The Neurophysiology Assessment
Introduction
The neurological assessment can be expanded through by nerve conduction studies and electromyography (EMG). Nerve conduction studies are highly technical and require objective attention to detail. EMG is more of an art and requires subjective interpretation. Both studies should be thought of as an extension of the history and examination rather than as additional tests.
Nerve Conduction Studies
In nerve conduction studies, a stimulator is used to send an electrical pulse through the skin to a peripheral nerve. This produces an action potential (an event in which the membrane potential of a cell rises and falls) within the neuron that can be measured at a distant point over the same nerve using a recording electrode. If the nerve synapses with muscle, then more action potentials will be produced within the muscle cells innervated by that nerve. When recorded, the action potential appears as a wave. When performing nerve conduction studies on motor nerves, the compound muscle action potential (CMAP) is of major interest. The CMAP represents the summation of all the action potentials produced by the muscle cells innervated by a particular motor nerve. When performing nerve conduction studies on sensory nerves, the sensory nerve action potential (SNAP) is of major interest. The SNAP represents the summation of the sensory nerve action potentials at a distant point from the location of the stimulus. SNAPs can be recorded either orthodromically (the nerve is stimulated distally and recorded proximally) or antidromically (the nerve is stimulated proximally and recorded distally).
In all nerve conduction studies, several measurements are critical - latency, amplitude, conduction velocity, and F-wave latencies.
In all nerve conduction studies, several measurements are critical - latency, amplitude, conduction velocity, and F-wave latencies.
(1) Upper limb nerves.
(2) Lower limb nerves.
(3) Variants.
- These need to be watched for.
(a) Martin-Gruber anastomosis.
- This is a median to ulnar nerve anastomosis found in up to 30% of the general population (Gutmann, 1977; Werner and Andary, 2011).
- Median nerve elbow stimulation results in a higher CMAP amplitude than at the wrist as the anomalous fibers are also stimulated. Moreover, the median CMAP has an initial downward deflection and the velocity may be falsely elevated.
- Ulnar nerve wrist stimulation results in a higher CMAP amplitude than at the elbow as the anomalous fibers are also stimulated.
(b) Riche-Cannieu anomaly.
- This is an ulnar to APB and/or opponens pollicis connection that clinically results in the "all-ulnar hand."
- The median nerve CMAP amplitude may be reduced.
- To detect it, stimulate the ulnar nerve and record from APB and/or opponens pollicis.
(c) Accessory deep peroneal nerve.
- This is a superficial peroneal nerve to EDB connection found in up to 30% of the general population (Kimura, 1984).
- Peroneal nerve stimulation at the ankle results in a smaller amplitude than at the knee.
- These need to be watched for.
(a) Martin-Gruber anastomosis.
- This is a median to ulnar nerve anastomosis found in up to 30% of the general population (Gutmann, 1977; Werner and Andary, 2011).
- Median nerve elbow stimulation results in a higher CMAP amplitude than at the wrist as the anomalous fibers are also stimulated. Moreover, the median CMAP has an initial downward deflection and the velocity may be falsely elevated.
- Ulnar nerve wrist stimulation results in a higher CMAP amplitude than at the elbow as the anomalous fibers are also stimulated.
(b) Riche-Cannieu anomaly.
- This is an ulnar to APB and/or opponens pollicis connection that clinically results in the "all-ulnar hand."
- The median nerve CMAP amplitude may be reduced.
- To detect it, stimulate the ulnar nerve and record from APB and/or opponens pollicis.
(c) Accessory deep peroneal nerve.
- This is a superficial peroneal nerve to EDB connection found in up to 30% of the general population (Kimura, 1984).
- Peroneal nerve stimulation at the ankle results in a smaller amplitude than at the knee.
EMG
In EMG, a needle is inserted into a skeletal muscle so as to record its electrical activity. Unlike motor nerve conduction studies, which measure the summation of the action potentials for the muscle (CMAPs), EMG measures the summation of the action potentials for motor units (defined as one motor neuron plus all of the muscle cells that it innervates, which can number from one hundred to one thousand), called motor unit potentials (MUAPs). Thus, the waves recorded in EMG each represent one MUAP. The needle records the MUAPs from all active motor units in the vicinity.
For each muscle assessed, there are three observations that need to be made with regards to spontaneous activity, motor recruitment, and the MUAP morphology.
(1) Spontaneous activity.
- Refers to the activity of the muscle at rest. Normal muscle is silent; some anomalies break that silence.
For each muscle assessed, there are three observations that need to be made with regards to spontaneous activity, motor recruitment, and the MUAP morphology.
(1) Spontaneous activity.
- Refers to the activity of the muscle at rest. Normal muscle is silent; some anomalies break that silence.
(a) Fibrillations and positive sharp waves.
- Spontaneous regular discharges from denervated individual muscle cells. - Fibrillations show a negative deflection (point up). - Positive sharp waves show a positive deflection (point down). (b) Fasciculations. - Spontaneous irregular discharges from denervated individual motor units. - Large and appear and disappear abruptly. (c) Complex repetitive discharges. - Rhythmic discharges from denervated groups of muscle cells in which one cell acts as a pacemaker and drives the others ephaptically. - Start or stop abruptly and like a motorboat; only in chronic conditions. (d) Myokymia. - Rhythmic discharges from denervated groups of motor units. - Like the footsteps of marching soldiers and is always pathological. (e) Myotonic discharges. - Delayed relaxation of muscle cells - electrical counterpart of myotonia. - Waxes and wanes in frequency like a dive bomber or motorcycle. |
(2) Recruitment.
- Refers to the successive activation of more motor units with increasing voluntary muscle contraction strength (American Association of Electrodiagnostic Medicine, 2001). Normally, motor units are recruited at 6-7 Hz (Chan, 2002). The strength of muscle contraction can be increased by spatial recruitment (increasing the number of active motor units) and temporal recruitment (increasing the firing rate of the individual motor units). Both of these mechanisms occur concurrently. Spatial recruitment predominates at low levels of muscle contraction. Temporal recruitment predominates at high levels of muscle contraction.
- Refers to the successive activation of more motor units with increasing voluntary muscle contraction strength (American Association of Electrodiagnostic Medicine, 2001). Normally, motor units are recruited at 6-7 Hz (Chan, 2002). The strength of muscle contraction can be increased by spatial recruitment (increasing the number of active motor units) and temporal recruitment (increasing the firing rate of the individual motor units). Both of these mechanisms occur concurrently. Spatial recruitment predominates at low levels of muscle contraction. Temporal recruitment predominates at high levels of muscle contraction.
