Medsci 206 Laboratory Report 6: Human Nerve Conduction Velocity
- To enter the EMG and detect the alterations in the recording with different degrees of voluntary musculus contraction
- speeds of both the ulnar and the average nervousnesss that are located in the human forearm.
- To analyse and contrast illustrations of normal and unnatural nervus conductivity measurings
The currents that courses through our motor nerve cells, during the voluntary activation of our musculuss, generates an electrical signal that can be detected outside the activated musculus itself ( Kandel, Schwartz & A ; Jessell, 2000 ) .
Through observation of electromyographic activity, we are able to find the physiological activity that underlies muscle contraction. To make this, we use an EMG ; which uses simple electrodes that records the complex form of electrical potencies when placed over the surface of the overlying tegument ( Kandel, Schwartz & A ; Jessell, 2000 ) .
The currents that are noticed in our nervousnesss upon stimulation are known as action potencies ( Totara & A ; Derrickson, 2006 ) .
The finding factor of whether an action potency occurs is the gap of voltage-gated Na channels, which itself is, in bend, dependent on the initial depolarisation of cell ; normally a specific ‘threshold ‘ stimulation is required before gap of the Na channels can happen ( Totara & A ; Derrickson, 2006 ) . Once these channels are opened, an copiousness of Na ions will deluge into the cell. The happening of this terrible depolarisation that consequences from the inflow of Na ions is synonymous with the happening of an action potency. However, we must observe that there is a clear difference between an action potency in a individual nerve cell and the compound nervus action potency. In the action potency of a individual nerve cell, the action potency recorded is representative of the depolarisation of a individual nerve cell entirely. However, as a compound nervus consists of multiple nerve cells, the ensuing action potency recorded represents the figure of nerve cells that are active when stimulation was applied which is, basically, the accrued consequence of multiple action potencies ( Kandel, Schwartz & A ; Jessell, 2000 ) . The larger the action potency, the more nerve cells were depolarized sufficiently to threshold value for an action potency to happen ( Kandel, Schwartz & A ; Jessell, 2000 ) . In our experiments, as we did non insulate one nerve cell but observed the musculus as a whole, the action potencies recorded represent the compound nervus action potency.
The two nervousnesss that will be capable to our experiment are the ulnar nervus and the average nervus. The ulnar nervus can be found on the arm merely anterior of the tricep, ramifying off the median chord of the brachial rete ( Elizaga 1998 ) . Besides ramifying off the brachial rete is the average nervus which, down the radial portion of the forearm and via the carpal tunnel of the carpus, innervates the sidelong musculuss of the thenar of the manus ( Totara & A ; Derrickson, 2006 ) .
The obtained the compound musculus action potency, combined with the cognition of the physiology of neuromuscular activity, can supply penetration on the abnormalcies of nervus map. The chief usage of nervus conductivity surveies is to find the presence in neuropathies in patients ( Oh, 2002 ) . The many variables, such as latency or conductivity speed, that are identified in nervus conductivity surveies allow specific penetration in the exact mistake with the nervus depending on which variables is or is non unnatural. This farther allows the designation of the pathophysiological nature of the neuropathy ( Oh, 2002 ) .
Measurement of the Voluntary EMG:
- The tegument was prepared for adhesion with electrodes by cleaning with intoxicant and lightly scouring with emery paper.
- The recording electrodes were so applied. The active electrode ( negative ) was placed over the hypothenar musculuss, which are located at the lateral-dorsal boundary line. We were careful that the electrode was placed over the country where there is maximal concentration of end-plates as it was there that the initial possible alteration is negative and the amplitude of the musculus action potency is optimal.
- The mention electrode ( positive ) was placed over a sinew that is located merely distal to the 5th metacarpal-phalangeal articulation ; on the sidelong surface of the 5th figure.
- The land electrode was steadfastly attached to the dorsum of the manus at the back of the carpus.
- Once the electrodes are in topographic point, recording, utilizing the ‘Scope version 5 ‘ package, may get down. The first recording was used merely to find the truth of which the electrodes were attached. This, therefore, represented the musculus in its resting province.
- Measure 5 was so repeated for different strengths of musculus contraction. The degrees of strength are little, medium and maximum force. Small force can be applied by utilizing the little finger finger to defy against a weight, medium force is to be generated against a heavier weight and maximum force can be generated by trying to raise against a weight that is forcing down against the finger. We were careful that the contraction is sustained for a certain period of clip.
Measurement of Nerve Conduction Velocity:
- Ensure that the apparatus of the recording and land electrodes are as were used in the measuring of the voluntary EMG.
