Compound Nerve Action Potential Amplitude Research Articles

Computational models of compound nerve action potentials: Efficient filter-based methods to quantify effects of tissue conductivities, conduction distance, and nerve fiber parameters.

Peripheral nerve recordings can enhance the efficacy of neurostimulation therapies by providing a feedback signal to adjust stimulation settings for greater efficacy or reduced side effects. Computational models can accelerate the development of interfaces with high signal-to-noise ratio and selective recording. However, validation and tuning of model outputs against in vivo recordings remains computationally prohibitive due to the large number of fibers in a nerve. We designed and implemented highly efficient modeling methods for simulating electrically evoked compound nerve action potential (CNAP) signals. The method simulated a subset of fiber diameters present in the nerve using NEURON, interpolated action potential templates across fiber diameters, and filtered the templates with a weighting function derived from fiber-specific conduction velocity and electromagnetic reciprocity outputs of a volume conductor model. We applied the methods to simulate CNAPs from rat cervical vagus nerve. Brute force simulation of a rat vagal CNAP with all 1,759 myelinated and 13,283 unmyelinated fibers in NEURON required 286 and 15,860 CPU hours, respectively, while filtering interpolated templates required 30 and 38 seconds on a desktop computer while maintaining accuracy. Modeled CNAP amplitude could vary by over two orders of magnitude depending on tissue conductivities and cuff opening within experimentally relevant ranges. Conduction distance and fiber diameter distribution also strongly influenced the modeled CNAP amplitude, shape, and latency. Modeled and in vivo signals had comparable shape, amplitude, and latency for myelinated fibers but not for unmyelinated fibers. Highly efficient methods of modeling neural recordings quantified the large impact that tissue properties, conduction distance, and nerve fiber parameters have on CNAPs. These methods expand the computational accessibility of neural recording models, enable efficient model tuning for validation, and facilitate the design of novel recording interfaces for neurostimulation feedback and understanding physiological systems.

Relationship between Gravidity, Parity, and Neurophysiological Features in Carpal Tunnel Syndrome (CTS) Patients with a History of Pregnancy.

It is not yet clear if gravidity and parity have any relationships with the electrodiagnostic parameters of carpal tunnel syndrome (CTS). To determine whether there is a relationship between electrodiagnostic findings, gravidity, and parity number in CTS. Female patients over 18 years of age with CTS were included in this retrospective cohort study. The gravidity/parity number, median nerve compound muscle action potential (CMAP), and compound nerve action potential (CNAP) of the patients were analyzed. The two subgroups of the Boston carpal tunnel syndrome questionnaire (BCTSQ): The Symptom Severity Scale (SSS) and Functional Severity Scale (FSS) were applied to the patients. CTS patients were divided into two groups aged at first pregnancy ≤20 years and >20 years. One hundred and eight CTS extremities (seven right-sided CTS, three left-sided CTS, 49 bilateral CTS) of 59 patients were included. The median (interquartile range: 25%-75%) number of gravidity, parity, and abortion were 3 (2-5), 3 (2-4), and 0 (0-0), respectively. Right-sided CTS patients at the age of first pregnancy ≤20 years had higher BCTSQ-SSS/FSS scores and median nerve CMAP latency compared to patients at the age of first pregnancy >20 years (P = 0.029 for SSS; P = 0.042 for FSS; and P = 0.041 for CMAP latency). A negative correlation was found between the gravidity/parity numbers and median nerve CNAP/CMAP amplitudes (P = 0.028/0.031, r = -0.293/-0.289 for CNAP amplitude; and P = 0.006/0.035, r = -0.363/-0.283 for CMAP amplitude). Neurophysiological findings worsen as the number of gravidity and parity increase. Electrodiagnostic and clinical features of CTS may be worsening in females below 20 years at first pregnancy.

ANXIETY AND DEPRESSION IN TYPE 2 DIABETES MELLITUS: A STUDY INCLUDING NERVE CONDUCTION STUDY AND NEUROPATHIC PAIN

Objective: It is known that neuropathy, neuropathic pain and psychiatric disorders are associated with diabetes mellitus (DM). It was aimed to find out whether there is a relationship between nerve conduction study findings, neuropathic pain, depression and anxiety.
 
