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For an undergrad assignment I read a biology paper that mentioned the speed of nerve imuplses to be 440 km/h in myelinated fibers. However, our biology teacher told us that this reported conduction speed is not true. So my question is:
What is the actual speed of myelinated fibers?
A conduction velocity of 440 km/h is possible in thick, myelinated fibers. However, this number is probably more representative of the upper range of conduction velocities, rather than a conservative average.
First off, there are a heap of variables that affect neural conduction velocities (in myelinated fibers) in complex ways (Waxman, 1980), including but not limited to:
- axon diameter;
- myelin thickness;
- internode distance;
- axonal milieu;
- age of the subject.
Having said that, in humans myelinated, thin A-delta fibers the average conduction speed was established at 19 m/s (Gyberls et al, 1983), or 68 km/h. A range of pain-conducting fibers exist, with different diameters. As a result, they range in their conduction velocities from 0.5 m/s (2 km/h for thin C-type fibers) to 120 m/s (432 km/h for thick A-alpha type fibers).
Hence, the 440 km/h is certainly possible in thick myelinated fibers. Note I just highlighted pain-conducting fibers here as an example, and other classes of neurons may feature even faster conduction in their axons.
- Gybels et al., J Neurophysiol (1983); 49(1): 111-22
- Waxman, Muscle & Nerve (1980); 3(2): 141-50
Why are eye-foot and eye-hand reaction times different?
The brain controls your movement by sending nerve impulses down the nerves to the place in the body where movement is desired. The nerves are composed of nerve cells called neurons. Figure 1 shows a signal propagating from one neuron to another. Along the neurons the signal propagates by an electrical impulse which travels along the axon. The axon from one neuron does not touch the next neuron forming a gap called a synapse. The signal propagates across the synapse by chemical diffusion and causes the next neuron to ‘fire’ and send the signal electrically down its axon. The typical spacing of the synapse is about 20-30 nm  D.N. Wheatley, Diffusion theory, the cell and the synapse, Bio Systems 45 (1998) 151-163. . For an illustration see Ref.  http://upload.wikimedia.org/wikipedia/en/a/a6/Chemical_synapse_schema.jpg [2019-10-16]. .
The typical time it takes for a person to respond to a visual signal with their hands (for example pressing a button upon seeing a green light) is around 0.28 s  Journal of the American Optometric Association, 2000, vol. 71, no12, pp. 775-780 (32 ref.) . To respond with the feet takes longer, around 0.45 s  Journal of the American Optometric Association, 2000, vol. 71, no12, pp. 775-780 (32 ref.) . A portion of these reaction times is due to the brain processing the visual signal and initially sending out the signal to move. The remainder of the time is taken for the signal to travel down the nerves to the hands/feet. Assuming the same brain processing time in both circumstances the difference between the reaction times for the eye-hand and eye-foot reaction times is due to the difference in distance the signal has to travel from the brain to the hand or foot. Based on the times given and an approximation of distances between body parts we can calculate the average velocity that the signal propagates at.
The distance from your brain to your hands is approximately 1 meter, and from your brain to your feet is approximately 1.6 meters. The extra distance the nerve impulse has to travel to go to your feet is 0.6 m as compared to your hand. It takes (0.45 – 0.28) = 0.17s longer for the signal to reach your feet so the speed of the signal, vs propagating along the nerves is given by Eqn.1.
Note that this is an average speed of a signal traveling along one neuron. The actual time it takes for the signal to travel along the axon of one neuron can be greater than 25 m/s but to relay the signal to the next neuron across the synapse is about 1000 times slower  D.N. Wheatley, Diffusion theory, the cell and the synapse, Bio Systems 45 (1998) 151-163. .
The eye-foot reaction time is longer than the eye-hand reaction time due to the extra distance the nerve impulse has to travel. We calculated an approximate speed of signal propagation along the nerves to be 3.5 m/s. This is slower than the propagation of the signal along one neuron but takes into account that the signal must also cross the synapses by chemical diffusion.
When a neuron is not actively transmitting a nerve impulse, it is in a resting state, ready to transmit a nerve impulse. During the resting state, the sodium-potassium pump maintains a difference in charge across the cell membrane of the neuron. The sodium-potassium pump is a mechanism of active transport that moves sodium ions (Na+) out of cells and potassium ions (K+) into cells. The sodium-potassium pump moves both ions from areas of lower to higher concentration, using energy in ATP and carrier proteins in the cell membrane. The video below, “Sodium Potassium Pump” by Amoeba Sisters, describes in greater detail how the sodium-potassium pump works. Sodium is the principal ion in the fluid outside of cells, and potassium is the principal ion in the fluid inside of cells. These differences in concentration create an electrical gradient across the cell membrane, called resting potential . Tightly controlling membrane resting potential is critical for the transmission of nerve impulses.
