Author(s): Jason Kiene, MD, Benjamin Westerhaus, MD, David Sherwood, DO
Originally published: September 20, 2014 Last updated: April 19, 2020
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OVERVIEW AND DESCRIPTION

Electromyography (EMG) is an integral part of physical medicine and rehabilitation practice. A referral for electrodiagnostics should be made when the physician is uncertain about the etiology of symptoms, trying to confirm a clinical picture, or for prognostic information. The electrodiagnosis helps to clarify these situations. Therefore, it is essential for an electrodiagnostitian to understand the basic physiological principles of nerve conductions and needle EMG. This section will review and outline these principles.

RELEVANCE TO CLINICAL PRACTICE

Electrical activity occurs in a portion of muscle. The integrity of the muscle fiber membrane is an important factor in generating a source of electricity. In a resting state, the muscle and nerve membrane store an electrical charge, and when stimulated, release a burst of energy.

RESTING POTENTIAL

  1. In a resting state, the membrane is always negative on the inside as compared to outside. It is -70 mV in the nerve and -80 mV in the muscle.
  2. The membranes of both the nerve and muscle regulate the interchange of substances between exterior and interior. It allows certain ions to pass freely, but restricts the diffusion of others. The result is an unequal distribution of charged ions across the membrane. The difference in charge between outside and inside is referred to as resting potential. The membrane is selectively more permeable to K+ than Na+. While K+ is able to freely leak from the intracellular to extracellular space, an active transport mechanism maintains the Na+ concentration inside the membrane. Typically, inside a living cell, intracellular fluid is high in K+ and low in Na+ and Cl–. In the extracellular fluid, Na+ and Cl– are high., and K+ low.  Because of the cell membrane’s selective permeability, K+ freely leaks into the extracellular space leading to positive charges collecting on the outside and the creation of a negative charge on the inside, resulting in a polarized cell membrane.
  3. In a steady state, equilibrium of electrical charges is maintained, so that influx exactly matches the efflux. During the state of electro-chemical equilibrium, net movement of ions across the membrane is zero.  The potential difference between inside and outside of the cell is called resting potential. The calculated resting potential is derived by using the Nernst equation. For example, EK = (RT/PKF)ln[K+]o/[K+]i where R is the gas constant, T the temperature in Kelvin, z is the ion charge, F is Faraday’s constant (~96,500 coulombs/mol), PK is the permeability of the K+ ion, [K+]o is the extracellular concentration of the ion and [K+]i is the intracellular concentration of the ion. The equation results in -97 mV potential for K+.
  4. To determine the membrane resting potential for any cell the collective Nernst equations of K+,N+ and Cl– must be combined using the Goldman–Hodgkin–Katz equation (also called the Goldman Equation).  K+ is mainly responsible for the resting potential since Na+ concentration is much lower inside the cell. A sodium-potassium ATPase uses energy to move both Na+ and K+ across their concentration gradients, resulting in extracellular fluid with a large concentration of Na+ ions and the intracellular fluid with a large concentration of K+ ions.  Following an action potential, Na+ influxes into the cell and K+ effluxes out of the cell. These ions are then pumped back, maintaining appropriate concentration gradients.

To Summarize

A resting potential is continuously maintained across the membrane of normal nerve and muscle fibers. The resting potential is the result of the separation of electrical charges, negative inside and positive outside. Thus, the membrane acts as an insulator, separating two conductors.