 Material and Methods: Type 2 DM patients that applied to our clinical neurophysiology laboratory between September 2021 and January 2022 were included in this study. Median, ulnar, sural, peroneal and posterior tibial nerve conduction studies were performed on the patients. Douleur Neuropathique 4 Questions (DN4) was applied to the patients to evaluate neuropathic pain. Hospital Anxiety and Depression Scale (HADS) was applied to the patients. Anxiety (HADS-A) and depression (HADS-S) scores, which are the two subsections of HADS, were included in the analysis.
 
 Results: Forty DM patients (27 males, 13 females) were included in the study. The mean age of the patients was 57.9±12.7 (min-max 23-83) years. The number of patients with neuropathic pain, polyneuropathy according to neurophysiological findings, abnormal HADS-A and HADS-D scores were 32 (80%), 23 (58%), 17 (43%), and 24 (60%), respectively. Neuropathic pain was present in 22 (96%) and 10 (59%) of the patients with and without polyneuropathy, respectively. Neuropathic pain was found in 22 (92%) patients with depression and 16 (63%) patients without depression (p=0.046). Among patients with neuropathic pain, compound nerve action potential amplitudes of median, ulnar and sural nerves were lower than those without neuropathic pain (p=0.011, p=0.027, p

Early Expression of MMP-9 Predicts Recovery of Tibialis Anterior after Sciatic Nerve Crush Injury.

Background:The purpose of this study was to assess the expression of molecular markers and epineural blood flow after differing degrees of nerve injury to identify potential tools to predict nerve recovery in a rat sciatic nerve model.Methods:A total of 72 rats were divided into nine groups. Each group was subjected to one of three crush injuries, created by applying one of three vascular clamps for 30 seconds. Vascularity was assessed with laser Doppler flowmetry before and after crush, and at nonsurvival surgery. Nonsurvival surgeries were performed 6 hours, 2 weeks, or 6 weeks later with nerve conduction studies and muscle strength testing. Expression of matrix metalloproteinase 9 (MMP-9) and matrix metalloproteinase 2 (MMP-2) in each nerve was quantified using with enzyme linked immunosorbent analysis.Results:Persistent hyperemia was noted in the zone of injury compared with baseline at 2 weeks and 6 weeks in the groups that displayed incomplete recovery. Expression of MMP-9 at 6 hours increased with increasing severity of crush and was inversely related to tibialis anterior muscle force recovery. The ratio of MMP-9:MMP-2 expression correlated well with recovery of compound nerve action potential amplitude at 6 weeks.Conclusions:Resolution of nerve hyperemia may correlate with nerve recovery from trauma, but early measures of nerve blood flow after injury are not prognostic of recovery. Ratio of MMP-9:MMP-2 expression 6 hours after injury correlates with recovery of compound nerve action potential at 6 weeks, while MMP-9 expression alone predicts tibialis anterior recovery. These findings together suggest that increased MMP-9 expression is a potentially useful marker of more severe nerve injury.

PHYSIOLOGICAL RESPONSE OF PERIPHERAL NERVE TO REPETITIVE COMPRESSION: A RABBIT EXPERIMENTAL MODEL

Objective: The objective of this study is to clarify the differences in physiological responses following the different modality of repetitive compressions versus continuous compression (CC) of the peripheral nerve. Methods: Thirty-two rabbits were used. Under anesthesia, four conditions of compression; CC, low-frequency release compression (LFR, one second release time every 30 s), high-frequency release compression (HFR, one second release time every 10 s), and high-frequency compression (HFC, one second compression time every 10 s) were each applied with 80[Formula: see text]mmHg of pressure for 90[Formula: see text]min to the sciatic nerve. Compound nerve action potential (CNAP) and nerve blood flow were evaluated from the beginning of compression to 90[Formula: see text]min after compression release. Endoneurial microvascular permeability was evaluated histologically. Results: During compression, the nerve blood flow and the amplitude of CNAP decreased for all four groups. There were significant delays in the recovery of the amplitude and nerve blood flow in the LFR and HFR groups compared to CC group ([Formula: see text]). Endoneurial edema was observed in the repetitive compression groups. Conclusions: Even if the overall compression time was short, the accumulation of repetitive compression-release cycles causes to delay the recovery of nerve physiological function with endoneurial edema.