Sodium Potassium Pump, Amoeba Sisters, 2020.
Neural Stimulation of a Muscle Fiber
Muscle fibers contract by the action of actin and myosin sliding past each other. The signal to initiate the contraction comes from the brain as a part of the somatic nervous system.
The illustration below is a schematic representation of the process from the arrival of a nerve signal to the terminal bundle of the nerve axon to the contration of a muscle fiber. The stimulation of muscle action is associated with the neurotransmitter chemical acetylcholine.
When the nerve signal from the somatic nerve system reaches the muscle cell, voltage-dependent calcium gates open to allow calcium to enter the axon terminal. This calcium moves the acetylcholine-containing miceles to fuse with the presynaptic membrane and release their acetylcholine into the synapse, where it is bound by acetylcholine receptors on the postsynaptic surface. The acetylcholine receptors are examples of ligand-gated ion channels: upon binding the acetylcholine molecule, they open up a channel for sodium and potassium ions to enter the cell. In this case acetylcholine is the "ligand" that opens the gate for sodium.
When the opening of the Na channels sends a rush of Na into the cell, which, if it is strong enough, causes nearby voltage-gated Na channels to open and produces an action potential. This action potential is not one in a nerve cell, but in the muscle cell.
The muscle fiber structure has lots of tubes called T-tubules or transverse tubules. When the action potential travels down these tubules, it eventually triggers the voltage-sensitive proteins that are linked to the calcium channels in the structure called the sarcoplasmic reticulum (Wiki) that surrounds the nerve fibers. This membrane-enclosed structure has similarities to the endoplasmic reticulum in other cells. In the rest state, the sarcoplasmic reticulum will have a reserved supply of calcium because its walls have many Ca pumps which use ATP energy to store calcium. With the stimulus of the action potential, calcium rushes into the cell and interacts with the actin. Associated with the actin are the troponin complex and the tropomyosin strand which block the binding of myosin. The supplied calcium ions bind to the troponin and pulls the "gaurding" troponin and tropomyosin strand away from the site where myosin can bind.
In order to bind to the actin, the myocin must have a supply of energy, which it obtains from ATP . Having absorbed energy from ATP, a unit of the myosin fiber will be in a stressed or high energy state, like a stretched spring. With the action of the calcium to withdraw the troponin and tropomyosin, the myosin structure can bind and use the energy to pull the actin fiber, shortening or contracting the muscle fiber.
While the contraction of a muscle can be repeated by following the above steps, there must be a pathway back to a rest state since you don't want your muscles to be in a permanently contracted state. Those mechanisms for return to rest are provided. The initial stimulus by the motor nerve which started the process is under conscious control, so you can decide to relax the muscle. The free acetylcholine in the synaptic gap is removed by another molecule, acetylcholinesterase. The calcium pumps in the sarcoplasmic reticulum work to reclaim the calcium, and upon removal of the calcium from the receptors on the muscle, the "bodygaurd" troponin and tropomyocin move back to their blocking positions. The myosin and actin fibers return to their relaxed state.
2 Potassium Channels Key to Fast Transmission of Impulses Along Myelin-rich Nerve Fibers, Study Shows
Two potassium ion channels located at gaps between segments of myelin are required for high frequency and high-speed conduction of electrical impulses along myelin-rich nerves, a study shows.
Loss of the workings of these potassium channels in what are called the nodes of Ranvier slowed nerve conduction, and impaired the sensory response of a rat. These findings suggest that similar problems with these channels may exist in people with multiple sclerosis (MS).
Myelin, the fat-rich substance that wraps around nerve fibers (axons), works to insulate and increase the velocity of the signals relayed by nerve cells. Gaps between segments of myelin, or nodes of Ranvier, also work to amplify these signals.
Nerve impulses must travel and arrive at relay points extremely quickly for effective connection and communication between brain regions.
Researchers at the University of Alabama at Birmingham (UAB) showed for the first time that the nodes of Ranvier have potassium channels that allow the myelinated nerves to propagate nerve impulses at very high frequencies, and with high conduction speeds. This is key for fast transmission of sensations and rapid muscle control in mammals.
The nodes of Ranvier were first discovered in 1878 by the French scientist Louis-Antoine Ranvier. Later research, dating from 1939, showed that they work as relay stations placed along myelinated nerves — about 1 millimeter apart — for proper conduction of nerve impulses at rates of 50 to 200 meters per second.