Membrane excitability

  1. If a nerve is given enough electrical current or otherwise stimulated to change the trans-membrane potential close to neutral, an action potential is generated that propagates along the nerve or muscle membrane.
  2. Cells where action potentials can be triggered are called excitable. Thus, when a nerve or muscle membrane is triggered, depolarization (or ‘stimulation’) occurs. However, this current must be of a certain strength and of a certain duration to achieve depolarization.
  3. Another important factor is voltage gated Na+ channels. These are molecular pores which have gates that open and close in response to membrane potentials. When current is injected to the axon, depolarization occurs. Voltage sensors respond and open the gate to the channel, allowing Na+ to enter the axon. Every time the current exceeds 10-30 mV above the resting potential, it creates an action potential. As further depolarization continues, more Na+ channels open. This action potential is an all-or-none response and propagates away within about 1-2 ms.
  4. A second gate, called the inactivation gate, closes the channels, which causes the membrane to become unexcitable. The time period in which the membrane is unexcitable is referred to as the refractory period.
  5. The action potential continues to propagate away from the stimulation site. The speed, or conduction velocity (CV), of this action potential depends on the diameter of the axon. The larger the axon, the faster the conduction.
  6. In myelinated fibers, the fibers are surrounded by insulating material called myelin, supported by Schwann cells. In peripheral nerves, the myelin is laid in concentric spirals. Each of these segments covered by myelin is termed the internode.
  7. Between the internodes, the axons are exposed. These nodes are known as the nodes of Ranvier and are about 1-2 mm in length. The depolarization occurs only at the nodes of Ranvier by way of saltatory conduction, where ‘saltatory’ is Latin for ‘leaping’ or ‘bounding’. After depolarizing one node the action potential jumps to the next and continues.  During remyelination of damaged nerves, the number of nodes of Ranvier increase, thus decreasing the conduction velocity of the action potential.
  8. The CV of the action potential is faster in myelinated fibers than in unmyelinated fibers, since in an unmyelinated nerve, the entire nerve fiber needs to be depolarized. Unmyelinated axons CV ranges from 0.2-1.5 m/s.  Contrastingly, myelinated human nerve fibers conduct at 35-75 m/s.  As the action potential propagates down the nerve, these axons divide into many branches and finally end in muscle fibers.
  9. Depolarization of all the muscle fibers in a motor unit, defined as the anterior horn cell,  axon and all the muscle fibers that axon innervates, produces an electrical potential called motor unit action potential (MUAP). As the nerve terminals end in the muscle, they go through the neuromuscular junction (NMJ). The NMJ is essentially an electrochemical link between the nerve and the muscle.
  10. The muscle and nerve membranes are separated by a synaptic cleft. On the presynaptic side, acetylcholine (ACh) is stored in vesicles called quanta. The post-synaptic side contains several folds lined with ACh receptors.
  11. As the nerve action potential reaches the presynaptic side of the NMJ, voltage gated channels are activated, allowing influx of Ca2+, which causes presynaptic vesicles to fuse with the cell membrane, releasing ACh into the synaptic cleft.  Some quanta also fuse with the membrane spontaneously, resulting in miniature end-plate potentials (MEPPs).  The MEPPs are too small to trigger a normal action potential.
  12. As ACh diffuses across the synaptic cleft, it binds to post-synaptic ACh receptors. These receptors allow influx of Na+ and depolarization of the muscle begins.
  13. The muscle fiber contains two filaments, actin and myosin, which overlap.  In the resting state, the binding sites on actin are covered by tropomyosin. Depolarization of the muscle fiber causes Ca2+ to be released from sarcoplasmic reticulum, where it binds to troponin, causing tropomyosin to change configuration and expose the binding sites for myosin.  The myosin heads then use ATP to cause a muscle shortening contraction and generation of force.  Skeletal muscle contains many thousands of muscle fibers.
  14. Muscle fibers contain bundles of myofibrils, which in turn are composed of many filaments. These filaments contain sarcomere between Z lines. Actin, or thin filaments, inter-digitate with myosin, or thick filament. When a muscle contracts, the sarcomere becomes shorter because thin filaments move together. In relaxed state, the thin filaments move apart.
  15. When a muscle fiber membrane depolarizes at the end plate, a local circuit of current along the membrane occurs through the transverse fibular system which then travels deeper into the muscle fibers.

How are these potentials recorded?

Electrodiagnosis utilizes tools to record intracellular changes in the extracellular space.  Needle electrodes are used to record EMG potentials as the intracellular potentials are transmitted through tissue to the electrodes. Surface electrodes transmit potential during nerve conduction studies (NCSs). When potentials are recorded close to their source generation, they are called near-field potentials. These potentials produce a triphasic response, or wave form, as the advancing action potential approaches, passes under, and then away from the recording electrode. The electrical correlate is an initial positive, then a negative, and then a trailing positive phase. If a volume conducted near-field potential is directly under the recording electrode, then an initial negative phase is seen. The potential is biphasic and seen at the end plate. Examples of near-field potentials are compound motor action potential (CMAP), nerve action potential (NAP), sensory nerve action potential (SNAP) and motor unit action potentials (MUAPs).

Far-field potentials

Far-field potentials are routinely used in somatosensory evoked potential (SSEP) recordings.  Two recording electrodes are used – one closer and the other farther from the source, both which  see the source at the same time.  Far-field potentials have the potential to superimpose on near-field activity1 during NCSs.

CUTTING EDGE/UNIQUE CONCEPTS/EMERGING ISSUES

Over the past two decades significant improvements occurred in computer software, allowing better signal averaging. Automatic calculations of different parameters of NCSs by the computer are now possible. Some machines are very helpful to generate reports and have the capacity to interface with electronic medical records.

There is a growing number of electrodiagnosticians who are utilizing ultrasound while performing needle EMG. This technology can detect and isolate pathologies that may not be recognized without direct visualization of the muscle or nerve2. Recent studies have demonstrated correlation between pathologic appearance of peripheral nerves on ultrasonography and EMG-NCV studies3,4. This allows another dimension of understanding into neuromuscular pathology by visualizing the neuromuscular architecture under ultrasound.

