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Measuring the Conduction Velocity of Median Motor Nerve Axons

2679 words (11 pages) Essay in Biology

18/05/20 Biology Reference this

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Introduction

Electromyograhy (EMG) is a technique used to measure “changes in electrical potential that result from the conduction of action potentials along motor units during muscle contraction”1. EMG activity (measured in mV) is linearly related to the force produced by muscles2 and so it is used as a diagnostic procedure to assess pathology affecting the anterior horn cell, plexus, nerve roots, neuromuscular junction, peripheral nerve, and the muscle3. Recordings are made with an electrode which is either inserted directly into the muscle (needle electrode) or applied to the skin (extracellular electromyography using surface electrodes)4 and electrical activity picked up by the electrodes is displayed on an oscilloscope screen in the form of waves (EMG)5. An audio-amplifier is also used so that the activity can be heard as well as seen5. This set-up is known as an electromyography machine (fig 1). From the waveform output (graph), conduction velocity, amplitude (which depends on the synchrony and number of action potentials) and duration of action potentials (reflecting the degree of temporal dispersion) are key measurements for the diagnosis of neuromuscular disorders3. Electrical signals can be measured using a monopolar arrangement (i.e. measuring at only one site) or a bipolar electrode arrangement (i.e. measuring at two different sites) coupled with a differential amplifier to “increase the amplitude of the difference signal between the two recording electrodes with respect to the reference electrode”6.

Working of an EMG machine

All these recordings are made after a stimulating bar, having an anode (positively charged) and cathode (negatively charged) at a fixed distance, is placed on the subject and stimulates the selected nerve3. The nerve depolarizes (is stimulated) underneath the cathode, and the resulting action potential travels along the nerve in the customary physiological direction (orthodromically) and opposite to the physiological direction (antidromically)3. It is recorded using the two recording electrodes from the EMG machine which are attached to the muscle fibre3 using an electrode paste for low-impedance electrode contact7. These measure the electromagnetic field (EMF) that is generated by action potentials7. The potential voltage difference between the two separate electrodes can be calculated in order to provide information about the ability of that muscle to respond to stimulation7.  To calculate nerve conduction velocity from an electromyogram the distance from the centre of the cathode also needs to be recorded.

In this experiment the nerve conduction velocity of the median motor nerve axons innervating the abductor pollicis brevis (APB) or thumb abductor muscles, as well as other muscles in the arm, forearm and hand was determined using extracellular (surface) electromyography. The median nerve was stimulated at the wrist and elbow and the electrical activity was recorded using electrode stickers and an isolated stimulator. Since the muscle was stimulated by depolarization of the median nerve at two distinct locations bipolar EMG was performed. Onset latency (explained below) and time taken from delivery of stimulus to recording in the EMG electrodes were measured and the nerve conduction velocity calculated.

The procedure used has been described below along with calculations involved in determining the nerve conduction velocity of median axons innervating the APB. Afterwards, the subject’s median motor nerve conduction velocity has been compared to the average velocity range.

Protocol and set-up

To measure nerve conduction velocity of the median motor nerve the Evoked EMG and Nerve conduction velocity protocol from Kuracloud was followed8. An isolated stimulator and disposable ECG electrode stickers (recording electrodes) were used to collect the data inputted into the Kuracloud system. The recording electrodes were attached to the thumb and the ‘earth strap’ secured around the forearm as depicted in fig 1 and fig 2. 

Checking equipment

Prior to beginning the experiment, the equipment was checked to ensure it was functioning correctly. The subject was asked to press their thumb and ring finger together as hard as they could, to see if any signal would be generated if the muscle was contracted. Two graphs were produced. Since no electrical activity was detected in the absence of muscle contraction, there was a flat line. Voluntary contraction resulted in voluntary an asynchronous burst of activity/staggered line around a constant voltage). Since electrical activity was detected only once muscle contraction began, it was concluded that the equipment was working correctly.

