Radiculopathy is one of the most common diagnoses referred to any electromyography (EMG) laboratory. Even with the widespread use of magnetic resonance imaging, EMG continues to play an important role in the evaluation of radiculopathy. Although imaging studies usually are diagnostic in the more common radiculopathies caused by structural lesions, they often are unrevealing in radiculopathy caused by infection, infiltration, demyelination, or infarction. Whereas imaging studies do well in visualizing the spinal cord and nerve roots and their relationship to the vertebrae and intervertebral discs, they yield no information about how the nerve is functioning. In this regard, EMG complements magnetic resonance imaging with its ability not only to localize the lesion but also to functionally assess the nerve. However, every electromyographer should be aware that EMG has several significant limitations in assessing radiculopathy that can result in false-negative studies.
Clinical
The clinical hallmark of radiculopathy includes pain and paresthesias radiating in the distribution of a nerve root, often associated with sensory loss and paraspinal muscle spasm. Motor dysfunction may also be present. Radiculopathy caused by degenerative bone and disc disease most often affects the cervical (C3–C8) and lower lumbosacral (L3–S1) segments, resulting in well-recognized clinical syndromes ( Tables 29–1 and 29–2 ). Associated paraspinal muscle spasm commonly limits the range of motion, and movement of the neck or back may exacerbate symptoms.
| Root | Pain Location | Sensory Disturbance | Weakness | Reflex Change |
|---|---|---|---|---|
| C3–4 | Paraspinal muscles, superior shoulder | Neck | Diaphragm, nuchal muscles, strap muscles | None |
| C5 | Neck, shoulder, anterior arm | Shoulder | Deltoid, supraspinatus, infraspinatus, rhomboids, biceps, brachioradialis | Biceps, brachioradialis |
| C6 | Neck, shoulder, anterior upper arm extending to antecubital fossa | Thumb, index finger, radial forearm | Deltoid, supraspinatus, infraspinatus, rhomboids, biceps, brachioradialis, pronator teres, flexor carpi radialis, extensor carpi radialis | Biceps, brachioradialis |
| C7 | Neck, shoulder, dorsum of forearm | Middle finger | Triceps, latissimus dorsi, pronator teres, flexor carpi radialis, extensor carpi radialis | Triceps |
| C8 | Neck, shoulder, ulnar forearm | Ring, little fingers, hypothenar eminence | Intrinsic hand muscles, finger extensors, finger flexors | None |
| T1 | Neck, shoulder, ulnar arm | Ulnar forearm | Intrinsic hand muscles (Horner’s syndrome) | None |
| Root | Pain Location | Sensory Disturbance | Weakness | Reflex Change |
|---|---|---|---|---|
| L3 | Anterior thigh, groin | Anterior thigh | Iliopsoas, adductors, quadriceps | (Knee) |
| L4 | Anterior thigh | Medial calf, medial foot | Quadriceps, adductors, (iliopsoas) | Knee |
| L5 | Posterolateral thigh and calf, extending into great toe and dorsum of foot | Dorsum of foot, great toe, lateral calf | Tibialis anterior, tibialis posterior, extensor hallucis longus, peronei, gluteus medius, tensor fascia latae | None |
| S1 | Posterolateral thigh and calf, extending into lateral toes and heel | Lateral foot, posterior calf, sole of foot | Gastroc-soleus, hamstrings, gluteus maximus | Ankle |
The particular sensory and motor symptoms associated with a radiculopathy depend on which nerve root or roots are involved. Each nerve root supplies cutaneous sensation to a specific area of skin, known as a dermatome ( Figures 29–1 and 29–2 ), and motor innervation to certain muscles, known as a myotome ( Tables 29–3 and 29–4 ). Each dermatome overlaps widely with adjacent dermatomes. Consequently, it is very unusual for a patient with an isolated radiculopathy to develop a severe or dense sensory disturbance. Dense numbness usually is more indicative of a peripheral nerve lesion than a radiculopathy. In a patient with radiculopathy, sensory loss more often is vague, poorly defined, or absent, despite the presence of paresthesias.
