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Flashcards in Nerve Conduction and Electromyography Deck (35):
1

What is NCS and EMG used for

We measure mostly the PERIPHERAL NERVOUS SYSTEM. As such, this test is not designed to test central nervous system disorders. We test for disorders of the motor neuron and nervous system structures distal to this structure.

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Examples of diseases that can be diagnosed with NCS and EMG

Motor neuron disorder

Motor neuron disorder: lower motor neuron dysfunction in diseases such as polio, amyotrophic lateral sclerosis (ALS), spinal muscular atrophy.

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Examples of diseases that can be diagnosed with NCS and EMG

Nerve roots

Nerve roots (sensory and motor): cervical and lumbosacral radiculopathy, nerve root avulsion in trauma.

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Examples of diseases that can be diagnosed with NCS and EMG

DRG

Dorsal root ganglia: ganglionopathy/neuronopathy (mostly asymmetric sensory deficits due to damage of dorsal root ganglia).

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Examples of diseases that can be diagnosed with NCS and EMG

Brachial and Lumbosacral plexus

Brachial and lumbosacral plexus: due to trauma, inflammatory conditions, infections, neoplastic, related to prior radiation. Think of “Parsonage Turner Syndrome”, “Neuralgic Amyotrophy”, trauma, CMV (Cytomegalovirus lumbosacral polyradiculopathy), Lyme disease.

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Examples of diseases that can be diagnosed with NCS and EMG

Peripheral Nerve

Peripheral Nerve: sensory/motor/sensorimotor nerves, symmetric/asymmetric mono or poly- neuropathies, axonal or demyelinating. The most common cause of neuropathy in USA is diabetes, the most common cause of neuropathy worldwide is leprosy.

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Examples of diseases that can be diagnosed with NCS and EMG

NMJ

Neuromuscular Junction (NMJ): presynaptic like Lambert Eaton Syndrome and botulism, postsynaptic like Myasthenia Gravis (MG).

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Examples of diseases that can be diagnosed with NCS and EMG

Muscle Disorder

Muscle disorders: myopathy with and without membrane irritability, including inflammatory and toxic myopathies.

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Examples of diseases that can be diagnosed with NCS and EMG

Cranial nerves

Cranial Nerves: trigeminal nerve, facial nerve, spinal accessory nerve (trapezius, also innervated by ventral rami of C3 and C4 AND sternocleidomastoid), hypoglossal nerve (tongue).

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Spinal nerve divisions

Dorsal ramus: skin and paraspinal nerves.
Ventral ramus:
Brachial plexus: C5-T1,
Intercostal nerves: mostly thoracic,
Lumbosacral plexus and pudendal plexus: L1-L5, S1-S4, coccygeal nerve +/- T12.

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Brachial plexus

fun

The brachial plexus is responsible for cutaneous and muscular innervation of the entire upper limb, with two exceptions: the trapezius muscle innervated by the spinal accessory nerve (CN XI) and an area of skin near the axilla innervated by the intercostobrachial nerve.

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Brachial plexus

Divided into…

and an area of skin near the axilla innervated by the intercostobrachial nerve. The brachial plexus is divided into Roots, Trunks, Divisions, Cords, and Branches. There are five "terminal" branches and numerous other "pre-terminal" or "collateral" branches that leave the plexus at various points along its length.

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Review the brachial plexus

Do it

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Mnemonics for remembering the order of brachial plexus

Real Texans Drink Cold Beer
Read The Darn Cadaver Book
Real Teachers Drink Chilled Beer
Randy Travis Drinks Cold Beer

15

Neurophysiological basis of measuring nerve conduction/EMG

We measure the Extracellular action potentials of the various sensory, motor and muscle fibers. Routine nerve conductions measure large diameter fibers (small nerve fibers can be tested with other special testing, like QSART: Quantitative Sudomotor Axon Reflex Test)

The extracellular action potentials can be measured mostly because of the Na+/K+ pump, which is electrogenic. All the signals that we obtained are the result of the summation of individual cell signals.

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How is electrical activity measured

Technical perspective

From the technical perspective and as a very brief summary, we measure the electric activity with two electrodes: the active electrode and the reference electrode. Then there is a differential amplifier, that magnifies the signal to be measured. Then, specific filter parameters are applied to the signal. Then, the analog signal is made, and now is converted to a digital signal, which we see and hear.

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Nerve conduction study principles

Motor nerve conductions

mech

An electrical stimulus is applied over a motor nerve, inducing an action potential which travels down the nerve to the synapse and activates the muscle. The electrical activity of the muscle contraction, known as the compound motor action potential, is detected as a monophasic waveform by the recording electrode. The time between the stimulus and the onset of the compound motor action potential is known as the latency. The latency is made up of the time it takes the action potential to travel from the stimulus site to the synapse plus the time it takes for synaptic transmission plus the time it takes for the muscle to become activated. If the motor nerve is stimulated at a second site, the latency will differ only by the additional time required for the action potential to reach the synapse. If the distance between the two stimulation sites is divided by the difference in the two latencies, a motor nerve conduction velocity can be calculated, and represents the time it takes for an action potential to travel along the nerve segment between the two stimulation sites.