Between these nodes, the nerve is wrapped in myelin. When the nerve fires, the electrical impulse travels along the nerve (called action potential) from one node to the other at a speed 100 times faster than that of impulses in nerves lacking myelin.
Neuroscientists know that ions crossing the membrane of nerve cells are required to fire electrical impulses along nerves, but whether potassium ion channels were present in the nodes of Ranvier remained a matter of debate. No one had been able to use patch clamps — a technique that allows recording of whole-cell or single-ion channel currents flowing across membranes — to the nodes of the small intact nerves in mammals.
UAB researchers led by Jianguo Gu, PhD, worked with a rat and identified two ion channels, called TREK-1 and TRAAK, as the main potassium channels in the nodes of Ranvier of the rat’s myelinated nerve.
Most importantly, they showed these ion channels allow high-speed and high frequency conduction of nerve impulses along the myelinated afferent nerves — those carrying information from the sensory organs (like the eyes or skin) to the central nervous system (the brain and spinal cord). TREK-1 and TRAAK channels were highly enriched — 3,000 times higher — at the nodes of Ranvier in afferent nerves than in the nerve cell’s body.
When the scientists removed (knocked down) these channels, conduction speed in the rat’s nerve dropped by 50 percent, and the rat’s “aversion reaction” to its whisker being flicked was slower.
“TREK-1 and TRAAK are clustered at nodes of Ranvier of myelinated afferent nerves,” the researchers concluded, and “suppressing these channels retards nerve conduction and impairs sensory functions.”
Increasing evidence shows that dysfunction in the nodes of Ranvier are present in neurological diseases, including MS. Whether autoantibodies (antibodies that attack the body’s own tissues) target the TREK-1 and TRAAK to affect nerve conduction, leading to sensory and motor problems such as those seen in MS, remains to be investigated, Gu said in a UAB news release written by Jeff Hansen.
Peripheral Nervous System:
All our nerves are part of either the peripheral nervous system or the central nervous system. Most scientists classify the brain, spinal column, and the nerves associated with these masses of ganglia as part of the central nervous system. That leaves the peripheral nerves that control muscles, and our senses. These nerves make up the peripheral nervous system. The two major divisions of this system are the sensory division (nerves sending impulses from sensory organs) and the motor division (nerves controlling muscles).
It’s fairly easy to visualize nerves sending impulses to our muscles when we tell them to move. We move our fingers to type on the computer and we control where we walk. Yet, there are lots of muscles that are sent impulses without us even thinking about it. Muscles in our stomach move without use even knowing it. The motor division of the peripheral system also sends impulses to glands. We divide up the moto division into two classes – the autonomic nervous system and the somatic nervous system.
Somatic Nervous System:
The somatic nervous system consists of muscles that are controlled consciously. When we move our skeletal muscles we do this all consciously. Most of the time we have full control over our muscles. Only during times of stress might the nervous system take over. When you touch something hot for instance, its sometimes hard to stop yourself from pulling away. Your blinking reflex is another example. Try not blinking when you sneeze for instance.
Autonomic Nervous System:
The autonomic nervous system controls bodily functions that are not under conscious control. The movement of our digestive system would be part of this system. Most of the glands in our body are controlled by our nervous system yet we never know about it. The autonomic nervous system is further divided up into two more systems, the sympathetic nervous system and the parasympathetic nervous system. Just as a hang-glider controls his altitude by pushing or pulling on the bar in front of him, these two systems work to push and pull against each other, and thus maintain homeostasis. The control of heart rate is a classic example. The sympathetic nervous system increases heart rate and the parasympathetic nervous system decreases it. There are many other examples of how these two systems work in tandem, but the take home point is that both work together to help maintain equilibrium in the body.
The human boy has the ability to sense the environment and respond to it. We can sense chemicals in our food. They give us smells and tastes. Cells in the back of the eye respond to light and help us produce images of the world around us. Cells in the skin respond to pressure, and allow us to feel objects. Our ears allow us to detect sound waves and aid in our balance. Each of these systems is complex, but they all work because of mechanisms that send stimuli to our central nervous system. The following are but a few of the senses and sense organs that help send information to the brain.
- Touch – The Skin
- Smell – The Nose
- Taste – Taste Buds
- Hearing – The ear
- Sight – The Eye
Mechanism of Transmission of Nerve Impulse (explained with diagram)
All the nerve fibres carry information in the form of nerve impulse.
Nerve impulse is the sum total of physical and chemical disturbances created by a stimulus (electrical, chemical or mechanical) in a neuron or nerve fibre which result in the movement of a wave along the nerve fibre.