(a) Reduced.
- With maximal effort, low numbers of motor units are recruited. - Seen with pain, poor effort, or chronic partial denervation. In pain and poor effort, the MUAPs form intermittent, irregular bursts whereas in chronic partial denervation the MUAPs fire at a slow but regular frequency. (b) Early. - Even with minimal effort, all motor units are recruited. - Seen in neuromuscular junction disorders and primary muscle disease (though not necessarily; absence does not rule out myopathy). |
(3) MUAP morphology.
- Refers to the amplitude (maximum peak to peak voltage), duration (initial to final deviation from baseline), and phase number (the number of baseline crossings plus one) of the MUAP. Larger MUAPs with long durations may be seen in the elderly and with cold temperatures. Normally, MUAPs are triphasic, with a small positive peak followed by a larger negative peak and then another positive peak (Chan, 2002). Normal muscles have 10-20% polyphasic potentials.
- Refers to the amplitude (maximum peak to peak voltage), duration (initial to final deviation from baseline), and phase number (the number of baseline crossings plus one) of the MUAP. Larger MUAPs with long durations may be seen in the elderly and with cold temperatures. Normally, MUAPs are triphasic, with a small positive peak followed by a larger negative peak and then another positive peak (Chan, 2002). Normal muscles have 10-20% polyphasic potentials.
(a) Neurogenic (large amplitude, long duration, polyphasic).
- Seen in chronic partial denervation with re-innervation. (b) Myopathic (small amplitude, short duration, polyphasic). - Seen in neuromuscular junction disorders and primary muscle disease (although their absence does not rule out myopathy). |
Planning Studies
Studies ought to be modified according to the patient. For nerve conduction studies, avoid stimulating over skin infections or prosthetics and do not stimulate at Erb's point if there is a pacemaker. For EMG, avoid testing deep muscles such as iliopsoas and the paraspinals if the patient is anticoagulated or has a known clotting disorder.
(1) Carpal tunnel syndrome.
- Carpal tunnel syndrome is the most common referral one receives for a nerve conduction study. At least 20% of patients presenting with upper limb pain, numbness, tingling, and weakness have this diagnosis (Wang, 2013). The carpal tunnel forms an inelastic barrier that in certain situations may compress the median nerve and induce local ischemia (Werner and Andary, 2011) and focal demyelination with or without axonal loss (Siao et al, 2011).
- The ideal method for diagnosing carpal tunnel syndrome is to compare the median nerve peak SNAP latencies with the presumably normal ulnar or radial nerve latencies using three different measurements - thumbdiff, palmdiff, and ringdiff. If the first two disagree, perform a third to break the tie (Werner and Andary, 2011). Carpal tunnel syndrome can be so severe that no median CMAPs or SNAPs are recorded. In this case, a lumbrical to interosseus comparison is useful, as the median fibers to the second lumbrical are relatively spared compared with fibers to the thenar muscles (Werner and Andary, 2011). Using this technique, it is possible to make a latency comparison in over 90% of cases (Boonyapisit et al, 2002), proving that the median nerve compression is at the wrist and not elsewhere (Werner et al, 2011).
(1) Carpal tunnel syndrome.
- Carpal tunnel syndrome is the most common referral one receives for a nerve conduction study. At least 20% of patients presenting with upper limb pain, numbness, tingling, and weakness have this diagnosis (Wang, 2013). The carpal tunnel forms an inelastic barrier that in certain situations may compress the median nerve and induce local ischemia (Werner and Andary, 2011) and focal demyelination with or without axonal loss (Siao et al, 2011).
- The ideal method for diagnosing carpal tunnel syndrome is to compare the median nerve peak SNAP latencies with the presumably normal ulnar or radial nerve latencies using three different measurements - thumbdiff, palmdiff, and ringdiff. If the first two disagree, perform a third to break the tie (Werner and Andary, 2011). Carpal tunnel syndrome can be so severe that no median CMAPs or SNAPs are recorded. In this case, a lumbrical to interosseus comparison is useful, as the median fibers to the second lumbrical are relatively spared compared with fibers to the thenar muscles (Werner and Andary, 2011). Using this technique, it is possible to make a latency comparison in over 90% of cases (Boonyapisit et al, 2002), proving that the median nerve compression is at the wrist and not elsewhere (Werner et al, 2011).
Median and ulnar motors (include F-waves).
Standard median and ulnar sensories followed by thumbdiff and palmdiff (if they disagree, measure ringdiff).
If CMAPs and SNAPs are not recordable, measure lumbrical to interosseus comparison.
Antebrachials.
If C6/7 radiculopathy suspected, sample APB, FCR, FCU, EDC.
Standard median and ulnar sensories followed by thumbdiff and palmdiff (if they disagree, measure ringdiff).
If CMAPs and SNAPs are not recordable, measure lumbrical to interosseus comparison.
Antebrachials.
If C6/7 radiculopathy suspected, sample APB, FCR, FCU, EDC.
(2) Ulnar neuropathy.
- These are usually at the elbow. Slowing of 10 m/s and/or a drop in CMAP amplitude of >20% across the elbow is significant (Siao et al, 2011).
- If the ulnar (ADM) motor study is normal yet clinical suspicion is high, an ulnar (FDI) recording increases the yield by 10% (Siao et al, 2011).
- For localization, perform a dorsal cutaneous sensory branch recording which is normal in a wrist lesion but abnormal in an elbow lesion.
- These are usually at the elbow. Slowing of 10 m/s and/or a drop in CMAP amplitude of >20% across the elbow is significant (Siao et al, 2011).
- If the ulnar (ADM) motor study is normal yet clinical suspicion is high, an ulnar (FDI) recording increases the yield by 10% (Siao et al, 2011).
- For localization, perform a dorsal cutaneous sensory branch recording which is normal in a wrist lesion but abnormal in an elbow lesion.
Median and ulnar motors (include F-waves).
If ulnar (ADM) is normal but clinical suspicion is high, measure ulnar (FDI).
Standard median and ulnar sensories followed by thumbdiff and palmdiff (if they disagree, measure ringdiff).
If lesion not confirmed at the elbow, measure dorsal cutaneous sensory branch.