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Nerve conduction study principles

Sensory nerve conductions

mech

Sensory nerve differs from motor nerve in that the action potential in the nerve must be detected by recording electrode. The nerve action potential is a much smaller electrical signal than the compound motor action potential, requiring more amplification and greater possibilities of electrical interference in the measurement. The recorded sensory nerve action potential (SNAP) is usually bi- or triphasic, which results from the action potential traveling along the nerve past the recording electrode. As there is no synaptic transmission involved, a sensory nerve conduction velocity can be calculated by dividing the distance between the stimulation site and the recording site by the latency, but often the conduction velocity along different segments of the nerve is determined by stimulating at a single site while recording at different sites along the nerve. Here the segmental nerve conduction velocity is calculated as the distance between two recording sites (the segment length) divided by the difference in the two latencies.

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Nerve conduction study

Clinical applications





Demyelinating neuropathy: prolonged latency and conduction velocities, amplitude mostly unchanged.
Guillain Barre Syndrome, AIDP (acute inflammatory demyelinating polyneuropathy), CIDP (chronic inflammatory demyelinating polyradiculoneuropathy), some diabetic neuropathies, amiodarone neuropathy, etc.
Axonal neuropathy: reduced amplitude, latency and conduction velocity mostly unchanged.
Some diabetic neuropathies, alcohol neuropathies, most medication-related neuropathies, etc.

20

Repetitive stimulation in myasthenic syndromes (RNS)

MG

Myasthenia gravis causes a decrement in the response to repetitive stimulation on motor nerve conductions due to later stimuli releasing less acetylcholine. A decrease in amplitude of greater than 10% in the compound of motor action potential with stimulation at 3 Hz is abnormal, and is most likely to occur when muscle is exercised. A slide shows six series of seven compound motor action potentials, each slightly offset, in a rested patient and after 0, 1, 2, 3, and 4 seconds of exercise. Once the patient has exercised for two or more seconds, a substantial decrease in size is seen with each of the first three compound motor evoked potentials. Each time the neuromuscular junction synapse fires, acetylcholine is released from vesicles docked at the presynaptic membrane. With repetitive stimulation, especially in exercised muscle, the docked vesicles quickly become depleted of acetylcholine and must be replaced. The need to continually replace docked vesicles results in less acetylcholine being released each time the synapse fires after the first few stimuli. This normally makes little difference in the size of the compound motor action potential, because there are normally abundant acetylcholine receptors. In the myasthenic patient, there are fewer available acetylcholine receptors and the decrease in the amount of acetylcholine released results in a decrease in the compound motor action potential size.

21

Repetitive stimulation in myasthenic syndromes (RNS)

LEMS

In Lambert Eaton syndrome (LEMS), there is an increase in sequential compound motor action potentials when the nerve is stimulated at a rapid rate. A slide shows six series of seven consecutive compound motor action potentials, each slightly offset, at stimulation rates of one per second, two per second, three per second, five per second, 10 per second, 20 per second and 30 per second. At rates of 10 per second and 20 per second there is a clear increase in size with each subsequent compound motor action potential. Release of the acetylcholine from the presynaptic terminal requires entry of calcium through voltage gated calcium channels, and the number of these channels is decreased in the LEMS patient. At slow rates of repetitive stimulation, less acetylcholine is released and compound motor action potentials are smaller than they could be. The calcium which enters the presynaptic nerve terminal is removed before the next action potential can arrive. With more rapid stimulation, some calcium remains sequestered in the presynaptic nerve terminal and can be a released without passing through a voltage gated calcium channel. Each successive action potential arriving at the presynaptic nerve terminal can then mobilize more calcium despite the limited number of voltage gated calcium cannels, and more acetylcholine can be released, resulting in successively larger compound motor action potentials.

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H responses

The H-response is essentially the electrical measurement of a deep tendon reflex. The appropriate sensory nerve is stimulated to send an action potential towards the spinal column, where the mono-synaptic reflex arc then sends an action potential down the corresponding motor nerve, and the resulting compound motor action potential is detected. Technical considerations make this difficult to do in many parts of the body, so usually only tibial nerve H-responses are performed, corresponding to the ankle jerk reflex.

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F-response

The F-response can be performed on any motor nerve. The motor nerve is stimulated to send an action potential towards the spinal column (this is called antidromic transmission as the action potential is traveling backwards along the nerve). When the action potential reaches the motor neurons, about 5% of them will send an action potential back down the motor nerve (this is called orthodromic transmission as the action potential is traveling the usual direction along the nerve). The resulting (small) compound motor action potential is detected. The latency of the F- response results from transmission up the motor nerve from the stimulus site to the spine plus transmission along the root to and from the spinal cord plus transmission down the motor nerve from the root to the synapse plus synaptic transmission and muscle activation. If the segment conduction velocity along the nerve and the distal latency have already been tested, any remaining delay can be attributed to conduction along the root into and out from the spinal cord.