- The stimulating electrodes were so placed over the ulnar nervus or the average nervus, depending on which we wished to experiment on. The anode was placed proximal to the cathode which was placed straight over the nervus.
- Get downing with a weak stimulation ( 10 mA current ) we delivered a brief pulsation. We increased the current until a CMAP was recorded. If no CMAP was recorded beyond a current of 40 mas, we made the premise that the exciting electrodes were non right placed. If so, we repositioned the stimulating electrode and repeated this measure. We made certain that the topic ‘s arm was relaxed and the handheld exciting electrode was pressed steadfastly against the nervus.
- With a CMAP recorded, we have established the threshold stimulation. We continued increasing the current in a bit-by-bit manner until the amplitude of the CMAP did non increase which, therefore, indicated that the supramaximal stimulation has been reached
- We repeated stairss 3 and 4 for the staying nervus ( the nervus that was non stimulated in measure 2 )
- We repeated stairss 3 and 4 for each nervus at a different site of stimulation ; at a different distance from the entering electrodes.
Calculation of Speeds:
V=distance / time= ( ( distance at site 1- distance of site 2 ) x10^-2 ) ) / ( ( mean latency at site 1/ mean latency at site 2 ) x10^-3 ) )
Speed of Ulnar nerve= ( ( 26.5-10.7 ) x10^-2 ) ) / ( ( 7.28-3.1 ) x10^-3 ) ) = 50.97 ms^-1
Speed of Median nerve= ( ( 24.5-10.5 ) x10^-2 ) ) / ( ( 9.7-6.7 ) x10^-3 ) = 35.00ms^-1
The consequences obtained from Part A of our experiments ( Graph 1 ) , where we collated informations for different strengths of sustained muscular contraction, are an expected consequence ; accurately stand foring the underlying physiology behind the contraction of such musculuss.
A musculus is composed of 100s to 1000s of cells known as musculus fibers ( Totara & A ; Derrickson, 2006 ) and a motor unit consists of a motor nerve cell and the musculus fibers innervated by that nerve cell ( Kandel, Schwartz & A ; Jessell, 2000 ) . Knowing this, it becomes clear that the sum of force generated by a musculus is dependent on the figure of motor units recruited and active at any one clip ( Purves et al, 2008 ) . As, in Part A of our experiment, we are mensurating the electromotive force through a musculus, the figure of motor units active during the use of this musculus would straight impact the electromotive force end product measured by the recording electrodes. With more motor units utilised, more nerve urges from bodily motor nerve cells would be expected to happen, ensuing in an addition in the figure of musculus fibers stimulated in a musculus ( Totara & A ; Derrickson, 2006 ) . Our consequences followed this described map ( Graph 2 ) as there is an discernible correlativity between the strength of contractile force applied by the experimental topic and the size of the electromotive force measured by the recording electrodes. At maximum sustained contraction, we observed the largest electromotive force end product which exceeded 2 mVs whereas, when the musculus was in its relaxed province, the lowest electromotive force end product was obtained ; hardly any electromotive force was recorded as no motor units were active. As we experimented with sustained contraction, the frequence remained changeless throughout all strengths of muscular contraction.
The CMAP obtained from Part B of our experiments besides represented the physiological mechanisms involved in musculus contraction. First, we can see that musculus action potencies display an ‘all-or-none ‘ response. This is clearly seen in our consequences ( Tables 1, 2, 3 & A ; 4 ) , where stimulation at certain, lower, amperages provoked no response from a musculus whereas stimulation at higher, specific amperages was able to bring on a response. This is because a certain degree of depolarisation ( known as a threshold ) must be reached before the electromotive force gated Na channels will open ( Totara & A ; Derrickson, 2006 ) . Some of the lower currents did non do sufficient depolarization and ( Tables 1, 2, 3 & A ; 4 ) , as the threshold was non reached, no action potency occurred.
It was besides noticed that, upon stimulation with larger currents, the electromotive force end product recorded from the musculus increased. This consequence can be attributed to the all-or-nothing response in combination with the variable size of motor nerve cells. As smaller motor nerve cells have a smaller surface country, it hence has a higher overall opposition ( Kandel, Schwartz & A ; Jessell, 2000 ) . And, harmonizing to Ohm ‘s jurisprudence ( V=IR ) , with a higher opposition, a specific current that is applied to a smaller motor nerve cell would bring forth a larger electromotive force than if that same current was applied to a larger motor nerve cell with a smaller surface country ( which, accordingly, has a lower overall opposition ) . Knowing this, it becomes clear that, at some degrees of stimulation, smaller nerve cells would be recruited whilst larger nerve cells would stay inactive. At Supramaximal stimulation, the current applied is sufficient to let all nerve cells of all sizes to depolarise to threshold stimulation and go activated. Therefore, at currents larger than Supramaximal stimulation, the amplitude of CMAP is no larger than those ensuing from Supramaximal stimulation as there are no more nerve cells, of any size, to be activated. The physiology described above applies to both the average nervus and the ulnar nervus ; both nervousnesss displayed similar consequences with respect to both the ‘all-or-none ‘ response and the constructs of threshold and supramaximal stimulation.