| Root | Muscle | Nerve |
|---|---|---|
| C4 5 | Rhomboids | Dorsal scapular |
| C 5 6 | Supraspinatus | Suprascapular |
| C 5 6 | Infraspinatus | Suprascapular |
| C 5 6 | Deltoid | Axillary |
| C 5 6 | Biceps brachii | Musculocutaneous |
| C 5 6 | Brachioradialis | Radial |
| C 5 6 7 | Serratus anterior | Long thoracic |
| C5 6 7 | Pectoralis major: Clavicular | Lateral pectoral |
| C6 7 8 T1 | Pectoralis major: Sternal | Medial pectoral |
| C 6 7 | Flexor carpi radialis | Median |
| C 6 7 | Pronator teres | Median |
| C 6 7 | Extensor carpi radialis longus | Radial |
| C6 7 8 | Latissimus dorsi | Thoracodorsal |
| C6 7 8 | Triceps brachii | Radial |
| C6 7 8 | Anconeus | Radial |
| C 7 8 | Extensor digitorum communis | Radial |
| C7 8 | Flexor digitorum sublimis | Median |
| C7 8 | Extensor indicis proprius | Radial |
| C7 8 | Extensor carpi ulnaris | Radial |
| C7 8 T1 | Flexor pollicis longus | Median |
| C7 8 T1 | Flexor digitorum profundus | Median/Ulnar |
| C 8 T1 | Flexor carpi ulnaris * | Ulnar |
| C 8 T 1 | First dorsal interosseus | Ulnar |
| C 8 T 1 | Abductor digiti minimi | Ulnar |
| C 8 T 1 | Abductor pollicis brevis | Median |
* In some individuals, the flexor carpi ulnaris may have a C7 contribution.
| Root | Muscle | Nerve |
|---|---|---|
| L 2 3 4 | Iliacus | Femoral |
| L 2 3 4 | Rectus femoris | Femoral |
| L2 3 4 | Vastus lateralis and medialis | Femoral |
| L2 3 4 | Adductors | Obturator |
| L 4 5 | Tibialis anterior | Deep peroneal |
| L4 5 | Extensor digitorum longus | Deep peroneal |
| L4 5 S1 | Extensor hallucis longus | Deep peroneal |
| L4 5 S1 | Extensor digitorum brevis | Deep peroneal |
| L4 5 S1 | Medial hamstrings | Sciatic |
| L4 5 S1 | Gluteus medius | Superior gluteal |
| L4 5 S1 | Tensor fascia latae | Superior gluteal |
| L 5 S1 | Tibialis posterior | Tibial |
| L 5 S1 | Flexor digitorum longus | Tibial |
| L 5 S1 | Peronei | Superficial peroneal |
| L 5 S 1 | Lateral hamstrings (biceps femoris) | Sciatic |
| L 5 S 1 2 | Gastrocnemius – lateral | Tibial |
| L5 S 1 2 | Gluteus maximus | Inferior gluteal |
| L5 S 1 2 | Abductor hallucis brevis | Tibial–medial plantar |
| S 1 2 | Abductor digiti quinti pedis | Tibial–lateral plantar |
| S 1 2 | Gastrocnemius – medial | Tibial |
| S 1 2 | Soleus | Tibial |
Just as with dermatomes, there is a wide overlap of myotomes. Indeed, nearly every muscle is innervated by at least two if not three myotomes (i.e., nerve roots). For instance, the triceps brachii muscle, predominantly a C7-innervated muscle, also receives some innervation from the C6 and C8 nerve roots. Consequently, paralysis of a muscle is very unusual in an isolated radiculopathy. Even in the case of a severe or complete C7 radiculopathy, the triceps brachii will become weak but not paralyzed, retaining some strength from its partial C6 and C8 innervation.
The deep tendon reflexes may be abnormal in a radiculopathy, depending on the root innervation to the muscle tendon being tested. The biceps and brachioradialis reflexes may be depressed in a lesion of the C5 or C6 nerve roots. The triceps reflex typically is most depressed with a lesion of the C7 nerve root but, because of its significant partial C6 innervation, may be abnormal with a lesion of that root as well. There is no routine reflex to check for a lesion of C8 or T1. In the lower extremities, the knee and ankle reflexes are commonly checked. The knee jerk may be reduced with a lesion of the L3 or L4 (rarely L2) nerve roots and the ankle jerk with a lesion of the S1 nerve root. Again, there is no useful routine reflex to assess the L5 root. Occasionally, a tibialis posterior or medial hamstring reflex can be elicited and, if asymmetric, suggests an L5 radiculopathy. However, both reflexes often are unobtainable in normal individuals.
Etiology
There are a vast number of causes of radiculopathy. The most common are structural lesions, including herniated discs, bony impingement from spondylosis, and mass lesions such as epidural abscesses and metastatic tumors to the spine.
