Applied Anatomy

The dorsal root axons originate from the sensory neurons of the DRG, which lie outside the spinal canal, within the intervertebral foramen, immediately before the junction of the dorsal and ventral roots (Figure C11-1). These sensory neurons are unique because they are unipolar. They have proximal projections through the dorsal root, called the preganglionic sensory fibers, to the dorsal horn and column of the spinal cord. The distal projections of these neurons, called the postganglionic peripheral sensory fibers, pass through the spinal nerve to their respective sensory end-organs. The ventral root axons, however, are mainly motor (some are sympathetic, with origins from the anterolateral horn of the cord). The motor axons originate from the anterior horn cells within the spinal cord. Passing through the spinal nerves and the peripheral nerve, these motor fibers terminate in the corresponding muscles.

Figure C11-1 Transverse section of the cervical spine, showing the usual site of root injury in cervical radiculopathy due to disc herniation (arrow). Note that the sensory fibers are injured proximal to the dorsal root ganglion, which is located within the intervertebral foramen.

(From Brown WF, Bolton CF. Clinical electromyography, 2nd ed. Boston, MA: Butterworth-Heinemann, 1993, with permission.)

The spinal nerves terminate as soon as they exit the intervertebral foramina, by branching into posterior and anterior rami. The small posterior rami innervate the paravertebral skin and deep paraspinal muscles of the neck, trunk, and back; the large anterior rami innervate the skin and muscles of the trunk and limbs.

In humans, there are 31 pairs of spinal nerve roots: 8 cervical, 12 thoracic, 5 lumbar, 5 sacral, and 1 coccygeal. In the cervical spine, each cervical root exits above the corresponding vertebra that shares the same numeric designation (Figure C11-2). For example, the C5 root exits above the C5 vertebra (i.e., between the C4 and C5 vertebrae). Because there are seven cervical vertebrae but eight cervical roots, the C8 root exits between the C7 and T1 vertebrae; subsequently, all thoracic, lumbar, and sacral roots exit below their corresponding vertebrae. For example, the L3 root exits below the L3 vertebra (i.e., between the L3 and L4 vertebrae).

Figure C11-2 Alignments of spinal segments and roots to vertebrae. The bodies and spinal processes of the vertebrae are indicated by Roman numerals, and the spinal segments and their respective roots by Arabic numerals. Note that the cervical roots (except C8) exit through intervertebral foramina above their respective bodies and that all other roots leave below these bodies.

(From Haymaker W, Woodhall B. Peripheral nerve injuries: principles of diagnosis. Philadelphia, PA: WB Saunders, 1953, with permission.)

Clinical Features

Cervical radiculopathy frequently is the result of a herniated intervertebral disc, or osteophytic spondylitic changes that result in mechanical compression of the cervical root. The symptoms may be acute, subacute, or chronic. Neck pain radiating to the parascapular area and upper extremity, made worse by certain neck positions, is common. The pain radiation tends to follow the dermatomal innervation of the compressed root. Subjective paresthesias within the involved dermatome is more common than objective sensory findings. The diminution of deep tendon reflexes helps in localizing the lesion to one or two roots. Weakness is uncommon; when present, it involves muscles innervated by the compressed root.

The classic study by Yoss et al., published in 1957, remains the best available clinicoanatomic study of cervical root compression. This detailed study analyzed the symptoms and signs of 100 patients with surgically proven single cervical lesions. C7 radiculopathy was the most common cervical radiculopathy, accounting for almost two thirds of patients (Figure C11-3). Figure C11-4 shows the common sensory symptoms and signs observed in these patients, while Figure C11-5 shows the weakened muscles caused by cervical radiculopathy. This study revealed the extreme variability of sensory manifestations in patients with cervical radiculopathy. Also, no single muscle was exclusively diagnostic of a specific root compression. However, based on the data, certain clinical conclusions can be made:

Figure C11-3 Incidence of cervical root involvement in a series of 100 patients with surgically proven single-level lesions.

(Data adapted from Yoss RE et al. Significance of symptoms and signs in localization of involved root in cervical disc protrusion. Neurology 1957;7:673–683, with permission.)

Figure C11-4 Sensory manifestation in patients with established single cervical root lesions (C5–C8). (A) patterns of paresthesias in 91 patients and (B) objective sensory impairment in 23 of the same patients.