Antebrachials.
If C8/T1 radiculopathy suspected, sample FDI, FCU, FPL, EDC.
If ulnar (ADM) is normal but clinical suspicion is high, measure ulnar (FDI).
Standard median and ulnar sensories followed by thumbdiff and palmdiff (if they disagree, measure ringdiff).
If lesion not confirmed at the elbow, measure dorsal cutaneous sensory branch.
Antebrachials.
If C8/T1 radiculopathy suspected, sample FDI, FCU, FPL, EDC.
(3) Radial neuropathy.
- Abnormalities are detected by side-to-side amplitude comparison; velocities are unreliable since distances cannot be measured accurately (Siao et al, 2011).
- Measure the superficial radial nerve bilaterally but remember that it may be spared in spinal groove lesions, and it will definitely be spared in PIN lesions as well as C7 radiculopathy.
- Abnormalities are detected by side-to-side amplitude comparison; velocities are unreliable since distances cannot be measured accurately (Siao et al, 2011).
- Measure the superficial radial nerve bilaterally but remember that it may be spared in spinal groove lesions, and it will definitely be spared in PIN lesions as well as C7 radiculopathy.
Median and ulnar motors (include F-waves).
Radial (EIP) motors with side to side comparison.
Standard median and ulnar sensories followed by thumbdiff and palmdiff (if they disagree, measure ringdiff).
Superficial radial sensories with side to side comparison.
Antebrachials.
If C6/7 radiculopathy suspected, sample EDC, BR, triceps, FCR, FCU.
Radial (EIP) motors with side to side comparison.
Standard median and ulnar sensories followed by thumbdiff and palmdiff (if they disagree, measure ringdiff).
Superficial radial sensories with side to side comparison.
Antebrachials.
If C6/7 radiculopathy suspected, sample EDC, BR, triceps, FCR, FCU.
(4) Brachial plexopathy.
- There are various injuries that may occur to the brachial plexus indicative of a pan, patchy, upper, or lower brachial plexopathy.
- Neuralgic amyotrophy presents with one to several weeks of shoulder, neck, and/or scapular pain with sensory symptoms and weakness, wasting, and/or scapular winging all affecting C5/6. Nerve conduction studies may show pan or patchy abnormal SNAPs. EMG may show spontaneous activity in the cervical paraspinals.
- Erb palsy presents with weakness of C5/6 muscles. Nerve conduction studies show an upper brachial plexopathy with abnormal median SNAPs, superficial radial SNAPs, and lateral antebrachial SNAPs. EMG shows denervation in one or more of supraspinatus, infraspinatus, rhomboids, serratus anterior, deltoid, biceps brachii, and BR.
- Klumpke palsy and thoracic outlet syndrome present with weakness of C8/T1 muscles. Nerve conduction studies show a lower brachial plexopathy with abnormal median CMAPs, ulnar CMAPs, ulnar SNAPs, and medial antebrachial SNAPs. EMG shows denervation in one or more of FPL, APB, FDI, and EDC.
- There are various injuries that may occur to the brachial plexus indicative of a pan, patchy, upper, or lower brachial plexopathy.
- Neuralgic amyotrophy presents with one to several weeks of shoulder, neck, and/or scapular pain with sensory symptoms and weakness, wasting, and/or scapular winging all affecting C5/6. Nerve conduction studies may show pan or patchy abnormal SNAPs. EMG may show spontaneous activity in the cervical paraspinals.
- Erb palsy presents with weakness of C5/6 muscles. Nerve conduction studies show an upper brachial plexopathy with abnormal median SNAPs, superficial radial SNAPs, and lateral antebrachial SNAPs. EMG shows denervation in one or more of supraspinatus, infraspinatus, rhomboids, serratus anterior, deltoid, biceps brachii, and BR.
- Klumpke palsy and thoracic outlet syndrome present with weakness of C8/T1 muscles. Nerve conduction studies show a lower brachial plexopathy with abnormal median CMAPs, ulnar CMAPs, ulnar SNAPs, and medial antebrachial SNAPs. EMG shows denervation in one or more of FPL, APB, FDI, and EDC.
Median and ulnar motors (include F-waves).
Standard median and ulnar sensories (do not chase carpal tunnel syndrome).
Superficial radial sensories with side to side comparison.
Antebrachials.
For upper plexus, sample supraspinatus, infraspinatus, rhomboids, serratus anterior, deltoid, biceps brachii, BR.
For lower plexus, sample FPL, APB, FDI, EDC.
C6 paraspinal.
Standard median and ulnar sensories (do not chase carpal tunnel syndrome).
Superficial radial sensories with side to side comparison.
Antebrachials.
For upper plexus, sample supraspinatus, infraspinatus, rhomboids, serratus anterior, deltoid, biceps brachii, BR.
For lower plexus, sample FPL, APB, FDI, EDC.
C6 paraspinal.
(5) Peripheral neuropathy.
- These may be classified into acute demyelinating, chronic demyelinating, and axonal neuropathies.
- In general, an acute or chronic demyelinating neuropathy must fulfill three of the following criteria, with two or more nerves affected (Siao et al, 2011). If the criteria are not stringently met, a diagnosis of probable demyelinating neuropathy may still be made.
- These may be classified into acute demyelinating, chronic demyelinating, and axonal neuropathies.
- In general, an acute or chronic demyelinating neuropathy must fulfill three of the following criteria, with two or more nerves affected (Siao et al, 2011). If the criteria are not stringently met, a diagnosis of probable demyelinating neuropathy may still be made.
- An axonal neuropathy is indicated by a CMAP amplitude <LLN. Since it involves axonal loss, some of the fastest conducting fibres will be lost and so the CMAP latency may additionally be slightly prolonged and the CMAP velocity slightly reduced.
- In the normal elderly, the sural nerve should always be measurable (Siao et al, 2011). If it is not, move the cathode closer to the active recording electrode to find it, then return to the normal measured distance.
- In the normal elderly, the sural nerve should always be measurable (Siao et al, 2011). If it is not, move the cathode closer to the active recording electrode to find it, then return to the normal measured distance.
Peroneal and tibial motors (include F-waves).
Sural sensories.
Median and ulnar motors (include F-waves).
Standard median and ulnar sensories (do not chase carpal tunnel syndrome).
If a demyelinating neuropathy is clinically suspected, measure more nerves as needed.