Less well appreciated is that radiculopathy can occur on a microscopic level without evidence of a mass lesion. The cause can be infiltration by tumor (carcinomatous or lymphomatous meningitis), infiltration by granulomatous tissue (e.g., sarcoid), or infection (e.g., Lyme disease, herpes zoster, cytomegalovirus, herpes simplex). Rarely, cases of pure radiculopathy or polyradiculopathy may be due to acquired demyelinating neuropathy (e.g., early Guillain–Barré syndrome). In addition, radiculopathy can be seen as a result of infarction of the nerve root, which may occur in vasculitic neuropathy and presumably occurs commonly in diabetic polyradiculopathy. These nonstructural etiologies illustrate how a patient may have a clinical radiculopathy with completely normal imaging studies. It is in such cases that EMG is especially useful in demonstrating a physiologic radiculopathy.
Differential Diagnosis
The differential diagnosis of pain and radiating paresthesias includes not only radiculopathy but also proximal neuropathy, plexopathy and entrapment neuropathy. Although plexopathies are much less common than radiculopathies, separating plexopathy from radiculopathy on clinical grounds can be quite difficult. In addition, some entrapment neuropathies may be mistaken for radiculopathy, especially when the symptoms are mild. Because an entrapped nerve can cause referred pain and paresthesias, it is possible for distal entrapment to cause symptoms in more proximal segments. For instance, in ulnar neuropathy at the elbow, pain radiating into the upper arm or shoulder is not unusual. Some cases of carpal tunnel syndrome (CTS) are associated with pain in the forearm, the arm, and rarely the shoulder. The presence of referred pain along with distal paresthesias from entrapment neuropathies may suggest radiculopathy. However, pain in the neck or back and exacerbation of symptoms with neck or back movement do not occur in the common entrapment neuropathies and thus provide an important clinical clue pointing to radiculopathy.
Besides plexopathy, proximal neuropathy, and entrapment neuropathy, the major differential diagnosis of radiculopathy includes local orthopedic problems that result in pain and secondary muscle spasm. Often the key task in the EMG laboratory is to try to separate pain due to muscle spasm alone from pain due to true nerve root dysfunction.
Electrophysiologic Evaluation
Nerve Conduction Studies
In patients with radiculopathy, nerve conduction studies typically are normal, and the electrodiagnosis is established with needle EMG ( Box 29–1 ). Although some motor abnormalities are occasionally seen in radiculopathy, the more important reason to perform nerve conduction studies is to exclude other conditions that may mimic radiculopathy, especially entrapment neuropathy and plexopathy. In cases of upper extremity lesions, ulnar neuropathy at the elbow and CTS must be excluded. Ulnar neuropathy and C8 radiculopathy both can present with pain in the arm associated with numbness of the little and ring fingers. Likewise, pain in the arm with paresthesias involving the thumb, index, and middle fingers may be seen in C6–C7 radiculopathy and CTS. In the case of lower extremity symptoms, one must exclude peroneal neuropathy at the fibular neck. Both peroneal palsy and L5 radiculopathy may present with pain in the leg, accompanied by footdrop and paresthesias over the dorsum of the foot and lateral calf. In more severe cases, the clinical differentiation between a radiculopathy and a common entrapment usually is straightforward. In mild or early cases, however, the distinction often is more difficult, and nerve conduction studies are useful to either demonstrate or exclude an entrapment neuropathy.
Upper Extremity
Motor studies:
- •
Perform median and ulnar motor conduction studies, recording abductor pollicis brevis and abductor digiti minimi, respectively. Be sure to exclude carpal tunnel syndrome in suspected C6–C7 radiculopathy and ulnar neuropathy at the elbow in suspected C8 radiculopathy. Ideally, studies should be performed bilaterally if CMAP distal latency, amplitude, or conduction velocity is abnormal or borderline.
Sensory/mixed studies:
- •
Perform at least one sensory study, ideally in the distribution of the suspected radiculopathy (see Table 29–6 ). It is best to perform the sensory studies bilaterally if the amplitude on the symptomatic side is low or borderline.
- •
In suspected C6–C7 radiculopathy (paresthesias into thumb, index, and middle fingers), perform at least one median versus ulnar internal comparison study (e.g., median versus ulnar palm-to-wrist mixed studies), as a sensitive internal control, to definitely exclude electrophysiologic evidence of median neuropathy across the wrist.
Late responses:
- •
Perform median and ulnar F responses. In suspected C8 radiculopathy, these should be performed bilaterally if the results are abnormal or borderline on the symptomatic side.
Lower extremity
Motor studies:
- •
Perform peroneal and tibial motor conduction studies, recording extensor digitorum brevis and abductor hallucis brevis, respectively. Be sure to exclude peroneal palsy at the fibular neck, especially in suspected L5 radiculopathy. Ideally, studies should be performed bilaterally if CMAP distal latency, amplitude or conduction velocity is abnormal or borderline.