The nerve fibre or axon is like a cylinder, the interior of which is filled with axoplasm (i.e., the cytoplasm of the nerve cell) and the exterior of which is covered with a thin membrane, the axon membrane or axolemma.
The axon is immersed in the extracellular fluid (ECF). Through axolemma movement of solute takes place between the axoplasm and ECF. Generally the solutes in ECF and axoplasm are in ionic form. In the axoplasm -vely charged protein molecules are present which are neutralized due to the presence of large amount of K + ions. In the ECF (outside the axon) the -vely charged CI – ions are neutralized by the presence of +vely charged Na + ions.
Conduction of nerve impulse is an electro-chemical process. Membrane of a non-conducting nerve cell or neuron is positive on the outside and negative inside. The difference in charge is about 70 to 90 millivolts which is called as resting potential and the membrane is said to be polarized. To maintain resting potential, sodium potassium metabolic pump operates.
This pump which is located on the axon membrane pump Na + from axoplasm to ECF and K + from ECF to axoplasm. It pumps more positive charges (3 Na + ) from axoplasm to ECF than in the reverse direction (2K + ), and is run by an enzyme called Sodium Potassium-ATPase. The concentration of sodium ions will be about 14 times more in ECF (outside) and concentration of potassium ions will be about 28-30 times more in axoplasm (inside).
When a stimulus (may be mechanical, electrical or chemical) is applied to the membrane of the nerve fibre, its permeability changes and sodium potassium pump stop operating. Sodium ions rush inside and potassium ions rush outside. This results in the positive charge inside and negative charge outside.
The nerve fibre is said to be in action potential or depolarized. The resting potential inside the membrane is about -70 mV and the action potential inside the membrane is about +30 mV. The travelling of action potential along the membrane is a nerve impulse. After a period of action potential, again sodium pump operates and axon membrane will get resting potential by repolarization.
During this process the sodium ions will rush outside and potassium ions will move inside (reversal of the process taken place during action potential). Refractory period is the period of complete inexcitibility (restoration of nerve fibre) between deplorization and repolarization (1-6 milli seconds in mammals). During refractory period nerve fibre never transmits impulse.
In medullated nerve fibres (white fibres), the impulse jumps from node to node, it is called saltatory propagation (Fig. 1.21). It increases the speed of nerve impulse which is about 20 times faster in medulated than in non-medullated nerve fibres. The speed of transmission of nerve impulse also depends upon the diameter of the fibre. Fibres with larger diameter conduct impulse faster.
The velocity of conduction of nerve impulse in frog is 30 metres per second and that of mammal is 120 metres per second. The threshold value of any nerve fibre is the minimum strength of stimulus which initiates action potential in that nerve fibre.
Why myelinated mammalian nerves are fast and allow high frequency
University of Alabama at Birmingham researchers, for the first time ever, have achieved patch-clamp studies of an elusive part of mammalian myelinated nerves called the Nodes of Ranvier. At the nodes, they found unexpected potassium channels that give the myelinated nerve the ability to propagate nerve impulses at very high frequencies and with high conduction speeds along the nerve. Both qualities are necessary for fast conduction of sensations and rapid muscle control in mammals -- keys to an animal's survival in a predator-prey world.
Discovered by French scientist Louis-Antoine Ranvier in 1878, these tiny nodes have been known since 1939 to act like relay stations placed about 1 millimeter apart along the myelinated nerve to conduct mammalian nerve impulses at rates of 50 to 200 meters per second. Between each bare node, the nerve is wrapped with insulating sheaths of myelin. When the nerve fires, the electrical impulse hops from one node to the next, moving 100-times faster than the nerve impulse of an unmyelinated nerve. Neuroscientists have long known that release and uptake of ions at the nerve cell membrane is the mechanism of electrical nerve impulses. But whether any potassium ion channels were present in the Nodes of Ranvier -- and if so, what type -- has been a matter of debate for decades because no one had been able to successfully apply patch clamps to the 1 to 2 micron-wide nodes of intact nerves in mammals.
In a study published in the Cell Press journal Neuron, Jianguo Gu, Ph.D., his postdoctoral fellow Hirosato Kanda, Ph.D., and other colleagues at UAB report that two ion channels called TREK-1 and TRAAK act as the principal potassium channels in the Nodes of Ranvier of a rat myelinated nerve. More importantly, they showed that those two channels at the Nodes of Ranvier were required for high-speed and high-frequency saltatory, or "hopping," conduction along myelinated afferent nerves. Knockdown of the channels reduced nerve conduction speed by 50 percent, and behavioral experiments showed that knockdown in the nerve reduced a rat's aversive reaction to a flick of its whisker.