Sural sensories.
Median and ulnar motors (include F-waves).
Standard median and ulnar sensories (do not chase carpal tunnel syndrome).
If a demyelinating neuropathy is clinically suspected, measure more nerves as needed.
(6) Peroneal neuropathy.
- The lesion is usually at the fibular neck. Peroneal neuropathy should be differentiated from L5 radiculopathy during the study.
- Nerve conduction studies show abnormal superficial peroneal SNAPs (although they may remain normal for two weeks). EMG shows focal peroneal slowing and/or conduction block at the knee.
- The lesion is usually at the fibular neck. Peroneal neuropathy should be differentiated from L5 radiculopathy during the study.
- Nerve conduction studies show abnormal superficial peroneal SNAPs (although they may remain normal for two weeks). EMG shows focal peroneal slowing and/or conduction block at the knee.
Peroneal and tibial motors (include F-waves).
If focal slowing or conduction block not well demonstrated, measure peroneal (TA).
Sural and superficial peroneal sensories.
To differentiate from L5 radiculopathy, sample TA, TFL, TP.
If focal slowing or conduction block not well demonstrated, measure peroneal (TA).
Sural and superficial peroneal sensories.
To differentiate from L5 radiculopathy, sample TA, TFL, TP.
(7) Lumbosacral plexopathy.
- The usual etiology is diabetic amyotrophy which appears as a painful, asymmetric sensorimotor neuropathy. Patients present with unilateral pain and weakness largely involving the upper plexus as well as autonomic complaints (hypotension, tachycardia, bowel and bladder dysfunction, sexual dysfunction).
- If only the upper lumbosacral plexus (L1-3) is involved, nerve conduction studies show asymmetrically reduced lateral femoral cutaneous SNAPs. EMG shows denervation in iliopsoas, vastus lateralis, and the thigh adductors.
- If only the lower lumbosacral plexus (L4-S4) is involved, nerve conduction studies show asymmetrically reduced peroneal CMAPs, tibial CMAPs, sural SNAPs, and superficial peroneal SNAPs. EMG shows denervation in all lower limb muscles other than iliopsoas vastus lateralis, and the thigh adductors, although TFL, gluteus medius, and gluteus maximus may also be spared and if they are, a sciatic neuropathy is possible.
- The usual etiology is diabetic amyotrophy which appears as a painful, asymmetric sensorimotor neuropathy. Patients present with unilateral pain and weakness largely involving the upper plexus as well as autonomic complaints (hypotension, tachycardia, bowel and bladder dysfunction, sexual dysfunction).
- If only the upper lumbosacral plexus (L1-3) is involved, nerve conduction studies show asymmetrically reduced lateral femoral cutaneous SNAPs. EMG shows denervation in iliopsoas, vastus lateralis, and the thigh adductors.
- If only the lower lumbosacral plexus (L4-S4) is involved, nerve conduction studies show asymmetrically reduced peroneal CMAPs, tibial CMAPs, sural SNAPs, and superficial peroneal SNAPs. EMG shows denervation in all lower limb muscles other than iliopsoas vastus lateralis, and the thigh adductors, although TFL, gluteus medius, and gluteus maximus may also be spared and if they are, a sciatic neuropathy is possible.
Peroneal and tibial motors (include F-waves).
Sural and superficial peroneal sensories.
Lateral femoral cutaneous sensories.
For upper plexus, sample iliopsoas, vastus lateralis.
For lower plexus, sample TFL, gluteus maximus, biceps femoris, TA, medial gastrocnemius.
L4 paraspinal.
Sural and superficial peroneal sensories.
Lateral femoral cutaneous sensories.
For upper plexus, sample iliopsoas, vastus lateralis.
For lower plexus, sample TFL, gluteus maximus, biceps femoris, TA, medial gastrocnemius.
L4 paraspinal.
Electrodiagnosis Of Radiculopathy
Radiculopathy is the other common referral to the electrodiagnostic laboratory. A radiculopathy is a neuropathy of the nerve root as it exits the spinal cord, and most result from root compression due to disc herniation, ligamentous hypertrophy, or bony changes accompanying osteoarthritis (Barr, 2013). This can occur from damage at any level, but if a herniated disc is the problem, it is the disc above the nerve that is most often the culprit - for example, L5 lumbosacral radiculopathy results from posterolateral herniation of the L5 disc (Hsu et al, 2011). These degenerative changes are even common in asymptomatic people - in patients over 60 years of age, lumbar disc protrusions can be seen in 67%, and more than 20% have lumbar canal stenosis (Weishaupt et al, 1998). MRI imaging is highly sensitive at picking up these changes, but it provides no information about nerve function or whether the changes seen are actually the source of any symptoms a patient may be having.
In contrast, EMG is much more specific than MRI imaging. Since it assesses nerve function, if EMG shows evidence of a radiculopathy, the patient almost certainly has one (Barr, 2013). The criteria used to diagnose a radiculopathy are evidence of acute denervation (the presence of fibrillations and positive sharp waves) in either (1) one limb muscle plus paraspinal muscles at the corresponding level or (2) two limb muscles innervated by the same root. When using these criteria, EMG is 100% specific in both asymptomatic patients and patients with low back pain and sciatica (Barr, 2013). Using evidence of chronic denervation (the presence of large, long duration, polyphasic MUAPs), EMG is still 81-100% specific (Tong, 2011).
To achieve this high specificity, a certain number of muscles must be assessed. In one rather thorough study, it was determined that a five-muscle screen including paraspinals identified 94-98% of radiculopathies that could be detected by EMG (Dillingham et al, 2000). Looking for spontaneous activity in the paraspinal muscles was particularly essential to maintaining this high detection rate.
(1) Upper limbs.
- The most common cervical radiculopathy is C7, followed by C6, C8, and C5 (Radhakrishnan et al, 1994). A solid screen for cervical radiculopathy is to look at five muscles (Dillingham, 2000).
In contrast, EMG is much more specific than MRI imaging. Since it assesses nerve function, if EMG shows evidence of a radiculopathy, the patient almost certainly has one (Barr, 2013). The criteria used to diagnose a radiculopathy are evidence of acute denervation (the presence of fibrillations and positive sharp waves) in either (1) one limb muscle plus paraspinal muscles at the corresponding level or (2) two limb muscles innervated by the same root. When using these criteria, EMG is 100% specific in both asymptomatic patients and patients with low back pain and sciatica (Barr, 2013). Using evidence of chronic denervation (the presence of large, long duration, polyphasic MUAPs), EMG is still 81-100% specific (Tong, 2011).
