Physiological principles underlying electrodiagnosis and neurophysiologic testing

Author(s): Subhadra L. Nori, MD

Originally published:09/20/2014

Last updated:09/20/2014

1. OVERVIEW AND DESCRIPTION

Electromyography (EMG) is an integral part of physical medicine and rehabilitation practice. A referral to the electrodiagnosis is made when the physician is uncertain about etiology of symptoms or is trying to confirm a clinical picture. Sometimes it is the prognosis that is not clear. The electrodiagnosis helps to clarify these situations. Therefore it is essential for a electrodiagnostitian to understand the basic physiological principles of nerve conductions and needle EMG. This chapter will review and outline these principles.

2. 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 stage, the muscle and nerve membrane store an electrical charge, and when stimulated, release a burst of energy.

RESTING POTENTIAL

  1. In a resting stage the membrane is always negative on the inside as compared to outside. It is -70mv in the nerve and -80mv 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. This results in an unequal distribution of charged ions across the membrane. This potential difference between outside and inside is referred to as resting potential. The membrane is selectively more permeable to K+than Na+. An active transport mechanism maintains the Na concentration inside the membrane. Organic anions are not permeable. Normally, inside a living cell intracellular fluid is high in K+and low in Na+and Cl-. In the extra cellular fluid Na+and Cl-are high. K+tends to diffuse out of the cell and Cl-diffuses into the cell. The permeability of K+is 50 times more than that of Na+. When this happens positive charges collect on the outside and negative charges on the inside.
  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. When the outside is positive and inside negative, it is called polarized. The potential difference between inside and outside of the cell is called resting potential. The calculated resting potential using the Nernst equation, E = RT+/FZklogc[K+]o/[K+]I where R is the gas constant, F is the Faraday 96,500 coulombs is -97mV. K+is responsible for the resting potential since Na+ concentration is much lower inside the cell. The reason for this is because some innate mechanism in the living cell actively ejects Na+out into extracellular fluid. This energy is referred to as sodium pump. The same active transport process also brings K+into the cell, thus whenever Na+leaks into the cell, K+leaks out. These ions are 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 separation of electrical charges, negative inside and positive outside. Thus the membrane acts as an insulator, separating two conductors, i.e., the extracellular and intracellular fluids.

Membrane excitability

  1. If a nerve is given enough electrical current or stimulated to change the trans-membrane potential close to neutral, an action potential is generated which propagates along the nerve or muscle membrane.
  2. Cells in which action potentials can be triggered are called excitable. Thus, when a nerve or muscle membrane is triggered, depolarization occurs.
  3. This depolarization is called stimulation. But this current has to be of a certain strength and of a certain duration. Another important factor is a voltage gated Na+channel.
  4. These are molecular pores which have gates that open and close, in response to the level of membrane potentials. When current is injected with the axon, depolarization occurs.
  5. Voltage sensors respond and open the gate to the channel, allowing Na+to enter the axon. Every time the current exceeds 10 to 30 mv above the resting potential, it creates an action potential. As further depolarization continues, more Na+channels open.
  6. This action potential is an all-or-none response and propagates away within about 1 – 2 ms. A second gate called inactivation gate closes the channels. Now the membrane becomes unexcitable. This is called the refractory period. This action potential continues to propagate.
  7. The speed or velocity (CV) of this action potential depends on the diameter of the axon. The larger the axon, faster the conduction. In unmyelinated axons, the CV is very slow, in the ranges of 0.2 to 1.5 m/sec.
  8. 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.
  9. 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 by way of saltatory conduction, only at the nodes of Ranvier. After depolarizing one node the action potential jumps to the next and continues.
  10. The speed of the action potential is faster in myelinated fibers. It takes less time to depolarize the nerve, as compared to unmyelinated nerve where the entire nerve fiber needs to be depolarized. Myelinated human nerve fibers conduct at 35 to 75 m/sec. As the action potential propagates down the nerve, these axons divide into many branches and finally end in muscle fibers. The entire unit–the axon, anterior horn cell and all the muscle connected–is known as a motor unit.
  11. Depolarization of all the muscle fibers in a motor unit produces an electrical potential called motor unit action potential (MUAP). As the nerve terminals end in the muscle, they go through neuromuscular junction (NMJ). NMJ is essentially an electrochemical link between the nerve and the muscle.
  12. The muscle and nerve membranes are separated by a cleft. On the presynaptic side, collection of acetylcholine (Ach) called quantum are located. On the post-synaptic side, there are several folds lined with Ach receptors.
  13. As the nerve action potential reaches the presynaptic side of the NMJ, voltage gated channels are activated, allowing influx of CA, which in turn releases a neurotransmitter.
  14. Ach diffuses across the synaptic cleft and binds to the Ach receptors. These receptors allow influx of Na and depolarization of the muscle occurs. The muscle fiber filament action and myosin then overlap, causing muscle shortening contraction and generation of force. Skeletal muscle contains many thousands of muscle fibers.
  15. These contain bundles of myofibrils, which in turn are composed of many filaments. These filaments contain sarcomere or units, between Z lines. Actin/or thin filaments inter-digitate with thick filament or myosin. When a muscle contracts, sarcomere becomes shorter because thin filaments move together. In relaxed state, the thin filaments move apart.
  16. When a muscle fiber membrane depolarizes, at the end plate local circuit of current along the membrane occurs through the transverse fibular system. This contraction goes deeper into the muscle fibers.
  17. Calcium is released from sarcoplasmic reticulum and initiates contraction of actin and myosin – adenosine triphosphate (ATP) breaks the bridge coupling filaments and fibers relax, calcium is sequestered. The energy for this action is provided by the hydrolysis of ATP by myosin ATPase.

How are these potentials recorded?

Needle electrodes are used to record EMG potentials as the intracellular potentials are transmitted through tissue to the electrodes. Nerve conduction studies are surface recordings utilizing surface electrodes. This process of transmission of the electrical signals through tissues is called volume conduction. 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 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. This potential is biphasic and is seen at the end plate. Examples of near-field potentials are all routine nerve conduction studies, i.e., Compound motor action potential (CMAP), nerve action potential (NAP), sensory nerve action potential (SNAP) and motor unit action potentials (MUAPs).

Far-field potentials

Two recording electrodes are used – one closer and the other farther from the source. They see the source at the same time. An example of this is stimulus artifact. Seen at both proximal and distal site of recording during routine nerve conduction studies (NCS), these far-field potentials are routinely used in somatosensory evoked potential (SSEP) recordings.

3. CUTTING EDGE/UNIQUE CONCEPTS/EMERGING ISSUES

Over the past two decades significant improvements occurred in computer software, allowing better signal averaging. Automatic calculations of never conduction velocity (NCV) by the computer are now possible. Some machines are very helpful to generate reports and have the capacity to interface with electronic medical records.

4. GAPS IN KNOWLEDGE/EVIDENCE BASE

  1. At this time it is not completely understood how nerve conduction abnormalities are related to genetic conditions.
  2. Also, further research is needed to understand remyelination and nerve repair.
  3. Not enough research is available to understand the effects of medication on remyelination.

RECOMMENDED READING LIST

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.

Author Disclosure

Subhadra L. Nori, MD
Nothing to Disclose

Related Articles