29 Radiculopathy

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.

Table 29–1 Common Cervical Root Syndromes

Table 29–2 Common Lumbar Root Syndromes

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.

FIGURE 29–1 Cervical and thoracic dermatomes.

(From Aids to the examination of the peripheral nervous system. London: Baillière Tindall. With permission, 1986.)

FIGURE 29–2 Lower thoracic and lumbosacral dermatomes.

(From Aids to the examination of the peripheral nervous system. London: Baillière Tindall. With permission, 1986.)

Table 29–3 Root Innervation of Major Upper Extremity Muscles

Root	Muscle	Nerve
C4 5	Rhomboids	Dorsal scapular
C5 6	Supraspinatus	Suprascapular
C5 6	Infraspinatus	Suprascapular
C5 6	Deltoid	Axillary
C5 6	Biceps brachii	Musculocutaneous
C5 6	Brachioradialis	Radial
C5 6 7	Serratus anterior	Long thoracic
C5 6 7	Pectoralis major: Clavicular	Lateral pectoral
C6 7 8 T1	Pectoralis major: Sternal	Medial pectoral
C6 7	Flexor carpi radialis	Median
C6 7	Pronator teres	Median
C6 7	Extensor carpi radialis longus	Radial
C6 7 8	Latissimus dorsi	Thoracodorsal
C6 7 8	Triceps brachii	Radial
C6 7 8	Anconeus	Radial
C7 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
C8 T1	Flexor carpi ulnaris*	Ulnar
C8 T1	First dorsal interosseus	Ulnar
C8 T1	Abductor digiti minimi	Ulnar
C8 T1	Abductor pollicis brevis	Median

Note: Underlining indicates predominant root innervation.

^* In some individuals, the flexor carpi ulnaris may have a C7 contribution.

Table 29–4 Root Innervation of Major Lower Extremity Muscles

Root	Muscle	Nerve
L2 3 4	Iliacus	Femoral
L2 3 4	Rectus femoris	Femoral
L2 3 4	Vastus lateralis and medialis	Femoral
L2 3 4	Adductors	Obturator
L4 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
L5 S1	Tibialis posterior	Tibial
L5 S1	Flexor digitorum longus	Tibial
L5 S1	Peronei	Superficial peroneal
L5 S1	Lateral hamstrings (biceps femoris)	Sciatic
L5 S1 2	Gastrocnemius – lateral	Tibial
L5 S1 2	Gluteus maximus	Inferior gluteal
L5 S1 2	Abductor hallucis brevis	Tibial–medial plantar
S1 2	Abductor digiti quinti pedis	Tibial–lateral plantar
S1 2	Gastrocnemius – medial	Tibial
S1 2	Soleus	Tibial

Note: Underlining indicates predominant root innervation.

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.

Box 29–1

Recommended Nerve Conduction Study Protocol for Radiculopathy

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.

FIGURE 29–3 Sensory and motor potentials in axonal loss lesions distal and proximal to the dorsal root ganglion.

A: Normal. B: Lesion proximal to the dorsal root ganglion. C: Lesion at or distal to the dorsal root ganglion. In axonal loss lesions, both proximal and distal to the dorsal root ganglion, degeneration of motor fibers results in decreased compound motor action potential amplitudes. If larger motor fibers are lost, conduction velocities and distal latencies also may slow slightly. The situation is different for sensory fibers. Lesions proximal to the dorsal root ganglion result only in degeneration of sensory fibers proximally into the spinal cord. Because the dorsal root ganglion is a bipolar cell, it remains in continuity with the distal sensory fibers. Therefore, sensory nerve action potentials (SNAPs), when stimulated and recorded distally, remain normal. In axonal loss lesions at or distal to the dorsal root ganglion, distal sensory fibers degenerate, as do the motor fibers. Accordingly, SNAPs are reduced in lesions of the plexus and peripheral nerve but are normal in radiculopathies and other lesions proximal to the dorsal root ganglion.

FIGURE 29–4 Radiculopathy and sparing of the dorsal root ganglion.

Herniated intervertebral discs are a common cause of cervical and lumbosacral radiculopathy. Herniated discs are most often lateral and posterior, with the dorsal root ganglion located distal to the herniation. In disc herniations, this anatomic relationship results in injury to the roots but sparing of the dorsal root ganglion and the peripheral sensory nerves. Consequently, sensory conduction studies remain normal in radiculopathy.

(From Wilbourn, A.J., 1993 Radiculopathies. In: Brown, W.F., Bolton, C.F. (Eds.), Clinical electromyography, 2nd ed. Butterworth, Boston. With permission.)

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.

Table 29–5 Sensory Potentials to Check in Radiculopathy

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

SNAP, sensory nerve action potential.

Note: SNAPs are normal in lesions proximal to the dorsal root ganglion, including lesions resulting in radiculopathies. When evaluating a possible radiculopathy, one should examine at least one SNAP in the distribution of the suspected radiculopathy. For example, the ulnar SNAP to the little finger should be normal in a C8 radiculopathy. If it is abnormal, the lesion likely is not at the root, unless there is another reason for the SNAP to be abnormal, such as a superimposed ulnar neuropathy at the elbow.