Nerve Compound Action Potential Amplitude Research Articles

In Vivo Efficacy of a Novel, Sutureless Coaptation Device for Repairing Peripheral Nerve Defects.

Although microsuture neurorrhaphy is the accepted clinical standard treatment for severed peripheral nerves, this technique requires microsurgical proficiency and still often fails to provide adequate nerve approximation for effective regeneration. Entubulation utilizing commercially available conduits may enhance the technical quality of the nerve coaptation and potentially provide a proregenerative microenvironment, but still requires precise suture placement. We developed a sutureless nerve coaptation device, Nerve Tape®, that utilizes Nitinol microhooks embedded within a porcine small intestinal submucosa backing. These tiny microhooks engage the outer epineurium of the nerve, while the backing wraps the coaptation to provide a stable, entubulated repair. In this study, we examine the impact of Nerve Tape on nerve tissue and axonal regeneration, compared with repairs performed with commercially available conduit-assisted or microsuture-only repairs. Eighteen male New Zealand white rabbits underwent a tibial nerve transection, immediately repaired with (1) Nerve Tape, (2) conduit plus anchoring sutures, or (3) four 9-0 nylon epineurial microsutures. At 16 weeks postinjury, the nerves were re-exposed to test sensory and motor nerve conduction, measure target muscle weight and girth, and perform nerve tissue histology. Nerve conduction velocities in the Nerve Tape group were significantly better than both the microsuture and conduit groups, while nerve compound action potential amplitudes in the Nerve Tape group were significantly better than the conduit group only. Gross morphology, muscle characteristics, and axon histomorphometry were not statistically different between the three repair groups. In the rabbit tibial nerve repair model, Nerve Tape offers similar regeneration efficacy compared with conduit-assisted and microsuture-only repairs, suggesting minimal impact of microhooks on nerve tissue.

An invertebrate model in examining the effect of acute ferric iron exposure on proprioceptive neurons

Iron is an essential element for plant and animal life and is found in soil, fresh waters and marine waters. The Fe3+ ion is a vital prosthetic group and cofactor to mitochondrial electron transport complexes and numerous proteins involved in normal functioning. Despite its importance to life-sustaining processes, overexposure results in toxicity. For example, ferric iron (Fe3+) accumulation in the mammalian central nervous system is associated with various neurological disorders. Although current literature addresses the long-term effects of Fe3+ overload, fewer studies exist examining the effects of acute exposure. Using the blue crab (Callinectes sapidus), we investigate the effects of acute Fe3+ overload on proprioception within the propodite-dactylopodite (PD) nerve. For proprioceptive studies, 10- and 20-mM ferric chloride and ferric ammonium citrate solutions were used at 5- and 20- min exposure times. Exposure to 20 mM concentrations of ferric chloride and ferric ammonium citrate reduced excitability in proprioceptive neurons. Thus, Fe3+ likely blocks stretch-activated channels or voltage-gated Na+ channels. The depressive effects of Fe3+ are partly reversible following saline washout, indicating cells are not acutely damaged. Gadolinium (GdCl3, 1 and 10 mM) was used to examine the effects of an additional trivalent ion comparator. Gd3+ depressed PD nerve compound action potential amplitude while increasing the compound action potential duration. This study is relevant in demonstrating the dose-dependent effects of acute Fe3+ and Gd3+ exposure on proprioception and provides a model system to further investigate the mechanisms by which metals act on the nervous system.

Comparison of preseptal and pretarsal onabotulinum toxin an injection in patients with hemifacial spasm

Aim The aim of the present study was to evaluate the effects of different doses of onabotulinum toxin A on the amplitude and latency values of the blink reflex and facial nerve in the pretarsal and preseptal portions of the orbicularis oculi muscle in patients with hemifacial spasm. Materials and methods Thirty patients with hemifacial spasm were assigned in two equal groups: Pretarsal Group: Five units of onabotulinum toxin A were injected into each of 2 points of the pretarsal portion; Preseptal Group: Five units of onabotulinum toxin A was injected into 4 points of the preseptal portion. We compared the electromyographic features of the patients before and 5 weeks after botulinum toxin (BTX) injection. Results In comparison of pre- and post-treatment measurements of blink reflex amplitude responses, the decreases in R1 (p = 0.003), R2 (p < 0.001), and R2C amplitudes (p = 0.031) were found to be significant in the BTX injected side in the pretarsal group. In the comparison of pre- and post-treatment measurements of facial nerve compound action potential amplitude changes, decreases in the amplitudes of the BTX injected (ipsilateral), and uninjected (contralateral) side in the pretarsal group were found to be significant (p < 0.001 for both groups). Decreases in the amplitudes of the BTX injected, and uninjected side in the preseptal group were found to be significant (p < 0.001, and p = 0.008, respectively). Conclusion According to our hypothesis, the smaller amount of BTX applied to the pretarsal portion was found to be more effective than higher amount of BTX injected into the preseptal portion of the orbicularis oculi muscle.