Scalpel edge roughness affects post-transection peripheral nerve regeneration

BackgroundGentle and precise tissue dissection reduces collateral tissue damage and preserves its structural quality for optimizing healing. This is particularly true for peripheral nerve neurorrhaphy. Axon regeneration kinetics across the repair is dependent on the amount of intraneural fibrosis. The purpose of this study was to determine whether scalpel blade smoothness was a deterministic factor in the kinetics of postneurorrhaphy peripheral axon regeneration. MethodsScalpel transection of the saphenous nerve was performed in 18 female Hartley guinea pigs either by a standard #15 stainless steel scalpel blade or a highly polished version of the same blade. Compound nerve action potential recordings and histochemical assay of neurofilament density proximal and 1 cm distal to the site of nerve transection were quantified postneurorrhaphy at postoperative weeks 5, 9, and 12. ResultsThere was no action potential transmission observed in the distal axons immediately after neurorrhaphy. A substantial acceleration of axonal conduction recovery was observed in nerves transected with polished scalpel blades observed by high compound nerve action potential amplitudes at postneurorrhaphy weeks 5 and 9 (P < .05). In addition, an increased recovery of intra-axonal neurofilament density in nerves transected with polished scalpel blades was observed by postoperative week 5 (P < .05). ConclusionThe quality of the scalpel blade is an important determinate of postsurgical healing. Gentle handling of tissue matters.

Effects of microRNA-338 Transfection into Sciatic Nerve on Rats with Experimental Autoimmune Neuritis

Nerve demyelination or axonal lesions are characteristic of experimental autoimmune neuritis (EAN). Previous studies have demonstrated that microRNA-338 can regulate the differentiation and maturation of oligodendrocytes and Schwann cells and promote injured peripheral nerves in rats. In this study, we used microRNA-338 coded lentivirus vector (miR-338-LV) in a Lewis rat EAN model, in with the conjunction P0 peptide 180-199 which was injected into the footpads of animals to induce immunization. The clinical scores of miR-338-LV and intravenous immunoglobulin (IVIg) (positive drug) groups were significantly superior to those of untreated group at disease peak and disease plateau (p < 0.05). The nerve conduction velocity and the compound nerve action potential amplitude of miR-338-LV and IVIg groups increased significantly compared to those of the untreated group at disease peak (p < 0.01). At disease peak, myelin swelling, cavity formation, and lamellae separation showed improvement in miR-338-LV and IVIg groups compared to untreated group. S100 and NF200 expression in miR-338-LV and IVIg groups increased compared to that in untreated group. Iba1 and S100 co-expression in Schwann cells in miR-338-LV and IVIg groups decreased compared to that in untreated group, which was indicative of the reduced conversion of Schwann cells into inflammatory cells. Overall, miR-338-LV in sciatic nerves might improve neuromuscular function in EAN by inhibiting the conversion of Schwann cells into inflammatory cells.

Nerve conduction study of the association between glycemic variability and diabetes neuropathy

BackgroundIt remains unclear whether glycemic variability is related to diabetes microvascular disease, especially diabetes peripheral neuropathy (DPN). We investigated the association between glycemic variability and DPN with type 1 or 2 diabetes.MethodsForty patients (23 males and 17 females; aged 34–79 years) underwent continuous glucose monitoring (CGM) and a nerve conduction study (NCS). Glycemic variability was estimated by mean amplitude of glycemic excursions (MAGE) in CGM. DPN was quantitatively evaluated by NCS in the median, tibial, sural and medial plantar nerves.ResultsMAGE had a significantly positive correlation with disease duration and low-density lipoprotein cholesterol level (r = 0.462, p = 0.003; and r = 0.40, p = 0.011, respectively), and a significantly negative correlation with BMI and medial plantar compound nerve action potential amplitude (r = − 0.39, p = 0.012; and r = − 0.32, p = 0.042, respectively). Multivariate linear regression analysis with adjustment for clinical background showed that MAGE (β = − 0.49, p= 0.007) was independently associated with a higher risk of medial plantar neuropathy.ConclusionsGlycemic variability may be an independent risk factor for DPN.

