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.

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