The truth of our experiment and the information resulting is, nevertheless, questionable. With respects to our experimental process, it was non the most precise of methods and the usage of such methods could halter the truth of our consequences. For illustration, the placement of the stimulating electrodes is important. If the stimulating electrode is non straight over the nervus, the current produced by the electrode will non be transferred wholly to the nervus. Thus, though the device indicates that, for illustration, 30 milliamps ( Table 3 ) was applied ; if merely 10 of the 30 milliamps reached the nervus due to hapless placement, we would wrongly presume that 30 milliamps was applied alternatively of 10milliamps.
This could explicate why, despite experimenting on the same nervus, the threshold and supramaximal stimulation differs between the different sites ( Tables 3 & A ; 4 ) . It is wholly possible that 10 milliamps was all that was required for threshold to be reached but we falsely believed that 30 milliamps was required due to faulty placement ( Tables 3 & A ; 4 ) . This theory can be farther supported by our consequences which show that, in both the median and the ulnar nervus, the threshold stimulation required was at a lower current at the 2nd site of stimulation, near the carpus, compared to the 1st site of stimulation, near the cubitus ( Tables 1, 2, 3 & A ; 4 ) . As the country near the carpus is smaller than near the cubitus, the opportunities of ill positioning the stimulating electrode is less likely and, therefore, more likely that most of the current applied reaches the nervus which, accordingly consequences in an seemingly lower current required for threshold at the 2nd site relation to the 1st site. The lone consequence that should differ between the two sites is the latency. With a greater distance to the recording electrodes the latency would, logically, be longer. The conductivity speed through the nervus and the stimulus strength required for both threshold and supramaximal should be the same for the same nervus ( Totara & A ; Derrickson, 2006 ) . Major differences within/between these consequences are declarative of faulty or inaccurate experimental process.
If we are to look at the category informations ( Table 5 ) the bulk of the obtained consequences lie within the normal values for the conductivity speeds of both the ulnar ( 50-80ms^-1 ) ( Schubert, 1964 ) and average nervus ( 45-70ms^-1 ) ( Kandel, Schwartz & A ; Jessell, 2000 ) . Between topics, there are differences present in the resulting conductivity speeds, but non to an dismaying grade. The differences in obtained consequences can be attributed to the expected differences between persons. For illustration, the differences between the organic structure temperatures of experimental topics could ensue in 1 to 2 metres per 2nd difference per grade of temperature ( Kandel, Schwartz & A ; Jessell, 2000 ) . Furthermore, non all topics used their dominant manus in the experiment ; it is known that the conductivity speeds in the nervousnesss of the dominant manus differ to that of the non-dominant manus ( Kandel, Schwartz & A ; Jessell, 2000 ) . A few more factors to be considered is age ( Norris, Shock & A ; Wagman, 1953 ) , use of temperamental equipment in experimental processs and perchance even merely mistakes in measuring.
Analysis of Clinical Motor Study:
- ( ( 25.5-5.5 ) x 10^-2 ) / ( ( 5.2-2.4 ) x 10^-3 ) = 71.4286 ms^-1
- ( ( 36.8-5.5 ) x10^-2 ) / ( ( 6.9-2.4 ) x 10^-3 ) = 69.5556ms^-1
Median Motor Study – Convention
- ( ( 32.5-6.0 ) x 10^-2 ) / ( ( 7.3-2.8 ) x 10^-3 ) = 58.8889ms^-1
Ulnar Motor Study – Convention
Ulnar Motor Study – Abnormal
- The clip base for this recording is 50 msecs, which differs from the clip base of the old Ulnar Nerve recording of 20 msecs.
- The morphology of this CMAP is rather jagged as oppose to the usual smooth curve observed in normal patients. Furthermore, though non obvious visually, if we consider the difference in graduated table, we can that that the continuance of this action potency is far longer than that of a normal patient.