Axonal excitability and conduction alterations caused by levobupivacaine in rat.

In this study, effects of the long-acting amide-type local anesthetic levobupivacaine on axonal conduction and excitability parameters of the rat sciatic nerve were thoroughly examined both in vitro and in vivo. In order to deduce its effects on isolated nerve conduction, compound nerve action potential (CNAP) recordings were performed using the suction method over sciatic nerves of Wistar rats before and after administration of 0.05 % (1.7 mmol L-1) levobupivacaine. Levobupivacaine caused complete CNAP area and amplitude depression by blocking conduction in a time-dependent manner. To assess the influence of levobupivacaine on in vivo excitability properties, threshold-tracking (TT) protocols were performed at sciatic nerves of rats injected with perineural 0.05 % (1.7 mmol L-1) levobupivacaine or vehicle alone. Charge-duration TT results revealed that levobupivacaine increases the rheobase and decreases the strength-duration time constant, suggesting interference of the anesthetic with the opening of Na+ channels. Twenty and 40 % threshold electrotonus curves were found for both groups to follow the same paths, suggesting no significant effect of levobupivacaine on K+ channels for either the fastest or relatively slow conducting fibers. Current-threshold relationship results revealed no significant effect on axonal rectifying channels. However, according to the results of the recovery cycle protocol yielding the pattern of excitability changes following the impulse, potential deviation was found in the recovery characteristics of Na+ channels from the absolute refractory period. Consequently, conduction blockage caused by levobupivacaine may not be due to the passive (capacitive) properties of axon or the conductance of potassium channels but to the decrease in sodium channel conductance.

Prevention of vincristine-induced peripheral neuropathy by genetic deletion of SARM1 in mice.

Peripheral polyneuropathy is a common and dose-limiting side effect of many important chemotherapeutic agents. Most such neuropathies are characterized by early axonal degeneration, yet therapies that inhibit this axonal destruction process do not currently exist. Recently, we and others discovered that genetic deletion of SARM1 (sterile alpha and TIR motif containing protein 1) dramatically protects axons from degeneration after axotomy in mice. This finding fuels hope that inhibition of SARM1 or its downstream components can be used therapeutically in patients threatened by axonal loss. However, axon loss in most neuropathies, including chemotherapy-induced peripheral neuropathy, is the result of subacute/chronic processes that may be regulated differently than the acute, one time insult of axotomy. Here we evaluate if genetic deletion of SARM1 decreases axonal degeneration in a mouse model of neuropathy induced by the chemotherapeutic agent vincristine. In wild-type mice, 4 weeks of twice-weekly intraperitoneal injections of 1.5 mg/kg vincristine cause pronounced mechanical and heat hyperalgesia, a significant decrease in tail compound nerve action potential amplitude, loss of intraepidermal nerve fibres and significant degeneration of myelinated axons in both the distal sural nerve and nerves of the toe. Neither the proximal sural nerve nor the motor tibial nerve exhibit axon loss. These findings are consistent with the development of a distal, sensory predominant axonal polyneuropathy that mimics vincristine-induced peripheral polyneuropathy in humans. Using the same regimen of vincristine treatment in SARM1 knockout mice, the development of mechanical and heat hyperalgesia is blocked and the loss in tail compound nerve action potential amplitude is prevented. Moreover, SARM1 knockout mice do not lose unmyelinated fibres in the skin or myelinated axons in the sural nerve and toe after vincristine. Hence, genetic deletion of SARM1 blocks the development of vincristine-induced peripheral polyneuropathy in mice. Our results reveal that subacute/chronic axon loss induced by vincristine occurs via a SARM1 mediated axonal destruction pathway, and that blocking this pathway prevents the development of vincristine-induced peripheral polyneuropathy. These findings, in conjunction with previous studies with axotomy and traumatic brain injury, establish SARM1 as the central determinant of a fundamental axonal degeneration pathway that is activated by diverse insults. We suggest that targeting SARM1 or its downstream effectors may be a viable therapeutic option to prevent vincristine-induced peripheral polyneuropathy and possibly other peripheral polyneuropathies.