In the classic experiments that led to a Nobel Prize in 1963 for the nerve impulse mechanism, nerves used a voltage-gated potassium channel (meaning a change in voltage makes it fire) to release potassium ions from an unmyelinated squid giant nerve. Gu and his colleagues initially expected to find such channels at the Nodes of Ranvier.
However, their earliest experiments confounded that expectation -- so much so that they dropped the study for a year. When they added known inhibitors of voltage-gated potassium channels, they saw no significant decrease in the electrical spikes at the Node of Ranvier. That finding challenged dogma, and it meant some other unidentified potassium channel or channels instead were serving as the workhorses at each node.
Possible candidates included three members of a family of 15 proteins known as "leak" potassium channels, which are constitutively open rather than voltage-gated and were known to have large conductance, says Gu, the Edward A. Ernst, M.D., Endowed Professor and director for pain research in the UAB Department of Anesthesiology and Perioperative Medicine's Division of Molecular and Translational Biomedicine. Gu's lab found that two of them, TREK-1 and TRAAK, are the active channels in the Nodes of Ranvier. Their tests to show this included the pressure-patch-clamp recording technique the researchers developed for the nodes, along with immunohistochemical, genetic and pharmacological approaches.
Furthermore, the UAB team found that TREK-1 and TRAAK -- which are thermosensitive and mechanosensitive two-pore-domain potassium channels -- are highly clustered at the nodes of the rat trigeminal A-beta nerve, with a current density that is 3,000-fold higher than that of the cell body.
Leak potassium channels and voltage-gated potassium channels act to repolarize the nerve membrane after a nerve impulse, known as an action potential. TREK-1 and TRAAK in the Nodes of Ranvier acted quite differently from the voltage-gated potassium channels that are found in the cell body, or soma, of the rat nerve. During a stimulation of the soma at 50-times per second, the action potentials that use the voltage-gated potassium channels typically failed. But Gu and colleagues found that action potentials at the Nodes of Ranvier with the "leak" channels showed no significant failures at stimulation frequencies up to 200-times per second.
In other words, the two leak potassium channels allowed very rapid repolarization at the Nodes of Ranvier, and high frequency as well as rapid conductance of the myelinated rat nerves. Interestingly, the TREK-1 and TRAAK two-pore-domain potassium channels appeared to form heterodimers in the Nodes of Ranvier.
Gu says these new fundamental findings have implications in neurological diseases or conditions where nodal dysfunctions affect action potential conduction. These include carpal tunnel syndrome, Guillain-Barré syndrome, multiple sclerosis, spinal cord injuries and amyotrophic lateral sclerosis.
Predicting How Humans Estimate Speed
Psychologists at the University of Pennsylvania and the University of Texas at Austin have reversed this process. Operating more like physicists, they analyzed all of the steps involved in estimating how fast an object is moving, from light bouncing off the object, passing through the eye’s lens, hitting the retina and transmitting information to the brain through the optic nerve, in order to build an optimal model.
Such a model, that uses all the available information in the best way possible, is known as an “ideal observer.” They then tested this ideal observer model against people’s performance in a speed-estimation experiment.
That people are about as good as the optimal model at this task means that the neural mechanisms associated with speed estimation can be very precisely understood and predicted. It also suggests that engineers can similarly optimize technological applications that need to estimate the speed of a moving object, like cameras on a self-driving car, by mimicking biological systems.
Most previous studies of this aspect of visual processing used only artificial images. By employing small patches of natural images, the researchers’ model is more generally applicable to how speed estimation is accomplished in natural conditions in the real world.
The research was conducted by Johannes Burge, assistant professor in the Department of Psychology in Penn’s School of Arts and Sciences, and Wilson Geisler, professor and director of Center for Perceptual Systems at UT-Austin.
It was published in Nature Communications.
“There have been many descriptions of what visual systems do when estimating motion, but there have not been many predictions for how they should do it,” Burge said. “We use a best-case scenario as a starting point for understanding what the visual system actually does. If we get a close match between the performance of the ideal observer model and the performance of humans, then we have evidence that humans are using the visual information in the best way possible.”
The aspect of the visual system that Burge and Geisler set out to model was its ability to estimate the speed of images of objects in motion.
Because this ability is critical to survival, there was reason to believe that evolutionary pressures had selected for visual systems that make very accurate estimates.