- Conduction Velocity= ( ( 26.2-5.2 ) x 10^-2 ) / ( ( 17.5- 5.7 ) x 10^-3 ) = 18.050 ms^-1. This conductivity speed is far slower than the expected conductivity speed of a normal patient. A likely cause for this is that harm has occurred to the myelin sheaths of the nervus. By moving as an electric dielectric, the myelination of nerve cells can greatly increase conductivity speed ( Purves et al, 2008 ) therefore ; it logically follows that conductivity speeds will be decreased in the absence or harm of these myelin sheaths. It has been observed in mice that have shortages in the cistron look of the protein proteolipids that make myelin sheaths, the conductivity speeds of nervousnesss that contain these defective sheaths are decreased ( Tanaka et al, 2009 ) .
Median Nerve Motor Study – Abnormal
- The latency to section 1 is 9 msecs. This is approximately 3 times longer than that of a normal survey.
- Conduction Velocity = ( ( 29.5-6.5 ) x10^-2 ) / ( ( 12.7-8.6 ) x10^-3 ) = 56.09756 ms^-1
- As the conductivity speed lies within the expected value, we can presume that there is no mistake with the carry oning ability of the nerve cell. The abnormalcy seems to shack in the significantly long latency period. As mentioned earlier, a cardinal constituent that contributes to the latency period is the clip taken for the neuromuscular transmittal of chemicals. Therefore, a longer latency period ensuing from two motor surveies of equal distances, given that conductivity speed is more or less the same, indicates that possibly there is an mistake in the neuromuscular transmittal of chemicals. Therefore, a possible cause of this abnormalcy might be Lambert-Eaton myasthenic syndrome, where acetylcholine release is hampered due the suppression of the electromotive force gated Ca channels in the pre-synaptic membrane ( Newson-Davis J, 2004 ) . With less acetylcholine released, sufficient depolarisation to threshold would take longer if it even occurs at all and, therefore, we will see a significantly larger latency period.
Furthermore, we notice that the amplitude of the unnatural average nervus is about merely a 3rd of that seen in a normal average nervus. This is provides more weight to the possibility of Lambert-Eaton Myasthenic syndrome as, with a shortage in acetylcholine release, nerve cells with a higher depolarisation threshold would non be depolarized sufficiently to be stimulated. With less nerve cells active when stimulation is applied, and, since we ‘re mensurating compound nervus action potency, the amplitude would be expected to be lower.
Through our experiments, we were able to accurately enter an EMG during voluntary musculus contraction and besides accurately find the conductivity speed of the ulnar and average nervousnesss in the forearm of a human topic. Overall, despite the fluctuations in obtained consequences, this experiment possessed sufficient truth as it reflected the consequence expected from the physiological mechanisms of musculus contraction and the actions of nervousnesss. The all-or-nothing response and the specificity of a threshold and a supramaximal stimulation are all features of neuromuscular action and were all observed in our consequences.
Tanaka H, Ma JM, Tanaka KF, Takao K, Komada M, Tanda K, Suzuki A, Ishibashi T, Baba H, Isa T, Shigemoto R, Ono K, Miyakawa T, Ikenaka K ( July 2009 ) Mice with Altered Myelin Proteolipid Protein Gene Expression Display Cognitive Deficits Accompanied by Abnormal Neuron-Glia Interactions and Decreased Conduction Velocities, Journal of Neuroscience Volume 29, Issue 26, Pages 8363-8371
Newson-Davis J ( February 2004 ) Lambert-Eaton Myasthenic syndrome Rev. Neurol. ( Paris ) Volume: 160, Issue 2, Pages 177-180
Norris, A. H. , Shock, N. W. , Wagman I. H. ( 1953 ) Age Changes in the Maximum Conduction Velocity of Motor Fibers of Human Ulnar Nerves. Journal of Applied Physiology, Volume: 5, Issue 10, Pages 589-593.
Elizaga, A. , M. ( 1998 ) . Illustrated Notes in Regional Anesthesia ( October 1998 )
Oh, S. , J. ( 2002 ) . Clinical Electromyography: Nerve Conduction Studies, pp. 1-20
Derrickson, Bryan. Tortara, Gerard J. ( 2006 ) Principles of Anatomy and Physiology 11th Edition
Kandell, Eric R. Schwartz, James H. Jessell, Thomas M. ( 2000 ) Principles of Neuroscience 4th Edition
Purves, Dale et Al ( 2008 ) Neuroscience 4th Edition
Cite this Human Nerve Conduction Velocity
Human Nerve Conduction Velocity. (2017, Jul 20). Retrieved from https://graduateway.com/human-nerve-conduction-velocity/