(From Yoss RE et al. Significance of symptoms and signs in localization of involved root in cervical disc protrusion. Neurology 1957;7:673–683, with permission.)

Figure C11-5 Incidence and severity of weakness of muscles or groups of muscles in cervical radiculopathy (C5–C8).

Rights were not granted to include this figure in electronic media. Please refer to the printed book.

(From Yoss RE et al. Significance of symptoms and signs in localization of involved root in cervical disc protrusion. Neurology 1957;7:673–683, with permission.)

However, despite the variability in sensory and motor presentations of cervical radiculopathies, certain classical symptoms and signs exist and are extremely helpful in localizing the compressed root. Table C11-1 reveals the common presentations of cervical radiculopathies.

Electrodiagnosis

Goals of the Electrodiagnostic Study

The EDX examination plays a pivotal role in the diagnosis, and sometimes the management, of cervical radiculopathy. The diagnostic aims of the EDX examination in radiculopathy are to:

1. Exclude a more distal lesion (i.e., plexopathy or a mononeuropathy).

2. Confirm evidence of root compression.

3. Localize the compression to either a single or multiple roots.

4. Define the age and activity of the lesion.

5. Define the severity of the lesion.

Exclude a More Distal Nerve Lesion

Differentiating a mononeuropathy from radiculopathy is relatively easy when the focal peripheral nerve lesion is associated with conduction block or focal slowing, such as in carpal tunnel syndrome or ulnar mononeuropathy at the elbow. Also, in mononeuropathy, fibrillation potentials and MUAP reinnervation changes are limited to muscles innervated by the involved peripheral nerve. However, these abnormalities in radiculopathy are more widespread and involve muscles that share the same root innervation, regardless of their peripheral nerve.

Differentiating a brachial plexus lesion from cervical radiculopathy involves mostly evaluating the SNAPs and needle EMG of the cervical paraspinal muscles as well as very proximal muscles.

• The presence of fibrillation potentials in paraspinal muscles is not consistent with a brachial plexus lesion because these muscles are innervated by the dorsal rami before the formation of the plexus. Unfortunately, fibrillation potentials in paraspinal muscles are not always present in radiculopathy, presumably due to of effective reinnervation of these very proximal muscles.

• Detecting signs of denervation and reinnervation in muscles innervated by peripheral nerves arising before the formation of the brachial plexus is a strong support for the diagnosis of cervical radiculopathy. These muscles are the rhomboids (C5 root via the thoracodorsal nerve) and serratus anterior (C6, C7, C8 roots via the long thoracic nerve) (see Figure C13–2 in Case 13). One caveat is that these nerves may be selectively injured along with the brachial plexus during shoulder trauma or with a bout of neuralgic amyotrophy (see Case 16).

• In brachial plexopathy, the SNAPs usually are abnormally low in amplitude, or they are absent, because the lesion affects the postganglionic fibers. In contrast, these studies are normal in cervical radiculopathy, in which compression involves the preganglionic fibers only (i.e., sensory fibers proximal to the DRG). However, the utility of the SNAP in the confirmation of cervical radiculopathy has few limitations:

(a) The C5 cervical root does not have a technically feasible SNAP.

(b) The medial brachial SNAP, which assesses the T1 root, may be difficult to evoke or is absent bilaterally in a significant number of individuals, especially in the elderly, obese, and those with limb edema.

(c) The SNAP amplitudes may be low or absent if the DRGs are involved by the pathological condition that may affect the DRG preferentially or extend from the intraspinal space through the neural foramen to the extraspinal space or vice versa. Examples include infiltrative malignancy such as lymphoma, infection such as herpes zoster, tumor such as schwannoma or meningioma, or autoimmune attack on DRG such as in Sjogren syndrome or with small-cell lung cancer.

Confirm Evidence of Root Compression

Two criteria are necessary to establish the diagnosis of cervical radiculopathy.

1. Denervation in a segmental myotomal distribution (i.e., in muscles innervated by the same roots via more than one peripheral nerve), with or without denervation of the cervical paraspinal muscles. At least two muscles, and preferably more, should reveal evidence of denervation (fibrillation potentials and/or reinnervation MUAP changes and reduced recruitment). Fibrillation potentials in the paraspinal muscles are strong evidence of a root lesion within the spinal canal. However, they may be absent particularly in chronic radiculopathies, likely due to effective reinnervation.

