Nerve Conduction and Electromyography Flashcards
(35 cards)
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.
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.
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.
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).
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.
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.
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).
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.
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).
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.
Brachial plexus
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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.
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.
Review the brachial plexus
Do it
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
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.
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.
Nerve conduction study principles
Motor nerve conductions
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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.
Nerve conduction study principles
Sensory nerve conductions
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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.
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.
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.
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.
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.
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.
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.