Cordycepin Decreases Compound Action Potential Conduction of Frog Sciatic Nerve In Vitro Involving Ca (2+) -Dependent Mechanisms.

Cordycepin has been widely used in oriental countries to maintain health and improve physical performance. Compound nerve action potential (CNAP), which is critical in signal conduction in the peripheral nervous system, is necessary to regulate physical performance, including motor system physiological and pathological processes. Therefore, regulatory effects of cordycepin on CNAP conduction should be elucidated. In this study, the conduction ability of CNAP in isolated frog sciatic nerves was investigated. Results revealed that cordycepin significantly decreased CNAP amplitude and conductive velocity in a reversible and concentration-dependent manner. At 50 mg/L cordycepin, CNAP amplitude and conductive velocity decreased by 62.18 ± 8.06% and 57.34% ± 6.14% compared with the control amplitude and conductive velocity, respectively. However, the depressive action of cordycepin on amplitude and conductive velocity was not observed in Ca2+-free medium or in the presence of Ca2+ channel blockers (CdCl2/LaCl3). Pretreatment with L-type Ca2+ channel antagonist (nifedipine/deltiazem) also blocked cordycepin-induced responses; by contrast, T-type and P-type Ca2+ channel antagonists (Ni2+) failed to block such responses. Therefore, cordycepin decreased the conduction ability of CNAP in isolated frog sciatic nerves via L-type Ca2+ channel-dependent mechanism.

80. Neurophysiological evaluation of the ulnar nerve at the elbow

In clinical practice there are many neurophysiological evaluations of mononeuropathies of ulnar nerve at the elbow. Our aim was to determine the most highly sensitive nerve conduction studies for the ulnar nerve entrapment at the elbow. We evaluate ulnar and median nerve in 10 healthy subjects; we study latency, amplitude and conduction velocity of compound nerve action potential (CNAP) at 10 cm proximal medial epicondyle and motor nerve conduction velocity (mNCV) across the elbow recorded from adductor digiti minimi (ADM), first dorsal interosseous (FDI) and flexor carpi ulnaris (FCU) before and after anodal DC stimulation (2 mA, 20 min) at the elbow. Anodal nerve stimulation reduces ulnar CNAP amplitude by 27% (p = 0.0102) and mNCV recorded from FCU by 11% (p = 0.049) without any changes in median CNAP and ulnar mNCV recorded from ADM and FDI. Anodal DC stimulation induces a partial conduction block at the elbow; our findings suggest that evaluation of ulnar CNAP amplitude and mNCV recorded from FCU are the most sensitive electrophysiological variable to identify ulnar block at the elbow.

Sensory Nerve Conduction Studies in the Diagnosis of Diabetic Sensorimotor Polyneuropathy: Electrophysiological Features

[Purpose] To analyze the electrophysiological characteristics of diabetic sensorimotor polyneuropathy (DSPN), also known as DPN, and to determine sensitive indicators of the disease using sensory nerve conduction studies (SNCSs). [Methods] SNCSs of the median, ulnar, and sural nerve were performed on 120 patients diagnosed with DSPN and compared with those of 77 healthy controls. We performed analysis to detect abnormal conduction velocities and the distal amplitude of the compound nerve action potential (CNAP). In addition, we determined the optimal cut-off values for the diagnosis of DSPN. [Results] More severe abnormal nerve conduction was found in the lower limbs than in the upper limbs. The severity of the abnormal nerve conduction was more apparent in the distal CNAP amplitude than in the conduction velocity. [Conclusion] Our findings suggest that SNCSs of the lower limb nerve seem to be more sensitive at detecting DSPN than SNCSs of the upper limb. In particular, the sural nerve is the best indicator for the early detection of DSPN.