2. Normal SNAP of the corresponding dermatome. Once myotomal denervation is detected by needle EMG, the lesion must be confirmed as preganglionic (i.e., within the spinal canal) and not postganglionic (i.e., due to a brachial plexus injury). This can be achieved by recording one or more dermatomal SNAPs, appropriate for the myotome involved, and then establishing SNAP normality. For example, in a suspected C7 radiculopathy, the median SNAP recording middle finger should be performed, preferably bilaterally for comparison. Table C11-2 lists technically feasible SNAPs with their corresponding roots that are helpful in confirming the diagnosis of cervical radiculopathy. Note that no SNAP has been devised to assess the C5 fibers, and the medial brachial SNAP is not always technically reliable in assessing the T1 fibers. These SNAP limitations, though much less significant than the lower extremity SNAPs, result in occasional difficulties in distinguishing a preganglionic lesion (i.e., cervical radiculopathy) from a postganglionic lesion (i.e., brachial plexopathy), unless fibrillation potentials are evident in the cervical paraspinal or very proximally innervated muscles (serratus anterior or rhomboids).

Table C11-2 Upper Extremity Sensory Nerve Action Potentials (SNAPs) and Their Segmental Representation

Root	SNAP
C6	Lateral antebrachial (Lateral cutaneous of forearm)
	Median recording thumb
	Median recording index
	Radial recording dorsum of hand
C7	Median recording index
	Median recording middle finger
	Radial recording dorsum of hand
C8	Ulnar recording little finger
	Medial antebrachial (Medial cutaneous of forearm)
T1	Medial brachial (Medial cutaneous of arm)

Localize the Compression to One or Multiple Roots

This requires meticulous knowledge of the segmental innervation of both limb muscles (myotomes) and skin (dermatomes). Many myotomal charts have been devised, with significant variability; this may lead to confusion and disagreement between the needle EMG and the level of root compression as seen by imaging techniques or during surgery. EMG-derived charts are also helpful and have had anatomic confirmation (see Levin et al. and Katirji et al.). Figure C11-6 reveals a common and most useful EMG-extracted myotomal chart.

Figure C11-6 Chart of upper extremity muscles useful in the electromyographic recognition of cervical radiculopathy. Solid squares indicate muscles that most often contain abnormalities, and checkered squares indicate muscles that are abnormal less frequently.

(From Brown WF, Bolton CF. Clinical electromyography, 2nd ed. Boston, MA: Butterworth-Heinemann, 1993, with permission.)

A minimal “root search” should be performed in all patients with suspected cervical radiculopathy to ensure that a radiculopathy is either confirmed or excluded. In other words, certain muscles of strategic value in EMG because of their segmental innervation should be sampled (Table C11-3). When abnormalities are found or when the clinical manifestations suggest a specific root compression, more muscles must be sampled after being selected based on their innervation (see Figure C11-6), to verify the diagnosis and establish the exact compressed root(s).

Table C11-3 Suggested Muscles to be Sampled in Patients With Suspected Cervical Radiculopathy^*

First dorsal interosseous	C8, T1
Flexor pollicis longus	C8, T1
Pronator teres	C6, C7
Biceps	C5, C6
Triceps	C6, C7, C8
Deltoid	C5, C6
Mid-cervical paraspinal	C5, C6
Low-cervical paraspinal	C7, C8

* Roots in bold type represent the major innervation.

Once myotomal denervation is detected by needle EMG, it is essential to confirm that the lesion is preganglionic (i.e., within the spinal canal) and not postganglionic (i.e., due to a brachial plexus injury). This can be achieved by recording one or more SNAPs appropriate for the myotome involved, and then establishing normality of SNAPs. For example, in a suspected C6 radiculopathy, the antidromic (or orthodromic) median SNAPs, recording the thumb and index, should be performed, preferably bilaterally for comparison (see Table C11-2).