To achieve this high specificity, a certain number of muscles must be assessed. In one rather thorough study, it was determined that a five-muscle screen including paraspinals identified 94-98% of radiculopathies that could be detected by EMG (Dillingham et al, 2000). Looking for spontaneous activity in the paraspinal muscles was particularly essential to maintaining this high detection rate.
(1) Upper limbs.
- The most common cervical radiculopathy is C7, followed by C6, C8, and C5 (Radhakrishnan et al, 1994). A solid screen for cervical radiculopathy is to look at five muscles (Dillingham, 2000).
Deltoid (C5)
Triceps (C7)
PT (C6/7)
APB (C8/T1)
Cervical paraspinal (C6)
Suspect C7 - Add FCR and FCU
Suspect C8 - Add EDC and FPL
Triceps (C7)
PT (C6/7)
APB (C8/T1)
Cervical paraspinal (C6)
Suspect C7 - Add FCR and FCU
Suspect C8 - Add EDC and FPL
- Using any abnormality in spontaneous activity, recruitment, or MUAP morphology as evidence of denervation, this screen catches 98% of detectable cervical radiculopathies, and using only fibrillations and positive sharp waves as evidence of denervation, this screen catches 80% of detectable cervical radiculopathies (Dillingham, 2000). If an abnormality is detected, the sampling should be expanded depending upon which nerve root is suspected.
- The important EMG muscles are as follows.
- The important EMG muscles are as follows.
Accessory - trapezius (C3/4).
Dorsal scapular - rhomboids (C5).
Subscapular - supraspinatus (C5), infraspinatus (C5).
Long thoracic - serratus anterior (C5/6/7).
Axillary - deltoid (C5).
Musculocutaneous - biceps brachii (C5/6).
Median - PT (C6/7), FCR (C7), FPL (C8), PQ (C8), APB (T1).
Ulnar - FCU (C7/8), ADM (C8/T1), FDI (C8/T1).
Radial - triceps (C7), BR (C6), EDC (C7/8), EIP (C8).
Dorsal scapular - rhomboids (C5).
Subscapular - supraspinatus (C5), infraspinatus (C5).
Long thoracic - serratus anterior (C5/6/7).
Axillary - deltoid (C5).
Musculocutaneous - biceps brachii (C5/6).
Median - PT (C6/7), FCR (C7), FPL (C8), PQ (C8), APB (T1).
Ulnar - FCU (C7/8), ADM (C8/T1), FDI (C8/T1).
Radial - triceps (C7), BR (C6), EDC (C7/8), EIP (C8).
- For FCR, insert the needle distal to the midpoint between the biceps tendon and the medial epicondyle.
- For FPL, insert the needle in the lateral forearm between the distal and middle third (not too distal or it may hit the radial artery). The muscle is very superficial. To activate it, flex the thumb DIP.
- For EDC, insert the needle 1 inch distal to the lateral epicondyle. The musle is very superficial. To activate it, extend the middle finger.
- For FPL, insert the needle in the lateral forearm between the distal and middle third (not too distal or it may hit the radial artery). The muscle is very superficial. To activate it, flex the thumb DIP.
- For EDC, insert the needle 1 inch distal to the lateral epicondyle. The musle is very superficial. To activate it, extend the middle finger.
(2) Lower limbs.
- The most common lumbosacral radiculopathy is L5, followed by S1 (Hsu et al, 2011). A solid screen for lumbosacral radiculopathy is to look at five muscles (Dillingham, 2000).
- The most common lumbosacral radiculopathy is L5, followed by S1 (Hsu et al, 2011). A solid screen for lumbosacral radiculopathy is to look at five muscles (Dillingham, 2000).
Vastus medialis (L3/4)
TA (L4/5)
TP (L5)
Medial gastrocnemius (S1)
Lumbar paraspinal (L4)
TA (L4/5)
TP (L5)
Medial gastrocnemius (S1)
Lumbar paraspinal (L4)
- Using any abnormality in spontaneous activity, recruitment, or MUAP morphology as evidence of denervation, this screen catches 98% of detectable lumbosacral radiculopathies, and using only fibrillations and positive sharp waves as evidence of denervation, this screen catches 91% of detectable cervical radiculopathies (Dillingham, 2000). If an abnormality is detected, the sampling should be expanded depending upon which nerve root is suspected.
- The important EMG muscles are as follows.
- The important EMG muscles are as follows.
Femoral - iliopsoas (L2/3), vastus lateralis (L3/4).
Superior gluteal - TFL (L5), gluteus medius (L5).
Inferior gluteal - gluteus maximus (L5/S1).
Sciatic - short head of biceps femoris (S1).
Deep peroneal - TA (L4/5), EHL (L5).
Superficial peroneal - peroneus longus (L5).
Tibial - TP (L5), medial gastrocnemius (S1).
Superior gluteal - TFL (L5), gluteus medius (L5).
Inferior gluteal - gluteus maximus (L5/S1).
Sciatic - short head of biceps femoris (S1).
Deep peroneal - TA (L4/5), EHL (L5).
Superficial peroneal - peroneus longus (L5).
Tibial - TP (L5), medial gastrocnemius (S1).
- For iliopsoas, insert the needle 1 inch lateral to the femoral artery.
- For TFL, insert the needle several centimeters distal to the midway point between the anterior superior iliac spine and the iliac crest.
- For gluteus medius, position the patient laterally and insert the needle between the iliac crest and the greater trochanter. To activate the muscle, abduct the leg.
- For gluteus maximus, position the patient prone and insert the needle in the upper medial quadrant. To activate the muscle, extend the hip or squeeze the buttocks.
- For the short head of biceps femoris, position the patient prone, go four fingerbreadths above the lateral knee, just medial to the tendon.
- For TFL, insert the needle several centimeters distal to the midway point between the anterior superior iliac spine and the iliac crest.
- For gluteus medius, position the patient laterally and insert the needle between the iliac crest and the greater trochanter. To activate the muscle, abduct the leg.
- For gluteus maximus, position the patient prone and insert the needle in the upper medial quadrant. To activate the muscle, extend the hip or squeeze the buttocks.
- For the short head of biceps femoris, position the patient prone, go four fingerbreadths above the lateral knee, just medial to the tendon.
