Applied Anatomy

The dorsal root axons originate from the sensory neurons of the dorsal root ganglia (DRG), which lie outside the spinal canal within the intervertebral foramen (Figure C2-1), and immediately before the dorsal and ventral roots are joined. These sensory neurons are unique because they are unipolar. They have proximal projections through the dorsal root, called the preganglionic sensory fibers, which extend to the dorsal horn and column of the spinal cord. The distal projections of these neurons, called the postganglionic sensory fibers, join the motor fibers in the ventral root to form the spinal nerve, and then pass through the corresponding peripheral nerve to reach their respective sensory end-organs. The ventral root axons are mainly motor, and 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. At each intervertebral foramen, a mixed spinal nerve is formed by the fusion of the dorsal (afferent, sensory) and ventral (efferent, motor, and sympathetic) roots. Nerve roots have no epineurium and less collagen than peripheral nerves, which result in increased susceptibility to compression, stretch, and infiltration.

Figure C2-1 Sagittal section of the lumbar spine, showing the location of the dorsal root ganglia in relation to the spinal canal. Note that the dorsal root ganglia are located in the distal cauda equina within the intervertebral foramen.

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

Each spinal nerve divides as soon as it exits the intervertebral foramina into posterior and anterior rami. The small posterior ramus innervates the paravertebral skin and the deep paraspinal muscles of the neck, trunk, or back. The large anterior ramus innervates the skin and muscles of the remaining trunk or 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. 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 (Figure C2-2). For example, the L3 root exits below the L3 vertebra (i.e., between the L3 and L4 vertebrae).

Figure C2-2 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 the 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.)

In adults, the spinal cord ends at the L1 vertebra, resulting in a disparity between the lengths of the vertebral column and the spinal cord. Hence, spinal cord segments, mostly the thoracic and lumbar, are higher than the corresponding vertebras. This disparity is most pronounced in the lumbar region where there is a difference of approximately three segments, while there is usually a two-segment disparity in the thoracic region (see Figure C2-2). Since the cord terminates at L1 vertebra, the lumbosacral roots traverse relatively long intraspinal courses before exiting through their respective intervertebral foramina, thus forming the cauda equina. Due to the intricate anatomic relationships between the cauda equina and lumbar spinal column, a disc herniation at one level may injure different nerve roots and the vertebral level of a lumbosacral root compression does not always correlate with its exit level. For example, the S1 root is most often compressed by a posterolateral L5–S1 disc herniation (Figure C2-3). Also, the L5 root may be compressed by any disc herniation up to the level of conus medullaris at or rostral to L5–S1 (see Figure C2-2), including a lateral L5–S1 disc herniation and a posterolateral L4–L5 disc herniation. Less often, the L4–L5 disc may protrudes laterally into the foramen at that level and compress the exiting L4 root. If large, the lateral disc may injure both the L4 and L5 roots. Finally, if the L4–L5 disc herniation is central, it may compress several roots on one or both sides of the cauda equina, often asymmetrically.

Figure C2-3 A 42-year-old woman presented with a severe right buttock pain radiating to posterior thigh and calf for 2 months. Neurological examination reveals depressed right ankle jerk only. EDX study reveals fibrillation potentials in the gastrocnemius, biceps femoris, gluteus maximus, and low lumbar paraspinal muscles with normal MUAP recruitment and morphology and normal sural sensory SNAP. The H reflex was absent on the right. T2-weighted MRI of the lumbar spine reveals a large right posterolateral L5–S1 disc herniation (arrows). Note also that several discs (L1–2, L2–3, L4–5, and L5–S1) reveal decreased T2-weighted signal consistent with multilevel degeneration of nucleus pulposus. The patient had complete relief of pain after laminectomy and diskectomy with no further symptoms with a 4-year follow-up.

Clinical Features

Low back pain is an extremely common symptom, but only a relatively small number of patients with low back pain have root compression in the lumbar region. Lumbosacral radiculopathy may be due to a variety of causes (Table C2-1), but is often caused by disc herniation, spondylitic changes (especially at the facetal joints leading to foraminal stenosis), or calcification of the ligamentum flavum. When combined, these changes can result in acquired lumbar canal stenosis. Disc herniation is more common in patients younger than 50 years while degenerative and spondylotic changes are more common in patients older than 50 years.