Magnetic resonance imaging (MRI) is another imaging modality that correlates well with electrodiagnostic findings, as noted by a growing body of evidence. Notably, these diagnostic tools can provide complementary information in certain pathologies5,6.

GAPS IN KNOWLEDGE/EVIDENCE BASE

  1. It is not completely understood how nerve conduction abnormalities are related to genetic conditions.
  2. The effects of medication on remyelination are still poorly understood.
  3. Due to limitations in sensitivity of signal processing as well as the size of the thinnest nerves, electromyography remains unable to detect pathologies in small fiber polyneuropathies, like diabetes-induced polyneuropathy.

REFERENCES

  1. Kimura J. Principles and pitfalls of nerve conduction studies. Ann Neurol. 1984 Oct; 16(4):415-429. doi: 10.1002/ana.410160402. PMID: 6093680.
  2. Gentile L, Coraci D, Pazzaglia C, Del Tedesco F, Erra C, Le Pera D, Padua L. Ultrasound guidance increases diagnostic yield of needle EMG in plegic muscle. Clin Neurophysiol. 2020 Feb;131(2):446-450. doi: 10.1016/j.clinph.2019.10.012. Epub 2019 Nov 9. PubMed PMID: 31887615.
  3. Domkundwar S, Autkar G, Khadilkar SV, Virarkar M. Ultrasound and EMG-NCV study (electromyography and nerve conduction velocity) correlation in diagnosis of nerve pathologies. J Ultrasound. 2017 Jun;20(2):111-122. doi: 10.1007/s40477-016-0232-3. eCollection 2017 Jun. Review. PubMed PMID: 28593000; PubMed Central PMCID: PMC5440331.
  4. Toia F, Gagliardo A, D’Arpa S, Gagliardo C, Gagliardo G, Cordova A. Preoperative evaluation of peripheral nerve injuries: What is the place for ultrasound?. J Neurosurg. 2016 Sep;125(3):603-14. doi: 10.3171/2015.6.JNS151001. Epub 2016 Jan 22. PubMed PMID: 26799303.
  5. Deroide N, Bousson V, Mambre L, Vicaut E, Laredo JD, Kubis N. Muscle MRI STIR signal intensity and atrophy are correlated to focal lower limb neuropathy severity. Eur Radiol. 2015 Mar;25(3):644-51. doi: 10.1007/s00330-014-3436-y. Epub 2014 Sep 26. PubMed PMID: 25257857.
  6. Kamath S, Venkatanarasimha N, Walsh MA, Hughes PM. MRI appearance of muscle denervation. Skeletal Radiol. 2008 May;37(5):397-404. doi: 10.1007/s00256-007-0409-0. Epub 2007 Nov 16. Review. PubMed PMID: 18360752.

Bibliography

Dumitru D. Electrodiagnostic Medicine. 2nd ed. Philadelphia, PA: Hanley & Belfus; 2002.

Dyck PJ, Thomas PK. Peripheral Neuropathy. 3rd ed. Philadelphia, PA: WB Saunders; 1993.

Friedli WH, Meyer M. Strength-duration curve: A measure for assessing sensory deficit in peripheral neuropathy.J Neurol Neurosurg Psychiatry. 1984;47:184-189.

Kandel ER, Schwartz JH, Jessell TM. Principles of Neuroscience. 4th ed. New York, NY: McGraw-Hill; 2000.

Kimura J. Electrodiagnosis in Disease of Nerve and Muscle: Principles and Practice. 3rd ed. New York, NY: Oxford University Press; 2001. 6. Patton HD, Sundsten JW, Crill WE, Swenson PD. Introduction to Basic Neurology. Philadelphia, PA: WB Saunders; 1976.

Rutkove SB. AAEM Minimonograph #14: The effects of temperature in neuromuscular electrophysiology.Muscle Nerve. 2001;24:867-882.

Seddon H. Surgical Disorders of the Peripheral Nerves. 2nd ed. Edinburgh, UK: Churchill Livingstone; 1975.

Sumner A.The Physiology of Peripheral Nerve Disease. Philadelphia, PA: WB Saunders; 1980.

Sunderland S.Nerves and Nerve Injuries. 2nd ed. Edinburgh, UK: Churchill Livingstone; 1978.

Original Version of the Topic

Subhadra L. Nori, MD. Physiological principles underlying electrodiagnosis and neurophysiologic testing. 9/20/2014.

Author Disclosure

Jason Kiene, MD
Nothing to Disclose

Benjamin Westerhaus, MD
Nothing to Disclose

David Sherwood, DO
Nothing to Disclose