(3) Timing.
- There is a typical evolution of EMG changes in acute or subacute radiculopathy such that the procedure must be timed appropriately.
- There is a typical evolution of EMG changes in acute or subacute radiculopathy such that the procedure must be timed appropriately.
- In chronic radiculopathy, proximal muscles may not show fibrillations or positive sharp waves if reinnervation has been successful, however the distal muscles may show fibrillations and positive sharp waves for years if reinnervation has not been entirely successful (Siao et al, 2011).
(4) Multilevel radiculopathy versus peripheral neuropathy.
- It can often be particularly difficult to differentiate between a multilevel radiculopathy and a peripheral neuropathy. Both result in bilateral lower limb numbness and weakness. Both can show motor and sensory nerve axonal loss on nerve conduction studies (multilevel radiculopathy will not actually result in sensory nerve axonal loss, but superficial peroneal SNAPs may be absent in the elderly) (Barr, 2013).
- Look at the upper limbs, the proximal muscles, and the surals closely.
- Abnormal nerve conduction studies in the upper limbs will occur with a neuropathy, but probably not with a multilevel radiculopathy.
- Abnormal EMG activity will occur in proximal muscles with a multilevel radiculopathy, but probably not with a neuropathy.
- The sural SNAPs will be absent in neuropathy, but should be detectable in multilevel radiculopathy.
- It can often be particularly difficult to differentiate between a multilevel radiculopathy and a peripheral neuropathy. Both result in bilateral lower limb numbness and weakness. Both can show motor and sensory nerve axonal loss on nerve conduction studies (multilevel radiculopathy will not actually result in sensory nerve axonal loss, but superficial peroneal SNAPs may be absent in the elderly) (Barr, 2013).
- Look at the upper limbs, the proximal muscles, and the surals closely.
- Abnormal nerve conduction studies in the upper limbs will occur with a neuropathy, but probably not with a multilevel radiculopathy.
- Abnormal EMG activity will occur in proximal muscles with a multilevel radiculopathy, but probably not with a neuropathy.
- The sural SNAPs will be absent in neuropathy, but should be detectable in multilevel radiculopathy.
Electrodiagnosis Of Scapular Winging
Scapular winging is when the shoulder blade, or scapula, protrudes from the back in an abnormal position. There are five possibilities.
(1) Weak serratus anterior.
- Usually from neuralgic amyotrophy or a damaged long thoracic nerve.
- The scapula is medially and inferiorly displaced.
- Winging is increased by shoulder flexion.
(2) Weak trapezius.
- Usually from a damaged accessory nerve, often from a cervical lymph node biopsy.
- The scapula is laterally and superiorly displaced, with SCM often atrophied.
- Winging is increased by shoulder abduction.
(3) Weak rhomboid.
- Usually from a C5 radiculopathy, but this is a rare source of winging.
(4) FSH dystrophy.
- Associated with weakness in all three muscles.
(5) Scoliosis.
- From an abnormal spinal conformation.
(1) Weak serratus anterior.
- Usually from neuralgic amyotrophy or a damaged long thoracic nerve.
- The scapula is medially and inferiorly displaced.
- Winging is increased by shoulder flexion.
(2) Weak trapezius.
- Usually from a damaged accessory nerve, often from a cervical lymph node biopsy.
- The scapula is laterally and superiorly displaced, with SCM often atrophied.
- Winging is increased by shoulder abduction.
(3) Weak rhomboid.
- Usually from a C5 radiculopathy, but this is a rare source of winging.
(4) FSH dystrophy.
- Associated with weakness in all three muscles.
(5) Scoliosis.
- From an abnormal spinal conformation.
Median and ulnar motors (include F-waves).
Standard median and ulnar sensories (do not chase carpal tunnel syndrome).
Superficial radial sensories with side to side comparison.
Antebrachials.
Sample trapezius.
For upper plexus and C5/6, sample supraspinatus, infraspinatus, rhomboids, serratus anterior, deltoid, biceps brachii, BR.
For lower plexus and C8/T1, sample FPL, APB, FDI, EDC.
C6 paraspinal.
Standard median and ulnar sensories (do not chase carpal tunnel syndrome).
Superficial radial sensories with side to side comparison.
Antebrachials.
Sample trapezius.
For upper plexus and C5/6, sample supraspinatus, infraspinatus, rhomboids, serratus anterior, deltoid, biceps brachii, BR.
For lower plexus and C8/T1, sample FPL, APB, FDI, EDC.
C6 paraspinal.
Electrodiagnosis Of Neuromuscular Disease
The approach depends on the suspected condition.
(1) Myasthenia gravis.
- Postsynaptic disorder that displays postexercise exhaustion (maximal with one minute of exercise) both clinically and on repetitive nerve stimulation.
- Nerve conduction studies to exclude neuropathy. EMG may show "myopathic" MUAPs and varying amplitudes during sustained muscle contraction.
- Repetitive nerve stimulation is important. Normally, low frequency repetitive nerve stimulation produces a progressive decline in quantal content (number of vesicles released per nerve impulse) during the first three to five stimulations due to synaptic vesicle depletion, shown as reduced but not clinically relevant end plate potential amplitudes. An equilibrium is then reached. However, in a postsynaptic disorder the decline in quantal content is clinically relevant and results in transmission failure in a subpopulation of neuromuscular junctions (Siao et al, 2011). On repetitive nerve stimulation this shows up as CMAP amplitude decrement, with a decrement of >10% being abnormal. The decrement-increment pattern is the most common pattern seen in myasthenia gravis though it may also be seen in Lambert-Eaton myasthenic syndrome, motor neuron disease, peripheral neuropathy, and radiculopathy (Siao et al, 2011).
- Following are the best muscles for repetitive nerve stimulation (stimulate at 1, 3, 5 Hz both at rest and postexercise).
(1) Myasthenia gravis.
- Postsynaptic disorder that displays postexercise exhaustion (maximal with one minute of exercise) both clinically and on repetitive nerve stimulation.
- Nerve conduction studies to exclude neuropathy. EMG may show "myopathic" MUAPs and varying amplitudes during sustained muscle contraction.