Table C2-1 Causes of Lumbosacral Radiculopathy

Clinically, root compression often manifests by involvement of the sensory fibers, sensory and motor fibers, or rarely motor fibers only. Hence, the symptoms of lumbosacral radiculopathy include pain, tingling, numbness, or weakness. The pain and the sensory symptoms may be provoked by coughing, sneezing, or other Valsalva maneuvers, and often follow typical dermatomal distributions (radicular pain) that are useful in localization. Similarly, when weakness or reflex changes occur, they follow a corresponding segmental distribution.

Table C2-2 lists common findings in patients with the various lumbosacral radiculopathy. Straight leg raise test is a maneuver that causes stretching of the sciatic nerve, sacral plexus, and the L5 and S1 nerve roots. While the patient is supine, the pain is reproduced with passive straight leg raising or when the examiner flexes the leg at the hip and then extends it at the knee. The test is most reliable when it is positive between 30° and 70°. Reverse straight leg raise testing is performed by passive hip extension while the patient is prone and causes stretching of the femoral nerve, the lumbar plexus, and upper lumbar roots (L2, L3, or L4). Pain in the groin or anterior thigh is considered a positive test.

Lumbosacral root compression may involve a single root (monoradiculopathy) or multiple roots that are contiguous and may be bilateral (polyradiculopathy). Cauda equina lesions should be considered when more than two contiguous nerve roots are involved. Midline cauda equina syndrome results in early compression of sacral nerve roots, which lie medially within the cauda equina, leading to low back pain, sphincteric and sexual dysfunction, and paresthesias and sensory loss in sacral dermatomes (“saddle anesthesia”). When the lesion is large (such as with large midline L4–5 disc herniation), lumbosacral nerve roots may be involved resulting in leg weakness and sensory loss that may develop either early or later in the course, and sometimes result in paraplegia when multiple bilateral nerve roots are involved. Another clinically distinct cauda equina syndrome is the one caused by lumbar canal stenosis (Figure C2-4). This often presents with intermittent neurogenic claudication which is characterized by low back and leg pain, sometimes with paresthesias and weakness, brought on by standing and often worsened by walking. Typically, the symptoms are completely relieved several minutes after the patient sits down and are occasionally improved by bending at the waist. The symptoms are often bilateral but may be unilateral. The neurological examination in patients with lumbar canal stenosis may be entirely normal or show evidence of a single lumbosacral monoradiculopathy or patchy lumbosacral polyradiculopathy often involving the L4, L5, or S1 roots.

Figure C2-4 A 75-year-old woman developed neurogenic claudication (pain in both posterior thigh and legs upon standing and walking relieved by rest) and had a normal neurological examination (except for absent ankle jerks bilaterally). EDX study showed chronic reinnervation changes without fibrillation potentials in the tibialis anterior, extensor hallucis, gastrocnemius, and biceps femoris bilaterally, with normal sural and superficial peroneal sensory responses and absent H reflexes consistent with chronic bilateral L5 and S1 radiculopathies. MRI of the lumbar spine reveals multilevel lumbar canal stenosis, worst at L3–4. (A) Sagittal T2-weighted image. (B) Axial T2-weighted image through L3–4 disc (as shown in A). Note the significant lumbar canal stenosis at L3–4 mostly due to ligamentum flavum thickening and bilateral facetal hypertrophy. The enlarged facet joints encroach on the posterolateral aspect of the spinal canal, creating a trefoil appearance on axial section (arrow). The patient responded very well to an L3–4 epidural block with steroids.

Electrodiagnosis

General Concepts

It is essential to appreciate certain general concepts before one can make such a diagnosis in the EMG laboratory.

1. The SNAPs are normal in radiculopathy despite the presence of sensory loss. Compression of the dorsal (sensory) root, from either disc herniation or spondylosis, usually occurs within the spinal canal proximal to the DRG and results in injury of the preganglionic sensory fibers, but leaves the postganglionic sensory fibers intact (Figure C2-5).

2. Compression of the ventral (motor) root may cause demyelination or axon loss, or both. As with focal lesions of peripheral nerves, this leads to different EDX findings:

• With axon loss, wallerian degeneration occurs. Its effect is readily recognized by the presence of fibrillation potentials, long-duration and high-amplitude MUAPs, and, when severe, low-amplitude CMAPs. The needle EMG is the most sensitive electrodiagnostic test for the diagnosis of radiculopathy, since it may diagnose mild axonal loss by detecting fibrillation potentials generated by the loss of only a few motor axons.

• With pure demyelination, there is either focal slowing or conduction block; both cannot be evaluated well because roots are not accessible to conduction studies (despite attempts to use magnetic or direct needle stimulation). Thus, apart from weakness (and reduced MUAP recruitment), EDX studies might be otherwise normal.