 

Measuring nerve conduction

First, the median nerve was located by dipping a bar in water and firmly pressing it on the subject’s wrist near their tendons of abductor pollicis longus. This was done to ensure the nerve was stimulated and the electrode did not move around during stimulation (fig 2). Pulses of 3.6mA were emitted from the stimulating bar on pressing “start”. At this point the subject experienced light tingling in their hand and all fingers. The amplitude was increased in order to produce a clear contraction of the APB muscle alone. The electrode was also moved laterally until only the thumb was twitching. The final position was marked on the subject’s skin with a pen (fig 3). Electrical activity from the APB muscle was recorded at the chosen amplitude and position (fig 4). The median nerve was also stimulated at the elbow as is done in bipolar EMGs. This eliminates electromagnetic noise that can interfere with the displayed wave. Other precautions to minimise noise included not having the mains cable and recording cable touch each other or any other bioelectric bodies. For this second recording the stimulating bar was placed on the lateral side of the tendon of the biceps bacchhii and the amplitude of ‘pulse’ was set to 11.2mA. Stronger external force was applied here as the nerve is deeper in this tissue. Once again, the electrode was shifted slightly until a clear stimulation of the subject’s APB muscle was observed i.e. the thumb twitched. The position was marked, and an electromyogram recorded (fig 5).

Fig 3: Points of stimulation marked on subject’s right arm with a pen.

Fig 4: Electromyograph of median motor nerve stimulated at the wrist. Start of action potential marked with orange line.

Data analysis and Results

Fig 5: Electromyograph of median motor nerve stimulated at the elbow.

Nerve conduction velocity

Evoked EMG readings at the wrist

“The time interval between the stimulus at 0ms (can be confirmed by presence of stimulus artefact at 0ms)  and the initiation of an evoked potential is known as onset latency”9. This is also the time it takes the impulse to travel from the stimulation point at the wrist to the recording electrode7 and “it reflects conduction speed along the fastest fibres”9. At the wrist it was recorded as 4.90ms. The point selected on the electromyogram can be seen (fig 4).

Additionally, the maximum amplitude of the subject’s response to median nerve stimulation at the wrist was recorded as 7.07mV in the Kuracloud program. Motor axon loss, a conduction block or incorrect electrode placement can result in low-amplitude of compound muscle action potential, apart from temporal dispersion (mentioned above).

Evoked EMG readings at the elbow

The onset latency of the subject’s median nerve stimulated at the elbow was recorded as 9.8ms and the amplitude was noted as 4.57mV (fig5) in Kuracloud.

Calculating nerve conduction velocity

An electromyogram shows the response of a particular muscle following nerve stimulation. This means that nerve latency and amplitude vary according to the point of nerve stimulation. Onset latency increases when the stimulation occurs farther away from the targeted muscle. However certain times do not change with stimulation location: the time taken for the current to reach the electrode and from there to stimulate the nerve, action potential propagation, time taken for neurotransmitters to be released, and the time for the electrical signal from the movement to be picked up by the equipment are the same at all stimulation locations. The distance between the marked stimulation sites (elbow and wrist), measured to be 320mm, was needed to calculate the median nerve conduction velocity of the subject. The nerve conduction velocity, calculated by diving the distance between the two sites by the difference in onset latencies at the elbow and wrist, was found to be 65.31m/s (see Table 1).

Table 1: Showing latencies at different points, which were used to calculate conduction velocity.