Sensory studies:
- •
Perform at least one sensory study, ideally in the distribution of the suspected radiculopathy (see Table 29–6 ). It is best to perform these studies bilaterally if the amplitude on the symptomatic side is low or borderline.
Late responses:
- •
Perform tibial and peroneal F responses. It is best to perform these studies bilaterally if the results are abnormal or borderline on the symptomatic side.
- •
Perform H reflexes to soleus bilaterally, especially when considering S1 radiculopathy.
CMAP, compound muscle action potential.
Depending on the underlying pathophysiology and the level of the lesion, abnormalities occasionally may be seen on routine motor conduction and F response studies in radiculopathy. If the pathophysiology is predominantly demyelinating, the underlying axons remain intact. In that case, any motor study, stimulating and recording distally, will show a normal latency, conduction velocity, and compound muscle action potential (CMAP) amplitude. The only possible abnormality will be in the F responses. Because the F responses assess conduction both distally and proximally, abnormal F responses with normal distal conduction studies suggest a proximal lesion, either in the proximal nerve, plexus or roots. Of course, F waves will be abnormal only if the recorded muscle is innervated by the affected nerve roots.
In the upper extremity, F waves are routinely recorded only for the median and ulnar nerves, which are C8–T1 innervated. Thus, median and ulnar F-wave abnormalities may be seen in C8–T1 radiculopathy; however, these roots are infrequently affected by disc or bone impingement, the most common causes of radiculopathy. A radiculopathy at C5, C6, or C7, which are more common sites of root impingement, will not be reflected in the median or ulnar F responses. The situation is different in the lower extremities. The distally recorded peroneal and tibial muscles (extensor digitorum brevis, abductor hallucis brevis) are innervated predominantly by the L5 and S1 nerve roots, respectively. These levels are often affected by radiculopathy. Thus, in L5–S1 radiculopathies, peroneal and tibial F responses may be prolonged, especially in comparison with the contralateral side.
The H reflex occasionally is helpful in evaluating lower extremity radiculopathy. However, the H reflex, recorded from the soleus, can be used to evaluate only a possible S1 radiculopathy and is most useful when the symptomatic side is compared with the asymptomatic side. The H reflex is the electrical correlate of the ankle reflex; accordingly, it may be delayed or absent in any lesion that depresses the ankle jerk, including polyneuropathy, sciatic neuropathy, lumbosacral plexopathy, and S1 radiculopathy. Unfortunately, the combination of normal distal motor nerve conduction studies and an abnormal H reflex cannot help differentiate between plexopathy and radiculopathy, but can only suggest a proximal lesion.
If the pathophysiology also involves axonal loss, nerve conduction abnormalities may be seen in the motor conduction studies. Here again, abnormalities are seen only if the recorded muscle is innervated by the affected nerve root. Axonal loss may result in a decreased CMAP amplitude, with some slowing of conduction velocity and distal latency, especially if the largest fibers are involved. For instance, in an L5–S1 radiculopathy associated with axonal loss, the ipsilateral peroneal and tibial motor responses may have slightly slowed conduction velocities, slightly prolonged distal latencies, and reduced CMAP amplitudes, especially in comparison with the contralateral side. The distal latency prolongation and conduction velocity slowing, however, should never drop into the demyelinating range.
Sensory studies are the most important part of the nerve conduction studies in the assessment of radiculopathy . The sensory nerve action potential (SNAP) remains normal in lesions proximal to the dorsal root ganglion ( Figure 29–3 ). Nearly all radiculopathies, including those caused by compression from herniated discs and spondylosis, damage the root proximal to the dorsal root ganglion ( Figure 29–4 ). Conversely, lesions at or distal to the dorsal root ganglion result in decreased SNAP amplitudes if they are associated with axonal loss. Thus, lesions of the plexus and peripheral nerve (proximal and distal nerve) are associated with abnormal SNAPs, whereas lesions of the nerve root result in normal SNAPs.