3. The EMG examination determines the injured lumbosacral root(s), and not the vertebral level(s) of root compression or disc herniation. In the lumbar region only, and due to the intricate anatomic relationships between the nerve roots and spinal column, the vertebral level of root compression or disc herniation does not always correlate with the involved root. This is because the spinal cord ends at the L1 vertebral level in adults, and the roots have to travel a relatively long distance before they exit at their respective intervertebral foramina, thereby forming the cauda equina (see Figure C2-2). Thus, in contrast to the cervical and thoracic regions, the EMG performed in the lumbar region has a suboptimal value in predicting the site of the vertebral compression.

4. The needle EMG remains by far the most sensitive electrodiagnostic tool in patients with suspected radiculopathy. Other electrophysiologic studies, including somatosensory evoked potentials, nerve conduction studies, late responses, and thermography, are much less sensitive and their use in practice is limited.

5. By far, the most objective EMG finding in radiculopathy is the presence of fibrillation potentials. Decrease recruitment and large or polyphasic MUAPs are useful findings but when these abnormalities are mild they are more difficult to analyze and may be subject to debate by different observers. Hence, the accuracies of these MUAP findings vary according to the electromyographer’s experience.

6. Fibrillation potentials seldom are found in the entire myotomal distribution of the compressed root. This is best explained by one or more of the following reasons:

• Root compression usually results in partial motor axon loss. Hence, some muscles innervated by the injured root may “escape” denervation and remain normal.

• Proximal muscles innervated by the compressed root undergo more effective collateral sprouting and reinnervation than do distal muscles. This leads to the disappearance of fibrillation potentials in proximal muscles. Hence, in chronic radiculopathy it is more likely to find fibrillation potentials in distal than proximal muscles, despite being innervated by the same root. For example, in L5 radiculopathy, it is more likely to detect fibrillation potentials in the tibialis posterior than in the gluteus medius; both have a preponderant innervation by the L5 root.

• There is likely significant myotomal variability among individuals.

7. F waves are rarely abnormal in radiculopathy. Despite early enthusiasm about the utility of F waves, which test the integrity of the entire motor axon including the ventral roots, the F waves are not sensitive in the diagnosis of lumbosacral radiculopathies for the following reasons:

• The recorded muscle frequently is innervated by more than one root. Thus, in a single-level radiculopathy, normal conduction through the intact neighboring root results in normal F wave minimal latency. For example, in L5 radiculopathy, the peroneal F wave recorded from the extensor digitorum brevis muscle (innervated by L5 and S1 roots) frequently is normal because the compression is concealed by a normal S1 root.

• F wave latency is the most reproducible and clinically useful parameter. However, root compression resulting in significant motor axon loss can be associated with normal F wave latencies because the surviving axons are conducting normally.

• If focal slowing occurs at the root segment of the motor axon, the delay in F wave latency may be obscured, because the latency becomes diluted by the relatively long motor axon.

Figure C2-5 Axial section through the lumbar region showing a common site of root compression.

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

Goals of the Electrodiagnostic Study

The EMG examination plays a pivotal role in the diagnosis, and sometimes the management, of lumbosacral radiculopathy. The diagnostic aims of the EMG 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

Distinguishing a mononeuropathy from radiculopathy is relatively easy when the focal peripheral nerve lesion is associated with conduction block or focal slowing, such as in peroneal mononeuropathy at the fibular neck. Also, fibrillation potentials and MUAP denervation and reinnervation changes are limited to the muscles of the affected peripheral nerve in axon-loss mononeuropathy, while these abnormalities are widespread in radiculopathy and involve muscles that share a segmental innervation, irrespective of their peripheral nerves.

Distinguishing a lumbosacral plexus lesion from lumbosacral radiculopathy is clinically difficult because the same fibers are affected in both cases. Electrodiagnostically, the differential diagnosis depends mainly on two procedures: needle EMG of the paraspinal muscles and assessment of the SNAPs.

• The presence of fibrillation potentials in paraspinal muscles is not consistent with a lumbosacral plexus lesion because these muscles are innervated by the posterior primary rami that leave the spinal roots soon after the intervertebral foramina. Unfortunately, fibrillation potentials are not always present in the paraspinal muscles in chronic radiculopathy, presumably due to effective reinnervation of these muscles.