Discussion


The electromyograms (fig 4, fig 5) show the depolarisation and repolarisation of APB muscle fibres as the muscle contracts and the thumb ‘twitches’ following stimulation from an electrode. From this the subject’s median motor nerve conduction velocity was determined to be 65.31m/s. While this value varies between individuals, the accepted range for the normal median motor nerve conduction in healthy individuals is49.48m/s – 66.92m/s10. There might be slight variation in this figure due to age or height, which are negatively associated with nerve conduction velocity10,11 , but not due to gender11. Variation may also occur because of temperature or compression7. The subject in this experiment was 165cm tall, 19 years old and tested in a room of approximately 22⁰C. Low temperatures decrease nerve conduction velocity. The subject did not note any feeling of compression, and so it is thought that this did not affect the results. Given the subject’s profile, their nerve conduction velocity appears to be higher than the mean velocity of others in their age group (see ‘Young adult’ under ‘Age group’ in Table 2), however it is still considered to be in the global normal range mentioned above. It would be valuable to compare this value to that of other subjects tested under the same conditions (same temperature) to accurately assess if their conduction velocity is notably different from the group mean. Further trials also need to be conducted to determine if this result is consistent. It is important to note, that the ‘normal range’ values may have been taken at a different temperature as most nerve conduction velocity studies are carried out at 33⁰C – 34⁰C12. Hence, it is recommended that during future trials, the subject be maintained at this temperature to ensure comparable results. If the subject’s results are consistently high it is likely that their nerves are well myelinated and the diameters of their axons larger than average, such that leakage is prevented, and resistance is decreased within axons.

Table 2: Showing normal conduction velocity in axons of median motor nerves10.

Nerve conduction tests are traditionally used to non-quantitively13 test for  demyelination (caused by Guillan-Barrè syndrome) or axon loss (due to Friedrich’s ataxia) in large diameter axons, rather than the suspected pathology of the subject. This experiment tests the subjects median motor nerve; however, a variety of other peripheral nerves can also be tested: Sural sensory nerve, medial plantar nerve and the Ulnar sensory nerve14,15(for ‘normal’ velocities of different nerves see Table3). 

Table 3: Showing normal nerve conduction velocities of different nerves in healthy individuals

In Guillan – Barrè syndrome (GBS) the body’s immune system attacks parts of the peripheral nervous system and damages the myelin sheath surrounding axons. As a result, axons are exposed to damage16 and saltatory conduction is prevented, slowing down nerve conduction velocity. This causes muscle weakness and possible sensation changes as damaged nerves might pass on abnormal sensory signals from the body16. Studies have shown GBS to result in decreased amplitude and nerve conduction velocity17. This fall in amplitude is characteristic of a sub-type of GBS: acute motor axonal neuropathy, which is characterized by the immune system attacking the node of Ranvier instead of the Schwann cells making up the myelin sheath17.

Friedrich’s ataxia is an inherited disease which causes progressive nervous system damage which results in impaired muscle coordination18. The degradation of neuronal cell bodies and axons can be detected by a significant decrease in amplitude identified during nerve conduction studies. The nerve conduction velocity remains unchanged19.

References

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  14. 16 Ninds.nih.gov. (2019). Guillain-Barré Syndrome Fact Sheet | National Institute of Neurological Disorders and Stroke. [online] Available at: https://www.ninds.nih.gov/Disorders/Patient-Caregiver-Education/Fact-Sheets/Guillain-Barr%C3%A9-Syndrome-Fact-Sheet [Accessed 8 May 2019].
  15. 17 B. van den Berg, C. Walgaard, J. Drenthen, C. Fokke, B. C. Jacobs and P. A. van Doorn, Nat. Rev. Neurol., 2014, 10, 469-482 (DOI:10.1038/nrneurol.2014.121 [doi]).
  16. 18 Ninds.nih.gov. (2019). Friedreich Ataxia Fact Sheet | National Institute of Neurological Disorders and Stroke. [online] Available at: https://www.ninds.nih.gov/Disorders/Patient-Caregiver-Education/Fact-Sheets/Friedreichs-Ataxia-Fact-Sheet [Accessed 8 May 2019].
  17. 19 J. M. Peyronnard, L. Lapointe, J. P. Bouchard, A. Lamontagne, B. Lemieux and A. Barbeau, Canadian Journal of Neurological Sciences / Journal Canadien des Sciences Neurologiques, 1976, 3, 313-317 (DOI:10.1017/S0317167100025518).
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