Define the Age and Activity of the Radiculopathy

Changes seen on needle EMG help to determine the age of the lesion in an axon-loss cervical radiculopathy. As with many processes wherein motor axon loss occurs, increased insertional activity is the first abnormality seen and, when isolated, suggests that the process may be only 1–2 weeks old. Fibrillation potentials, which are spontaneous action potentials generated by denervated muscle fibers, develop soon after and become full after 3 weeks from acute motor axonal loss. These potentials often appear first in the cervical paraspinal muscles, then in proximal muscles, and lastly in distal muscles. They also disappear after reinnervation or following muscle fiber fatty degeneration. As time elapses, collateral sprouting from intact axons results in MUAPs with polyphasia and satellites potentials. These MUAPs, usually seen after 2 to 3 months from acute injury, are often unstable by showing moment-to-moment variation in morphology. With further time, MUAPs with high amplitude and long duration dominate, reflecting a more complete reinnervation and the chronicity of the root compression.

In assessing a patient with possible cervical radiculopathy, it is often important to comment on whether the root compression is chronic or ongoing (active). This is easy when one encounters large and stable MUAPs, reflecting chronicity, along with fibrillation potentials, reflecting ongoing (active) denervation. In contrast, when fibrillation potentials are absent, it is presumed that the findings are chronic and remote, such as in patients with a prior history of a severe cervical radiculopathy. This simplistic differentiation has, however, several limitations:

• It is not uncommon that the electromyographer cannot distinguish with certainty between a patient with chronic ongoing root compression (such as with spondylosis) from one with chronic remote (old) root compression (such as with a prior disc herniation). In situations where the rate of motor axon loss is slow, reinnervation may keep pace with denervation that no or minimal fibrillation potentials are seen on needle EMG. Some electromyographers may use erroneously the absence of fibrillation potentials as absolute evidence against ongoing root compression. A correlation with the clinical history, the neurological findings, and the imaging is warranted.

• A contrast situation rise in patients with remote radiculopathy that had resulted in severe axon loss. In these clinically inactive cases, some muscle fibers never fully reinnervate, especially in distal muscles located farthest from the injury site. In these radicular lesions, fibrillation potentials may continue to be seen in distal muscles, mistakenly suggesting that there is an ongoing root compression and axon loss process.

• The postoperative EDX evaluation of patients with cervical radiculopathy is challenging particularly when there was no preoperative EDX study. Since fibrillation potentials may persist for several months despite successive surgery, their presence does not mean a failed surgical procedure. Additionally, fibrillation potentials may be present in the paraspinal muscles after posterior cervical spine surgery because of muscle denervation during surgical exposure. Because of this, many electromyographers, including the author, will not sample the paraspinal muscles if a patient has a history of posterior cervical spine surgery. These postoperative EDX studies are often not satisfying to the electromyographer or clinician, since they cannot exclude or confirm persistent root compression.

Define the Severity of the Radiculopathy

In assessing the severity of a radiculopathy, one erroneously tends to rely on the degree of abnormalities seen on needle EMG, namely decreased recruitment (“neurogenic” MUAP firing pattern), fibrillation potentials, and MUAP configuration. Using these parameters in assessing severity of lesion (i.e., extent of axon loss) is suboptimal for the following caveats:

1. Although there is a correlation between the degree of reduced MUAP recruitment and the degree of weakness, decreased recruitment is not necessarily due to axon loss but may be due conduction block (segmental demyelination) at the root level. The latter has a very good prognosis for rapid recovery.

2. Although the presence of fibrillation potentials is consistent with motor axon loss, measuring the number of fibrillation potentials in a muscle is subjective and does not correlate with the degree of axon loss. Fibrillation potentials denote a recent axon loss but cannot assess its severity.

3. MUAP reinnervation changes are permanent. However, reinnervation may be quite robust that weakness may not or be minimally detected. Hence, finding very large MUAPs (giant MUAPs) does not always reflect severity or prognosis.

The best indicator of motor axon loss is the CMAP amplitude (or area) recorded during routine motor nerve conduction studies of the upper extremity. Although these studies are performed distally and do not include the roots, a root lesion causing demyelinative conduction block (or focal slowing), with little or no accompanying axonal degeneration, may result in weakness, but does not lead to any decrease in CMAP amplitude or other abnormalities on motor conduction studies. Only when significant axonal loss occurs at the root level does the CMAP recording from an involved muscle become low in amplitude (or occasionally absent when multiple adjacent roots are compressed). In acute lesions, this is only detected when sufficient time has elapsed for wallerian degeneration to occur (usually 7–10 days). For example, only in moderate or severe C8 radiculopathy is the ulnar CMAP, recording from abductor digiti minimi (C8, T1), borderline or low in amplitude at least after 10 days from onset of acute symptoms.