Burge and Geisler began by modeling the individual steps involved in processing moving images, such as the optics of the eye’s lens, how the retina translates stimuli into nerve impulses and how the early visual cortex interprets them.
The main challenge was determining what features in stimuli are truly critical for the latter task. Different sensory neurons have different receptive fields, which determine the stimulus features that cause the neuron to fire a signal. For example, one neuron might fire when it senses a bright patch of an image moving from right to left but not from left to right. Another neuron might have the opposite arrangement, firing only in response to images with bright patches that move left to right.
“We determine the small population of these different types of receptive fields that best supports accurate motion estimation,” Burge said. “We argue that these receptive fields constitute the population of receptive fields that visual systems ought to have if they want to maximize the accuracy of estimates of motion.”
By combining the receptive fields with the well-understood physical model of how photons reach these receptive fields in the first place, the researchers were able to predict how a person would estimate the speed of motion in natural images. . This was in contrast to previous studies of the topic, which tested models on abstract images in motion, such a black bars drifting across a white background. While accurate in those cases, such models begin to fail when applied to natural images.
To make their ideal observer as realistic and generalizable as possible, Burge and Geisler trained it on small patches of natural scenes, similar to those that would be seen by looking out a moving car window through a straw. The speed of the image on the retina depends on the distance to the object in the scene. Images associated with more distant objects move more slowly. Images associated with near objects move more quickly. How to combine local estimates of image speed to obtain accurate estimates of self-motion and object motion is a big question for future research.
Speed of retinal image motion in a natural scene for an observer walking briskly to the left at 3 miles per hour. Credit: The researchers/Nature Communications.
“With good local estimates, one will be in a better position to integrate them into an accurate global estimate of speed,” Burge said.
To compare human behavior to their model, the researchers had experiment participants view thousands of pairs of moving natural image patches. Each movie in the pair moved at a slightly different speed. Participants would indicate which movie in the pair was moving faster.
The participants’ responses closely matched what the ideal observer model predicted, when the two speeds were nearly identical and when the two speeds were quite different.
Ultimately, conduction velocities are specific to each individual and depend largely on an axon's diameter and the degree to which that axon is myelinated, but the majority of 'normal' individuals fall within defined ranges. 
Nerve impulses are extremely slow compared to the speed of electricity, where the electric field can propagate with a speed on the order of 50–99% of the speed of light however, it is very fast compared to the speed of blood flow, with some myelinated neurons conducting at speeds up to 120 m/s (432 km/h or 275 mph).
|Diameter||Myelin||Conduction velocity||Associated muscle fibers|
|α||Aα||13–20 μm||Yes||80–120 m/s||Extrafusal muscle fibers|
|γ||Aγ||5–8 μm||Yes||4–24 m/s  ||Intrafusal muscle fibers|
Different sensory receptors are innervated by different types of nerve fibers. Proprioceptors are innervated by type Ia, Ib and II sensory fibers, mechanoreceptors by type II and III sensory fibers, and nociceptors and thermoreceptors by type III and IV sensory fibers.
|Diameter||Myelin||Conduction velocity||Associated sensory receptors|
|Ia||Aα||13–20 μm||Yes||80–120 m/s ||Responsible for proprioception|
|Ib||Aα||13–20 μm||Yes||80–120 m/s||Golgi tendon organ|
|II||Aβ||6–12 μm||Yes||33–75 m/s||Secondary receptors of muscle spindle |
All cutaneous mechanoreceptors
|III||Aδ||1–5 μm||Thin||3–30 m/s||Free nerve endings of touch and pressure |
Nociceptors of neospinothalamic tract
|IV||C||0.2–1.5 μm||No||0.5–2.0 m/s||Nociceptors of paleospinothalamic tract |
|preganglionic fibers||B||1–5 μm||Yes||3–15 m/s|
|postganglionic fibers||C||0.2–1.5 μm||No||0.5–2.0 m/s|
|Nerve||Conduction velocity  |
|Median Sensory||45–70 m/s|
|Median Motor||49–64 m/s|
|Ulnar Sensory||48–74 m/s|
|Ulnar Motor||49+ m/s|
|Peroneal Motor||44+ m/s|
|Tibial Motor||41+ m/s|
|Sural Sensory||46–64 m/s|
Normal impulses in peripheral nerves of the legs travel at 40–45 m/s, and 50–65 m/s in peripheral nerves of the arms.  Largely generalized, normal conduction velocities for any given nerve will be in the range of 50–60 m/s. 
Nerve conduction studies Edit
Nerve Conduction Velocity is just one of many measurements commonly made during a nerve conduction study (NCS). The purpose of these studies is to determine whether nerve damage is present and how severe that damage may be.