- Repetitive nerve stimulation is important. Normally, low frequency repetitive nerve stimulation produces a progressive decline in quantal content (number of vesicles released per nerve impulse) during the first three to five stimulations due to synaptic vesicle depletion, shown as reduced but not clinically relevant end plate potential amplitudes. An equilibrium is then reached. However, in a postsynaptic disorder the decline in quantal content is clinically relevant and results in transmission failure in a subpopulation of neuromuscular junctions (Siao et al, 2011). On repetitive nerve stimulation this shows up as CMAP amplitude decrement, with a decrement of >10% being abnormal. The decrement-increment pattern is the most common pattern seen in myasthenia gravis though it may also be seen in Lambert-Eaton myasthenic syndrome, motor neuron disease, peripheral neuropathy, and radiculopathy (Siao et al, 2011).
- Following are the best muscles for repetitive nerve stimulation (stimulate at 1, 3, 5 Hz both at rest and postexercise).
- Single fiber EMG is also important. It uses a special needle electrode with a tiny recording surface to study the action potentials generated by single muscle fibers. In neuromuscular junction disease there is increased jitter (the variation in time interval between two muscle cell action potentials) as a result of spontaneous fluctuations in the rise time of the end plate potentials (Siao et al, 2011).
- In voluntary EMG, the patient cooperates to recruit motor units at a steady rate while the needle electrode is manipulated in the muscle. The recording surface of the needle electrode is placed somewhere between two muscle fibers of the same motor unit - the EMG specifically shows one of them to have a consistent latency while the other one varies (jitter). A study is abnormal if the mean jitter of 20 single fiber pairs exceeds normal limits, or if at least three of the pairs have jitters above normal limits (Siao et al, 2011).
- In stimulated EMG, the muscle fiber action potentials are elicited by microstimulation of motor axons in the endplate zone.
- Following are the best muscles for single fiber voluntary EMG.
- In voluntary EMG, the patient cooperates to recruit motor units at a steady rate while the needle electrode is manipulated in the muscle. The recording surface of the needle electrode is placed somewhere between two muscle fibers of the same motor unit - the EMG specifically shows one of them to have a consistent latency while the other one varies (jitter). A study is abnormal if the mean jitter of 20 single fiber pairs exceeds normal limits, or if at least three of the pairs have jitters above normal limits (Siao et al, 2011).
- In stimulated EMG, the muscle fiber action potentials are elicited by microstimulation of motor axons in the endplate zone.
- Following are the best muscles for single fiber voluntary EMG.
Peroneal and tibial motors (include F-waves).
Sural sensories.
Median and ulnar motors (include F-waves).
Standard median and ulnar sensories (do not chase carpal tunnel syndrome).
Sample vastus lateralis, TA, medial gastrocnemius, deltoid, triceps, FDI.
To assess for abnormal decrement or increment, repetitive nerve stimulation of at least two of ADM, trapezius, nasalis.
To assess for increased jitter, SFEMG of at least one of EDC, frontalis, orbicularis oculi.
Sural sensories.
Median and ulnar motors (include F-waves).
Standard median and ulnar sensories (do not chase carpal tunnel syndrome).
Sample vastus lateralis, TA, medial gastrocnemius, deltoid, triceps, FDI.
To assess for abnormal decrement or increment, repetitive nerve stimulation of at least two of ADM, trapezius, nasalis.
To assess for increased jitter, SFEMG of at least one of EDC, frontalis, orbicularis oculi.
(2) Lambert-Eaton myasthenic syndrome.
- Presynaptic disorder that displays postexercise facilitation (maximal with ten seconds of exercise) both clinically and on repetitive nerve stimulation.
- Nerve conduction studies to exclude neuropathy; may show small CMAPs. EMG shows no spontaneous activity.
- Repetitive nerve stimulation shows decrement with low-frequency stimulations and increment with higher frequencies and postexercise that lasts for several seconds.
(3) Botulism.
- Presynaptic disorder with similar electrographic features to Lambert-Eaton myasthenic syndrome.
- Nerve conduction studies may show small CMAPs. EMG may show spontaneous activity, unlike Lambert Eaton myasthenic syndrome.
- Repetitive nerve stimulation shows increment with higher frequencies and poxtexercise that is smaller in amplitude compared to Lambert Eaton myasthenic syndrome and may last for several minutes.
(4) Organophosphate poisoning.
- Repetitive nerve stimulation may show decrement or a decrement-increment response.
- Presynaptic disorder that displays postexercise facilitation (maximal with ten seconds of exercise) both clinically and on repetitive nerve stimulation.
- Nerve conduction studies to exclude neuropathy; may show small CMAPs. EMG shows no spontaneous activity.
- Repetitive nerve stimulation shows decrement with low-frequency stimulations and increment with higher frequencies and postexercise that lasts for several seconds.
(3) Botulism.
- Presynaptic disorder with similar electrographic features to Lambert-Eaton myasthenic syndrome.
- Nerve conduction studies may show small CMAPs. EMG may show spontaneous activity, unlike Lambert Eaton myasthenic syndrome.
- Repetitive nerve stimulation shows increment with higher frequencies and poxtexercise that is smaller in amplitude compared to Lambert Eaton myasthenic syndrome and may last for several minutes.
(4) Organophosphate poisoning.
- Repetitive nerve stimulation may show decrement or a decrement-increment response.
Electrodiagnosis Of Myopathy
There are four possible EMG patterns with myopathy. Always ensure that repetitive nerve stimulation studies are done to exclude a myasthenic syndrome.
Peroneal and tibial motors (include F-waves).
Sural sensories.
Median and ulnar motors (include F-waves).
Standard median and ulnar sensories (do not chase carpal tunnel syndrome).
Sample weak muscles - if uniform weakness, sample vastus lateralis, TA, medial gastrocnemius, deltoid, triceps, FDI.
To assess for abnormal decrement or increment, repetitive nerve stimulation of at least two of ADM, trapezius, nasalis.
Sural sensories.
Median and ulnar motors (include F-waves).
Standard median and ulnar sensories (do not chase carpal tunnel syndrome).
Sample weak muscles - if uniform weakness, sample vastus lateralis, TA, medial gastrocnemius, deltoid, triceps, FDI.
To assess for abnormal decrement or increment, repetitive nerve stimulation of at least two of ADM, trapezius, nasalis.
Evoked Potentials
Involves stimulation of peripheral nerves and recording over central pathways to assess the integrity of those pathways. The responses are very small compared with the EEG and so background noise is an issue. There are three types - visual evoked potentials (VEPs), auditory/brainstem evoked potentials (AEPs), and somatosensory evoked potentials (SEPs).