It is always imperative to check the SNAP that is in the distribution of the sensory symptoms ( Table 29–5 ). For instance, if a patient has pain down the arm with tingling and paresthesias of the middle finger, the median sensory response to the middle finger should be checked. In such a case, if the lesion is at or distal to the dorsal root ganglion (e.g., in the brachial plexus or median nerve) and there is axonal loss, the SNAP amplitude will be abnormal, if enough time has passed that wallerian degeneration has taken place. On the other hand, if the lesion is proximal to the dorsal root ganglion (e.g., C7 radiculopathy), the SNAP amplitude will be normal. The presence of a normal SNAP yields important diagnostic information. A normal SNAP in the same distribution as sensory symptoms and signs should always suggest a lesion proximal to the dorsal root ganglion (although a proximal demyelinating or acute peripheral nerve lesion also can result in a normal SNAP). One important rare exception to his rule is discussed below.
| SNAP | Root |
|---|---|
| Lateral antebrachial cutaneous | C5–C6 |
| Radial to the thumb | C6 |
| Median to the thumb | C6 |
| Radial to the snuffbox | C6–C7 |
| Median to the index finger | C6–C7 |
| Median to the middle finger | C7 |
| Median to the ring finger | C7–C8 |
| Ulnar to the ring finger | C7–C8 |
| Ulnar to the little finger | C8 |
| Dorsal ulnar cutaneous | C8 |
| Medial antebrachial cutaneous | T1 |
| Saphenous | L4 |
| Superficial peroneal sensory | L5 |
| Sural | S1 |
Superficial Peroneal SNAP and L5 Radiculopathy: the Rare Exception
If one follows the important tenet of EDX testing that SNAPs are normal in radiculopathy (or any lesion proximal to the dorsal root ganglia), and abnormal in disorders of the peripheral nerve associated with axonal loss (at or distal to the dorsal root ganglia), one will be correct over 99% of the time. However, there is one important exception that deserves comment: in some rare cases of L5 radiculopathy, the superficial peroneal SNAP may be abnormal (abnormal defined as absent, or reduced in amplitude either in an absolute sense or being 50% or less of the contralateral superficial peroneal SNAP). The reason behind this finding is not completely understood. In cadaver and other anatomic studies, the L5 dorsal root ganglion is actually located proximal to the intervertebral foramen in 10–40% of individuals, where it is theoretically susceptible to external intraspinal compression (e.g., from a disc). However, some S1 dorsal root ganglia are similarly located, but abnormalities of the sural sensory nerve are never seen in S1 radiculopathies. This discrepancy may be explained by the fact that in cadaver studies, some L5 dorsal root ganglia are found indented by the superior facet. The superior facet frames part of the intervertebral foramen. In contrast, there is no facet joint that frames the intervertebral foramen for the S1 root.
Regardless of the underlying etiology, this finding of an abnormal superficial peroneal SNAP can be seen, although very rarely, in L5 radiculopathy. The take-home message is the following: in an EDX study wherein all the clinical and electrophysiologic findings are consistent with an L5 radiculopathy, with the exception of an abnormal superficial peroneal SNAP, one can form an EDX impression of an L5 radiculopathy, with the important proviso in the report that these findings could also represent a lumbosacral plexus lesion. Conversely, if the EDX impression is that of a lumbosacral plexopathy, and the only abnormal sensory response is the superficial peroneal SNAP, it is likewise essential to put a proviso in the report that the findings could also represent an L5 radiculopathy with the very unusual variant that the superficial peroneal sensory fibers are involved.
Electromyographic Approach
The needle EMG strategy in radiculopathy is straightforward. Distal, proximal, and paraspinal muscles in the symptomatic extremity are sampled, looking for abnormalities in a myotomal pattern that are beyond the distribution of any one nerve ( Box 29–2 ). It is important to exclude a mononeuropathy, polyneuropathy, or more diffuse process that might account for the signs and symptoms.
- 1
Muscles innervated by the same myotome but by different nerves must be sampled to exclude a mononeuropathy . For example, the finding of fibrillation potentials and decreased recruitment of motor unit action potentials (MUAPs) in the triceps brachii (C6– C7 –C8), extensor carpi radialis ( C6–C7 ), and extensor carpi ulnaris ( C7–C8 ) could indicate an acute, predominantly C7 radiculopathy, since they all share this nerve root. However, because each of these muscles is also innervated by the radial nerve, one could not differentiate between a radial neuropathy and a C7 radiculopathy by sampling only these muscles. If, however, the flexor carpi radialis ( C6–C7 ) or pronator teres ( C6–C7 ) were also sampled and showed fibrillation potentials with reduced recruitment of MUAPs, the pattern of abnormalities could no longer be explained by a single nerve lesion (radial neuropathy) because the last two muscles are both innervated by the median nerve. Since all of these muscles have C7 innervation in common, despite different peripheral nerve innervation, this pattern of abnormalities points toward a radiculopathy as the lesion. Note that while nearly all muscles are innervated by multiple myotomes, certain muscles are predominantly innervated by one myotome, and these muscles are the most useful in the electrodiagnosis of radiculopathy ( Tables 29–6 and 29–7 ).
Table 29–6Related posts:
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