Modulation of the muscle and nerve compound muscle action potential by evoked pain

Background and aimsTo our knowledge there are no studies that have examined the effects of the experimental pain on muscle fibre excitability as measured by the amplitudes of the potentials evoked by direct muscle stimulation (DMS) in a muscle at rest. We hypothesized that evoked pain can modulate the muscle compound action potential (CMAP) obtained by DMS possibly due to changes in muscle fibre excitability. MethodsPain was evoked by intramuscular infusion of hypertonic saline in 50 men. Ten control subjects were infused with isotonic saline. The infusions were given distal to the motor endplate region of the dominant brachial biceps muscle (BBM) in a double-blind manner. The nerve CMAP was obtained by stimulating the musculocutaneous nerve and recording from the BBM using surface-electrodes. Muscle CMAPs were obtained by direct muscle stimulation with subdermal electrodes placed subcutaneously in the distal third of the muscle. A stimuli–response curve of the amplitudes from muscle CMAP was obtained by stimulating from 10 to 90mA. ResultsThere was a decrease of the nerve CMAP amplitudes after infusion of isotonic saline (from 13.78mV to 12.16mV), p-value 0.0007 and of hypertonic saline (from 13.35mV to 10.85mV), p-value 0.0000. The percent decrease from before to after infusion was larger in the hypertonic saline group (19.37%) compared to the isotonic saline group (12.18%), p-value 0.025.There was a decrease of the amplitudes of the muscle CMAP after infusion of both isotonic (at 90mA from 13.84mV to 10.32mV, p value 0.001) and of hypertonic saline (at 90mA from 14.01mV to 8.19mV, p value 0.000). The percent decrease was larger in the hypertonic saline group compared to the isotonic saline group for all the stimulations intensities. At 90mA we saw a 42% decrease in the hypertonic saline group and 24.5% in the isotonic saline group, p value 0.005.There were no changes in conduction velocity. ConclusionWe found a larger amplitude decrease of the muscle and nerve potentials following hypertonic saline infusion compared with that of isotonic saline. We suggest that this deferential outcome of hypertonic saline on muscle CMAP may be linked to the nociceptive effect on muscle fibre membrane excitability. ImplicationsThe study supplies with some evidence of the peripheral effect of muscle pain. However, further trials with other nociceptive substances such as capsaicin should be performed.

Contributing factors to hearing of diabetic patients in an in-hospital education program

Conclusion: In patients with poorly controlled diabetes mellitus (DM), hearing disturbance was associated with renal dysfunction and diabetic neuropathy, represented by decreases in median nerve compound action potential amplitude. Methods: The evaluation was conducted using 43 subjects who were hospitalized for the purpose of DM education. The mean age was 58.1 years (range 21–82 years). The mean HbA1c was 9.5%. The mean DM duration was 11.0 years. Renal function, retina condition, and nerve conduction were evaluated in relation to DM complications (nephropathy, retinopathy, and neuropathy). Nerve conduction studies were used to obtain detailed information on the condition of the peripheral nerves. After otological inspection, pure-tone audiometry, auditory steady-state response (ASSR), and distortion-product otoacoustic emissions (DPOAEs) were measured. Stepwise multiple linear regression was used to analyze the results in the better ear and worse ear. Results: Decreases in median nerve compound action potential amplitude were associated with deterioration in pure-tone audiometry and ASSR. Diabetic neuropathy, creatinine clearance, diabetic nephropathy, and retinopathy were related to hearing in ASSR and/or DPOAEs.

Prevention and reversal of motor and sensory peripheral nerve conduction abnormalities in streptozotocin-diabetic rats by the prostacyclin analogue iloprost.

The effects of the prostacyclin analogue iloprost on nerve function were examined in streptozotocin-diabetic rats. Rats were treated either with iloprost from induction of diabetes over 2 months in a preventive experiment, or for 1 month following a 1 month untreated period of diabetes in a reversal experiment. One and 2 months untreated diabetic control, non-diabetic control, and iloprost-treated non-diabetic groups were also used. Diabetes of 1 month duration caused a 21% (P < 0.001) reduction in sciatic motor conduction velocity and a 14% (P < 0.001) deficit in saphenous sensory conduction. This was not significantly changed over a subsequent month without treatment. Diabetic rats given iloprost treatment in both preventive and reversal studies had motor and sensory conduction velocities not significantly different from those of non-diabetic controls, but greater than for untreated diabetes (P < 0.01). Iloprost treatment did not have a significant effect on nerve conduction in non-diabetic rats. The time taken for sciatic nerve compound action potential amplitude to be reduced by 80% under hypoxic conditions in vitro was progressively elevated by 19% and 57% after 1 and 2 months diabetes respectively. Iloprost treatment significantly attenuated this for both preventive (47%, P < 0.001) and reversal (50%, P < 0.001) studies. There was no effect on hypoxic resistance for non-diabetic rats. In the preventive group there was a 28% increase in sciatic nerve endoneurial capillary density (P < 0.001), a lesser effect (16%, P < 0.05) in the reversal group, and no effect in non-diabetic rats.(ABSTRACT TRUNCATED AT 250 WORDS)

Transient conduction block following acute peripheral nerve ischemia

We studied the effects of transient focal ischemia on the electrophysiologic function of rat sciatic nerves. Focal and generalized impairment of impulse conduction, measured by falling evoked muscle and nerve compound action potential amplitudes, occurred within 10 minutes of femoral artery occlusion. Conduction failure reached a nadir at 45-60 minutes and then improved to normal within 24 hours. Fastest motor and mixed nerve conduction velocities were reduced less than 15% of baseline values during the period of acute conduction block. There were no detectable morphological abnormalities at the site of conduction failure. Transient ischemia produces reversible conduction block without evident structural changes. The fall in amplitude without significant conduction slowing implies that slower conducting myelinated fibers are relatively more sensitive to the effect of acute ischemia.

Human sensory nerve compound action potential amplitude: variation with sex and finger circumference.

The amplitude of human, antidromic, sensory compound action potentials (CAP) recorded from median and ulnar digital nerves is greater in females than males. This sex difference is probably due entirely to females having digits of smaller circumference, resulting in digital nerves being closer to the recording ring electrode enclosing the digit. The negative linear correlation between CAP amplitude and circumference holds true for persons of the same sex.