The characteristics of median nerve compound nerve action potential at different post injury and repair intervals and their correlation with nerve regeneration in rats

Objective To explore the characteristics of compound nerve action potential (CNAP) after rat median nerve transection and repair,and their correlation with neuromorphometry at various time points. Methods The median nerve was transected and sutured at mid-arm level. At various time points from 2 to 12 weeks postoperatively,CNAP recording was performed and the median nerve was harvested for morphological examination. Results CNAP could be recorded at 2 weeks after nerve repair. The CNAP amplitude,the area below the curve (Area) and conduction velocity (CV) of regenerated nerve were significantly lower than those of control group (P＜0.01). From 2 weeks to 6 weeks postoperatively,CNAP latency (Lat) was obviously longer than normal (P＜0.05). From 2 weeks to 8 weeks postoperatively,CNAP stimulus intensity (threshold intensity and the supramaximal stimulation intensity,THI and SSI) was significantly lower than that of the control group (P＜0.01). First peak amplitude (FPA),peak-peak amplitude (PPA),Area and CV of CNAP increased with time,while parameters such as Lat,THI and SSI decreased over time in regenerated median nerve. Regenerated axons could be seen at 2 weeks after nerve transection and repair. More and more regenerated axons were seen with the lapse of time. There was a strong positive correlation between CNAP amplitude and the number of myelinated nerve fibers,with a 0.953 correlation coefficient. Linear regression analysis revealed the existence of a linear relationship. The maturity of regenerated nerve at 8 weeks reflected by myelin sheath thickness was close to that of a normal median nerve. Conclusion CNAP recording is a valuable tool to evaluate the extent of early nerve regeneration after nerve suture repair. There might exist a linear relationship between CNAP amplitude of normal median nerve and the number of myelinated nerve fibers. CNAP parameters are inclined to stabilize and nerve myelin sheath maturation is close to normal 8 weeks postoperatively. Key words: Median nerve; Nerve regeneration; Compound nerve action potential

Evaluation of Na+/K+ pump function following repetitive activity in mouse peripheral nerve

After conduction of prolonged trains of impulses the increased Na+/K+ pump activity leads to hyperpolarization. The aim of this study was to develop a mouse model to investigate the Na+/K+ pump function in peripheral nerve by measuring the decrease in excitability during activity-dependent hyperpolarization. Acute electrophysiological investigations were carried out in seven adult mice. Nerve excitability was evaluated by tracking the change in threshold current after 5min of 100Hz stimulation of the tibial nerve at ankle. We developed a threshold tracking system that allowed us to follow several excitability measures simultaneously from the evoked plantar compound muscle action potential (CMAP) and sciatic compound nerve action potential (CNAP). Three minutes after repetitive supramaximal stimulation maximal CMAP and CNAP amplitudes recovered but the threshold was increased ∼40% for motor axons ∼34% for axons generating CNAP. The threshold recovered with a rate of 3.8%/minute that was similar for nerve and motor responses. By tracking the effect of polarizing currents we found evidence of activity dependent hyperpolarization, and our data suggest that the observed threshold change after repetitive stimulation of the mouse tibial nerve is an indicator of the Na+/K+ pump function in vivo. Evaluation of activity-dependent hyperpolarization may be an important indicator of axonal ability to cope with Na+ load.

Evaluation of sensory evoked potentials in Long Evans rats gestationally exposed to mercury (Hg0) vapor.

Mercury is known to alter neuronal function and has been shown to cross the placental barrier. These experiments were undertaken to examine if gestational exposure to mercury vapor (Hg(0)) would result in alterations in sensory neuronal function in adult offspring. Dams were exposed to 0 or 4 mg/m(3) Hg(0) for 2 h/day from gestational days 6-15. This exposure paradigm has been shown to approximate a maximal tolerated dose of Hg(0) for the dams. Between postnatal days 140-168, male and female offspring (one of each gender/dam) were examined using a battery of sensory evoked potentials. Peripheral nerve action potentials, nerve conduction velocity, somatosensory evoked responses (cortical and cerebellar), brainstem auditory evoked responses, pattern evoked potentials, and flash evoked potentials were quantified. Gestational exposure to 4 mg/m(3) Hg(0) did not significantly alter any of the evoked responses, although there was a suggestion of a decrease in compound nerve action potential (CNAP) amplitudes in male animals for the 3 mA stimulus condition. However, this possible change in CNAP amplitudes was not replicated in a second experiment. All evoked potentials exhibited predictable changes as the stimulus was modified. This shows conclusively that the evoked responses were under stimulus control, and that the study had sufficient statistical power to detect changes of these magnitudes. These results indicate that gestational exposure to 4 mg/m(3) Hg(0) did not result in changes in responses evoked from peripheral nerves, or the somatosensory, auditory, or visual modalities.