Nerve conduction studies are performed as follows: 
- Two electrodes are attached to the subject's skin over the nerve being tested.
- Electrical impulses are sent through one electrode to stimulate the nerve.
- The second electrode records the impulse sent through the nerve as a result of stimulation.
- The time difference between stimulation from the first electrode and pick-up by the downstream electrode is known as the latency. Nerve conduction latencies are typically on the order of milliseconds.
Although conduction velocity itself is not directly measured, calculating conduction velocities from NCS measurements is trivial. The distance between the stimulating and receiving electrodes is divided by the impulse latency, resulting in conduction velocity. NCV = conduction distance / (proximal latency-distal latency)
Many times, Needle EMG is also performed on subjects at the same time as other NCS procedures because they aid in detecting whether muscles are functioning properly in response to stimuli sent via their connecting nerves.  EMG is the most important component of electrodiagnosis of motor neuron diseases as it often leads to the identification of motor neuron involvement before clinical evidence can be seen. 
Micromachined 3D electrode arrays Edit
Typically, the electrodes used in an EMG are stuck to the skin over a thin layer of gel/paste.  This allows for better conduction between electrode and skin. However, as these electrodes do not pierce the skin, there are impedances that result in erroneous readings, high noise levels, and low spatial resolution in readings. 
To address these problems, new devices are being developed, such as 3-dimensional electrode arrays. These are MEMS devices that consist of arrays of metal micro-towers capable of penetrating the outer layers of skin, thus reducing impedance. 
Compared with traditional wet electrodes, multi-electrode arrays offer the following: 
- Electrodes are about 1/10 the size of standard wet surface electrodes
- Arrays of electrodes can be created and scaled to cover areas of almost any size
- Reduced impedance
- Improved signal power
- Higher amplitude signals
- Allow better real-time nerve impulse tracking
Anthropometric and other individualized factors Edit
Baseline nerve conduction measurements are different for everyone, as they are dependent upon the individual's age, sex, local temperatures, and other anthropometric factors such as hand size and height.   It is important to understand the effect of these various factors on the normal values for nerve conduction measurements to aid in identifying abnormal nerve conduction study results. The ability to predict normal values in the context of an individual's anthropometric characteristics increases the sensitivities and specificities of electrodiagnostic procedures. 
Normal 'adult' values for conduction velocities are typically reached by age 4. Conduction velocities in newborns and toddlers tend to be about half the adult values. 
Nerve conduction studies performed on healthy adults revealed that age is negatively associated with the sensory amplitude measures of the Median, Ulnar, and Sural nerves. Negative associations were also found between age and the conduction velocities and latencies in the Median sensory, Median motor, and Ulnar sensory nerves. However, conduction velocity of the Sural nerve is not associated with age. In general, conduction velocities in the upper extremities decrease by about 1 m/s for every 10 years of age. 
Sural nerve conduction amplitude is significantly smaller in females than males, and the latency of impulses is longer in females, thus a slower conduction velocity. 
Other nerves have not been shown to exhibit any gender biases. [ citation needed ]
In general, the conduction velocities of most motor and sensory nerves are positively and linearly associated with body temperature (low temperatures slow nerve conduction velocity and higher temperatures increase conduction velocity). 
Conduction velocities in the Sural nerve seem to exhibit an especially strong correlation with the local temperature of the nerve. 
Conduction velocities in both the Median sensory and Ulnar sensory nerves are negatively related to an individual's height, which likely accounts for the fact that, among most of the adult population, conduction velocities between the wrist and digits of an individual's hand decrease by 0.5 m/s for each inch increase in height.  As a direct consequence, impulse latencies within the Median, Ulnar, and Sural nerves increases with height. 
The correlation between height and the amplitude of impulses in the sensory nerves is negative. 
Hand factors Edit
Circumference of the index finger appears to be negatively associated with conduction amplitudes in the Median and Ulnar nerves. In addition, people with larger wrist ratios (anterior-posterior diameter : medial-lateral diameter) have lower Median nerve latencies and faster conduction velocities. 
Medical conditions Edit
Amyotrophic lateral sclerosis (ALS) Edit
Amyotrophic Lateral Sclerosis (ALS) aka 'Lou Gehrig's disease' is a progressive and inevitably fatal neurodegenerative disease affecting the motor neurons.  Because ALS shares many symptoms with other neurodegenerative diseases, it can be difficult to diagnose properly. The best method of establishing a confident diagnosis is via electrodiagnostic evaluation. To be specific, motor nerve conduction studies of the Median, Ulnar, and peroneal muscles should be performed, as well as sensory nerve conduction studies of the Ulnar and Sural nerves. 