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EMG
Types of electrical activity are observed

In electromyography (EMG) a needle electrode is used to detect the electrical activity in muscle. Three types of electrical activity are observed: electrical activity provoked by the insertion of the needle, spontaneous electrical activity in the resting muscle, and the electrical activity which results win the patient tries to activate (use) the muscle.

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EMG

Insertional activity

Insertional activity: normally some brief electrical activity is seen immediately after the needle electrode is inserted into the muscle. If the muscle is “irritable” the insertional activity may be increased and prolonged. This most often occurs in inflammatory conditions such as myositis, polymyositis, and dermatomyositis.

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EMG

Spontaneous activity

Spontaneous activity: resting muscle is normally silent, but the muscle fibers which have lost their innervation will show fibrillation potentials and positive sharp waves. These represent spontaneous firing of the denervated muscle fiber, which usually fires at regular intervals. Different fibers will tend to show different rates of spontaneous activity, so the number of different muscle fibers spontaneously active near the EMG electrode can often be determined.

27

EMG

activation

Activation: when the patient voluntarily contracts the muscle, motor units begin to fire. Each motor unit represents a group of muscle fibers innervated by a single alpha motor neuron. With very minimal effort, only one or a few motor units will fire, but with increasing effort the active units will fire more frequently and then additional motor units will become active. This is called “recruitment”. The pattern of firing produced by recruitment is called the “interference” pattern. Loss of lower motor neurons will result in fewer motor units firing even with maximal effort, but they will be firing quite rapidly. Loss of upper motor neurons (or their action) will also result in fewer motor units firing, but with much less increase in firing rate. Problems in the muscle will not affect the numbers or rates of motor units firing, but will reduce the amplitude of the interference pattern because the amplitude of the motor unit potentials (MUPs) will be reduced. Also, there will be “increased recruitment” (you will obtain an “interference pattern” more rapidly and with minimal effort) with myopathic disorders.

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Motor unit potential morphology

Neurogenic changes

Neurogenic changes: Increased amplitude, long duration, polyphasic motor units.

Loss of lower motor neurons will also result in an increase in the amplitude of motor unit potentials, which also may become polyphasic. This occurs because surviving motor neurons will sprout and re-innervate some of the muscle fibers from motor units that have lost their motor neurons. These surviving motor units will have more muscle fibers, resulting in larger amplitude of the motor unit potential, but the muscle fibers will be more dispersed and so fire less synchronously, resulting in polyphasia.

This changes can be seen with neuropathy, radiculopathy, motor neuron disease and all diseases that affect the motor fibers in any way.

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Motor unit potential morphology

Myopathic changes

Myopathic changes: Reduced amplitude, short duration, polyphasic motor units.

Myopathy, or a myogenic lesion, will also result in polyphasia of motor units, which are made up of more dispersed muscle fibers, but there will actually be fewer muscle fibers in these surviving motor units, so the amplitude of the motor unit potential is reduced and its duration shorter.

This changes can be seen in most inflammatory myopathies, toxic and necrotizing myopathies, muscular dystrophy and other congenital muscle diseases.

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Musculocutaneous nerve

From/roots/muscles/cutaneous

From
Roots
Muscles
Cutaneous

Lateral Cord
C5, C6, C7
Coracobrachialis, brachialis and biceps brachii
Becomes the lateral cutaneous nerve of the forearm

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Lateral Root of the Median Nerve

From/roots/muscles/cutaneous

From
Roots
Muscles
Cutaneous

Lateral Cord
C5, C6, C7
Fibers to the median Nerve
-

32

Axillary Nerve

From/roots/muscles/cutaneous

From
Roots
Muscles
Cutaneous

Posterior Cord
C5, C6
(Muscles) Anterior branch: deltoid and a small area of overlying skin
Posterior branch: teres minor and deltoid muscles
(Cutaneous) Posterior branch becomes upper lateral cutaneous nerve of the arm

33

Radial nerve

From/roots/muscles/cutaneous

From
Roots
Muscles
Cutaneous

Posterior Cord
C5, C6, C7, C8, T1
Triceps Brachii, supinator, anconeous, the extensor muscles of the forearm and brachioradialis
Skin of the posterior arm as the posterior cutaneous nerve of the arm

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Medial Root of the median nerve

From/roots/muscles/cutaneous

From
Roots
Muscles
Cutaneous

Medial cord
C8, T1
Fibers to the median nerve
Portions of hand not served by ulnar or radial

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Ulnar Nerve

From/roots/muscles/cutaneous

From
Roots
Muscles
Cutaneous

-Medial Cord
-C8, T1
-Flexor carpi ulnaris, the medial 2 bellies of flexor digitorum profundus, the intrinsic hand muscles except the thenar muscles and the two most lateral lumbricals
-the skin of the medial side of the hand and medial one and a half fingers on the palmar side and medial two and a half fingers on the dorsal side