• SNAPs usually are abnormally low in amplitude or are absent in axon-loss lumbosacral plexopathy, because the lesion affects the postganglionic fibers. In contrast, these studies are normal in radiculopathy, in which compression involves the preganglionic fibers only (i.e., sensory fibers proximal to the DRG). The utility of the SNAP in the confirmation of lumbosacral radiculopathy has however several limitations:

(a) The upper lumbar roots (L2 and L3) do not have a technically feasible SNAP.

(b) The saphenous SNAP, which assesses the L4 root, may be difficult to evoke or absent in a large number of individuals, especially in the elderly, obese, and those with leg edema.

(c) All the SNAPS of the lower extremities may be absent in the elderly, obese, and those with underlying polyneuropathy or leg edema.

(d) The superficial peroneal SNAP is occasionally low in amplitude or absent in L5 radiculopathy. This is explained by an intraspinal location of the L5 DRG rendering the ganglion itself vulnerable to compression by disc herniation or foraminal spondylosis.

(e) 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 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 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 lumbosacral 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 S1 radiculopathy, the sural SNAP should be performed, sometimes bilaterally for comparison. Table C2-3 lists technically feasible SNAPs with their corresponding roots that are helpful in confirming the diagnosis of lumbosacral radiculopathy. Note again that no SNAP has been devised to assess the L2 or L3 fibers, the saphenous SNAP is technically not reliable in assessment of the L4 fibers, and the superficial peroneal SNAP is occasionally low or absent in L5 radiculopathy. Also, all the lower extremity SNAPs frequently are often unevokable bilaterally in elderly or obese patients. These SNAP limitations result in difficulty to differentiate a preganglionic lesion (i.e., lumbosacral radiculopathy) from a postganglionic lesion (i.e., lumbosacral plexopathy), unless fibrillation potentials are evident in the paraspinal muscles.

Table C2-3 Lower Extremity Sensory Nerve Action Potentials (SNAPs) and their Segmental Representation

Root	SNAP
S1	Sural
L5	Superficial peroneal
L4	Saphenous*

* Saphenous SNAP is not always technically reliable especially in the elderly.

Localize the Compression to One or Multiple Roots

This requires meticulous knowledge of the segmental innervation of limb muscles (myotomes). Many myotomal charts have been devised, with significant variability; this may lead to confusion and disagreement between the EMG and the level of root compression as seen by imaging techniques or during surgery. EMG-derived charts also are very helpful and have had anatomic verification (see Tsao et al.). Figure C2-6 shows a common and most useful EMG-extracted myotomal chart.

Figure C2-6 Chart of lower extremity muscles useful in the needle electromyographic recognition of lumbosacral 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.)

A minimal “root search” should be performed in all patients with suspected lumbosacral radiculopathy to ensure that a radiculopathy either is confirmed or excluded. In other words, certain muscles of strategic value in EMG, because of their segmental innervation, should be sampled in these patients (Table C2-4). 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 C2-6), to verify the diagnosis and to establish the exact root(s) compressed. In contrast to limb muscles, fibrillation potentials in the paraspinal muscles are not useful in the diagnosis of the specific compressed root, though they often confirm that the lesion is intraspinal. This is due to observations that each primary posterior ramus has a highly variable segmental innervation that may extend up to 6 segments beyond the vertebral level of its root exit.

Table C2-4 Suggested Muscles to be Sampled in Suspected Lumbosacral Radiculopathy

Muscle	Root Innervation*
Tibialis anterior	L4, L5
Medial gastrocnemius	S1, S2
Flexor digitorum longus and tibialis posterior	L5, S1
Extensor digitorum brevis	L5, S1
Vastus lateralis and medialis	L2, L3, L4
Biceps femoris (short or long head)	L5, S1
Gluteus medius and tensor fascia lata	L5, S1
Mid: lumbar paraspinal
Low: lumbar paraspinal

* Roots in bold type represent the major innervation.

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 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 lumbar 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 satellite 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 lumbosacral 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 a patient with a prior history of a severe lumbosacral 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 erroneously use 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 contrasting situation arises in patients with remote radiculopathy that has resulted in severe axon loss. In these 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 axon loss process.

• The postoperative EDX evaluation of patients with lumbosacral 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 lumbar 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 lumbar 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 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 to conduction block (due to 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 so that weakness may not be or only 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 lower 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 n 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 L5 radiculopathy is the peroneal CMAP, recording from extensor digitorum brevis (L5, S1) or tibialis anterior (L4, L5), borderline or low in amplitude at least after 10 days from onset of acute symptoms.