Sensitivity of isolated rat facial nerve to chemical hypoxia altered by glucose availability and phenytoin

Ischemic lesions are presumed to play a role in the pathology of many facial nerve disorders, such as Bell's palsy. The response of facial nerve to anaerobic stress has not been evaluated previously in an in vitro model. In the present study, the effects of a transient anaerobic stress on functional parameters and their recovery were assessed. Isolated extratemporal rat facial nerves were superfused with solutions containing either 5 or 25 mM d -glucose. In some of the experiments, 40 μM phenytoin was added. Amplitude of compound nerve action potential (CNAP), latency of CNAP and extracellular direct current potential (DC) were measured simultaneously during and after 40 min of chemical hypoxia, induced by the addition of cyanide (2 mM). Two general observations were made with high glucose concentrations in the bathing solution: (a) there was an initial resistance of CNAP amplitude and DC potential to anaerobic stress and (b) the recovery of the amplitude was slowed. DC potential showed less depolarising changes in high glucose. The post-anaerobic restoration of initial values of DC potential and latency of CNAP was diminished in high glucose solution. Addition of phenytoin prolonged signal propagation during hypoxia and accelerated post-hypoxic recovery in low glucose. However, in high glucose, phenytoin showed no significant effects. These findings indicate that the presence of high glucose influences the liability to hypoxia induced lesions in vitro. Membrane stabilising drugs could show a protective effect against hypoxic damage and need further evaluation. This could suggest that in vivo, e.g. in Bell's palsy, similar mechanisms of damage and protective possibilities may occur.

Waveform analysis of compound nerve action potentials: A computer simulation

A compound nerve action potential (CNAP) recorded from surface of the skin is composed of single nerve fiber action potentials propagating at various conduction velocities (CVs). Based on this assumption, we constructed two CNAPs simulating those at the digit elicited by stimulation of the median nerve at the wrist (CNAP-Wr) and the elbow (CNAP-El). Distribution of the nerve fiber CVs used for the simulation was estimated from actual recordings of 12 healthy subjects. Mean ratio of the CNAP amplitude (CNAP-WrCNAP-El) was 2.2, and that of the duration was 0.76. First, to analyze how CV distributions affect CNAP waveforms artificially in our computer program, we altered mean CV or standard deviation (SD) of the estimated distribution, and reconstructed CNAPs. Results indicated that as the mean CV was made slower, the ratio of the CNAP amplitude increased and that of the duration decreased. Similar changes of the ratios were also shown when the SD of the CV distribution was increased without changing the mean CV. Secondly, to make constructed CNAPs more similar to actual recordings, we added artificial noise to the constructed waves and had 11 electromyographers read onset and peak latencies. The average of maximum CVs calculated from the onset latencies of CNAPs-Wr was 62m/sec, and that from the latency difference between CNAPs-Wr and -El was 70m/sec. Both CVs were slower than the genuine maximum (77m/sec) given to the simulation program. The mean CV calculated from latency difference of the major positive peaks of the CNAPs was 62m/sec being close to the mode (62m/sec) or mean (60m/sec) value of the given distribution.

Electrophysiological diagnosis of interdigital neuropathy of the foot.

We have devised a method of sensory nerve conduction in the interdigital nerves of the foot using the near-nerve needle and signal averaging techniques. In 40 normal controls between the ages of 20 and 59, there was no difficulty in recording sensory compound nerve action potential (CNAP) in the various interdigital nerves. The amplitude of sensory CNAP ranged from 0.4-8.8 muV. The mean maximum nerve conduction velocities ranged from 33.3-40.5 M/second. In the group between 50-59 years old, nerve conduction changes due to aging were noted. In five patients with interdigital neuropathy (IDN) of the foot, a selective marked decrease in the amplitude of the CNAP in the involved interdigital nerve ("abnormal dip phenomenon") was the most characteristic electrophysiological finding. The present technique is capable of recording the sensory CNAPs in the interdigital nerves of the foot and confirming the diagnosis of IDN electrophysiologically.