In patients with ALS, it has been shown that distal motor latencies and slowing of conduction velocity worsened as the severity of their muscle weakness increased. Both symptoms are consistent with the axonal degeneration occurring in ALS patients. 
Carpal tunnel syndrome Edit
Carpal tunnel syndrome (CTS) is a form of nerve compression syndrome caused by the compression of the median nerve at the wrist. Typical symptoms include numbness, tingling, burning pains, or weakness in the hand.   CTS is another condition for which electrodiagnostic testing is valuable.   However, before subjecting a patient to nerve conduction studies, both Tinel's test and Phalen's test should be performed. If both results are negative, it is very unlikely that the patient has CTS, and further testing is unnecessary. 
Carpal tunnel syndrome presents in each individual to different extents. Measurements of nerve conduction velocity are critical to determining the degree of severity.   These levels of severity are categorized as:  
- Mild CTS: Prolonged sensory latencies, very slight decrease in conduction velocity. No suspected axonal degeneration.
- Moderate CTS: Abnormal sensory conduction velocities and reduced motor conduction velocities. No suspected axonal degeneration.
- Severe CTS: Absence of sensory responses and prolonged motor latencies (reduced motor conduction velocities).
- Extreme CTS: Absence of both sensory and motor responses.
One common electrodiagnostic measurement includes the difference between sensory nerve conduction velocities in the pinkie finger and index finger. In most instances of CTS, symptoms will not present until this difference is greater than 8 m/s.  
Guillain–Barré syndrome Edit
Guillain–Barré syndrome (GBS) is a peripheral neuropathy involving the degeneration of myelin sheathing and/or nerves that innervate the head, body, and limbs.  This degeneration is due to an autoimmune response typically initiated by various infections.
Two primary classifications exist: demyelinating (Schwann cell damage) and axonal (direct nerve fiber damage).   Each of these then branches into additional sub-classifications depending on the exact manifestation. In all cases, however, the condition results in weakness or paralysis of limbs, the potentially fatal paralysis of respiratory muscles, or a combination of these effects. 
The disease can progress very rapidly once symptoms present (severe damage can occur within as little as a day).  Because electrodiagnosis is one of the fastest and most direct methods of determining the presence of the illness and its proper classification, nerve conduction studies are extremely important.  Without proper electrodiagnostic assessment, GBS is commonly misdiagnosed as Polio, West Nile virus, Tick paralysis, various Toxic neuropathies, CIDP, Transverse myelitis, or Hysterical paralysis.  Two sets of nerve conduction studies should allow for proper diagnosis of Guillain–Barré syndrome. It is recommended that these be performed within the first 2 weeks of symptom presentation and again sometime between 3 and 8 weeks. 
Electrodiagnostic findings that may implicate GBS include:   
- Complete conduction blocks
- Abnormal or absent F waves
- Attenuated compound muscle action potential amplitudes
- Prolonged motor neuron latencies
- Severely slowed conduction velocities (sometimes below 20 m/s)
Lambert-Eaton myasthenic syndrome Edit
Lambert–Eaton myasthenic syndrome (LEMS) is an autoimmune disease in which auto-antibodies are directed against voltage-gated calcium channels at presynaptic nerve terminals. Here, the antibodies inhibit the release of neurotransmitters, resulting in muscle weakness and autonomic dysfunctions. 
Nerve conduction studies performed on the Ulnar motor and sensory, Median motor and sensory, Tibial motor, and Peroneal motor nerves in patients with LEMS have shown that the conduction velocity across these nerves is actually normal. However, the amplitudes of the compound motor action potentials may be reduced by up to 55%, and the duration of these action potentials decreased by up to 47%. 
Peripheral diabetic neuropathy Edit
At least half the population with diabetes mellitus is also affected with diabetic neuropathy, causing numbness and weakness in the peripheral limbs.  Studies have shown that the Rho/Rho-kinase signaling pathway is more active in individuals with diabetes and that this signaling activity occurs mainly in the nodes of Ranvier and Schmidt-Lanterman incisures.  Therefore, over-activity of the Rho/Rho-kinase signaling pathway may inhibit nerve conduction.
Motor nerve conduction velocity studies revealed that conductance in diabetic rats was about 30% lower than that of the non-diabetic control group. In addition, activity along the Schmidt-Lanterman incisures was non-continuous and non-linear in the diabetic group, but linear and continuous in the control. These deficiencies were eliminated after the administration of Fasudil to the diabetic group, implying that it may be a potential treatment.