Evoked potentials can be useful in certain situations.
(1) Detecting lesions in multiple sclerosis.
- Using VEPs mainly, can detect and localize lesions in the CNS that may be missed by MRI. Can be useful in multiple sclerosis if the diagnosis depends on detecting multifocal lesions.
(2) Intraoperative monitoring.
- Using AEPs mainly, permits the early recognition of dysfunction and therefore damage during a surgical maneuver.
(3) Prognosis in coma.
- Using SEPs, bilateral absence of cortically generated components implies that cognition will not recover.
Evoked potentials can be useful in certain situations.
(1) Detecting lesions in multiple sclerosis.
- Using VEPs mainly, can detect and localize lesions in the CNS that may be missed by MRI. Can be useful in multiple sclerosis if the diagnosis depends on detecting multifocal lesions.
(2) Intraoperative monitoring.
- Using AEPs mainly, permits the early recognition of dysfunction and therefore damage during a surgical maneuver.
(3) Prognosis in coma.
- Using SEPs, bilateral absence of cortically generated components implies that cognition will not recover.
Conclusion
Unlike other tests and scans, nerve conduction studies and EMG require years of passion and experience to perform and interpret well; this is actually part of the appeal. We will now look at each of the major categories of neurological disease one at a time. The emphasis will be on practical aspects with regards to the assessment and treatment of common neurological conditions.
References
American Association of Electrodiagnostic Medicine. 2001. Glossary of terms in electrodiagnostic medicine. Muscle and Nerve supp 10, S1-50.
Barr. 2013. Electrodiagnosis of lumbar radiculopathy. Physical Medicine and Rehabilitation Clinics of North America 24, 79-91.
Boonyapisit et al. 2002. Lumbrical and interossei recording in severe carpal tunnel syndrome. Muscle and Nerve 25(1), 102-105.
Chan. 2002. Needle EMG abnormalities in neurogenic and muscle diseases. Neuromuscular Function and Disease. Saunders.
Dillingham et al. 2000. Identifying lumbosacral radiculopathies: an optimal electromyographic screen. American Journal of Physical Medicine and Rehabilitation 79(6), 496-503.
Gutmann. 1977. Median-ulnar nerve communications and carpal tunnel syndrome. Journal of Neurology, Neurosurgery, and Psychiatry 40, 982-986.
Hsu et al. 2011. Lumbosacral radiculopathy: pathophysiology, clinical features, and diagnosis. UpToDate.
Kimura. 1984. Principles and pitfalls of nerve conduction studies. Annals of Neurology 16, 415-429.
Preston and Shapiro. 2005. Electromyography and Neuromuscular Disorders. Elsevier.
Preston and Shapiro. 2013. Electromyography and Neuromuscular Disorders. Elsevier.
Radhakrishnan et al. 1994. Epidemiology of cervical radiculopathy. A population-based study from Rochester, Minnesota, 1976 through 1990. Brain 117(2), 325-35.
Siao et al. 2011. Practical Approach to Electromyography. Demos Medical, 1st edition.
Tong. 2011. Specificity of needle electromyography for lumbar radiculopathy in 55 to 79 year old subjects with low back pain and sciatica without stenosis. American Journal of Physical Medicine and Rehabilitation 90(3), 233-238.
Wang. 2013. Electrodiagnosis of carpal tunnel syndrome. Physical Medicine and Rehabilitation Clinics of North America 24(2013), 67-77.
Weishaupt et al. 1998. MR imaging of the lumbar spine: prevalence of intervertebral disk extrusion and sequestration, nerve root compression, endplate abnormalities, and osteoarthritis of the facet joints in asymptomatic volunteers. Radiology 209(3), 661-666.
Werner and Andary. 2011. Electrodiagnostic evaluation of carpal tunnel syndrome. Muscle and Nerve, AANEM Monograph #26, 597-607.
American Association of Electrodiagnostic Medicine. 2001. Glossary of terms in electrodiagnostic medicine. Muscle and Nerve supp 10, S1-50.
Barr. 2013. Electrodiagnosis of lumbar radiculopathy. Physical Medicine and Rehabilitation Clinics of North America 24, 79-91.
Boonyapisit et al. 2002. Lumbrical and interossei recording in severe carpal tunnel syndrome. Muscle and Nerve 25(1), 102-105.
Chan. 2002. Needle EMG abnormalities in neurogenic and muscle diseases. Neuromuscular Function and Disease. Saunders.
Dillingham et al. 2000. Identifying lumbosacral radiculopathies: an optimal electromyographic screen. American Journal of Physical Medicine and Rehabilitation 79(6), 496-503.
Gutmann. 1977. Median-ulnar nerve communications and carpal tunnel syndrome. Journal of Neurology, Neurosurgery, and Psychiatry 40, 982-986.
Hsu et al. 2011. Lumbosacral radiculopathy: pathophysiology, clinical features, and diagnosis. UpToDate.
Kimura. 1984. Principles and pitfalls of nerve conduction studies. Annals of Neurology 16, 415-429.
Preston and Shapiro. 2005. Electromyography and Neuromuscular Disorders. Elsevier.
Preston and Shapiro. 2013. Electromyography and Neuromuscular Disorders. Elsevier.
Radhakrishnan et al. 1994. Epidemiology of cervical radiculopathy. A population-based study from Rochester, Minnesota, 1976 through 1990. Brain 117(2), 325-35.
Siao et al. 2011. Practical Approach to Electromyography. Demos Medical, 1st edition.
Tong. 2011. Specificity of needle electromyography for lumbar radiculopathy in 55 to 79 year old subjects with low back pain and sciatica without stenosis. American Journal of Physical Medicine and Rehabilitation 90(3), 233-238.
Wang. 2013. Electrodiagnosis of carpal tunnel syndrome. Physical Medicine and Rehabilitation Clinics of North America 24(2013), 67-77.
Weishaupt et al. 1998. MR imaging of the lumbar spine: prevalence of intervertebral disk extrusion and sequestration, nerve root compression, endplate abnormalities, and osteoarthritis of the facet joints in asymptomatic volunteers. Radiology 209(3), 661-666.
Werner and Andary. 2011. Electrodiagnostic evaluation of carpal tunnel syndrome. Muscle and Nerve, AANEM Monograph #26, 597-607.