Numbness, pain, and/or weakness involving one or both arms are common reasons for referral to the neuromuscular clinician. These symptoms may be due to radiculopathy, brachial plexopathy, or one or more mononeuropathies. Some systemic etiologies for these focal neuropathic disorders have been discussed in preceding chapters (e.g., Lyme disease, vasculitis, and diabetes mellitus). This chapter will focus mainly on radiculopathies secondary to compression (e.g., degenerative joint disease and herniated discs), brachial plexitis, traumatic plexopathies, and focal mononeuropathies related to compression or entrapment. Before discussing the evaluation and management of these disorders, a review of the normal anatomy would be helpful.

SPINAL NERVES

Recall that there are seven cervical vertebrae, the first of which, the atlas, articulates with the skull’s occipital condyles. The orientation of this joint allows primarily for flexion/extension movements. The second cervical vertebra, the axis, has a superiorly directed bony prominence, the dens, which articulates with the atlas and allows for rotational movements of the head and neck. The third through seventh cervical vertebrae are composed of the vertebral bodies themselves as well as short pedicles giving rise to laminae, which end in comparatively short and often bifid spinous processes. The transverse processes arise near the junctional zone of the pedicle and lamina. Between the transverse processes at each vertebral level lies a sulcus for the spinal nerves.

The spinal nerves are composed of a dorsal root and a ventral root (Fig. 23-1). The dorsal root consists of sensory fibers emanating from the dorsal root ganglia that lie outside the spinal cord. These dorsal root fibers enter the posterolateral aspect of the spinal cord and into the dorsal horn. Along the anterior aspect of the spinal cord, two or as many as 12 individual rootlets arising from anterior horn cells, fila radicularia, fuse to form the ventral root. Just distal to the dorsal root ganglion, the ventral and dorsal roots merge to form the spinal nerve. In the cervical region, there are eight cervical spinal roots on each side but only seven cervical vertebrae (Fig. 23-2). The first cervical spine nerve arises between the skull and atlas. As a result, each numbered cervical nerve root is related to the bony level immediately inferior to it down to the T1 vertebra. For example, the fifth cervical nerve root exits the spinal column just superior to the fifth cervical vertebrae. The eighth cervical nerve root exits the spinal column superior to the first thoracic vertebra.

At the intervertebral foramina, the spinal nerves are joined by the gray rami from the cervical sympathetic chain ganglia (Fig. 23-1). The superior cervical ganglion communicates with C1–4 spinal roots, the middle cervical ganglion with the C5 and C6 spinal nerves, and the inferior cervical ganglion with C8 and T1 spinal roots. Importantly, the sympathetic nerves to head and neck arise from the first thoracic segment. Thus, injuries to the T1 nerve root may result in ipsilateral Horner syndrome (miosis, ptosis, and anhidrosis). Just distal to the entry point of the gray rami, the cervical spinal nerves branch to form an anterior and posterior primary ramus. The nerve fibers in the posterior primary ramus innervate the paraspinal muscles, while the anterior primary rami of C5–T1 cervical spinal nerves form the brachial plexus (Fig. 23-3).

A dermatome refers to the cutaneous region supplied by a specific spinal nerve root segment (Fig. 23-4). Notably, there is some overlap of the cutaneous innervation by individual spinal nerves. The motor fibers emanating from the anterior horn cells, which course through the ventral root, spinal root, brachial plexus, and finally individual nerves, innervate specific muscle groups. Most muscles are supplied by motor nerves arising from at least two spinal cord segments (e.g., the deltoid muscle is innervated by motor fibers within the C5 and C6 spinal roots).

BRACHIAL PLEXUS

The brachial plexus is composed of three trunks (upper, middle, and lower), with two divisions (anterior and posterior) per trunk. Subsequently, the trunks divide into three cords (medial, lateral, and posterior), and from these arise the multiple terminal nerves innervating the arm (Table 23-1,Fig. 23-4).^1–3 More specifically, the anterior primary rami of C5 and C6 fuse to form the upper trunk; the anterior primary ramus of C7 continues as the middle trunk, while the anterior rami of C8 and T1 join to form the lower trunk. Of note, in approximately 62% of anatomic dissections of the brachial plexus, the C4 spinal nerve contributes to the upper trunk.^1,4 In this situation, the brachial plexus is said to be a “prefixed plexus,” in which all of the spinal nerve contributions usually are shifted up one level. As a result, the contribution from the T1 spinal segment to the lower trunk of the brachial plexus may be minimal. In contrast, in approximately 7% of anatomic dissections of the brachial plexus, C5 contributes minimally to the brachial plexus, a so-called “postfixed plexus.”¹ In such cases, the spinal nerve contributions may be shifted down by one level; therefore, C7 contributes to the upper trunk while the lower trunk might receive nerves from the T2 spinal segment. However, the frequency of contributions of C4 and T2 to the brachial plexus is controversial, based on surgical explorations in patients following trauma.^1,5

The anterior divisions of the upper and middle trunks fuse to form the lateral cord, while the anterior division of the lower trunk continues as the medial cord. The three posterior divisions of the upper, middle, and lower trunks join forming the posterior cord. The designations medial, lateral, and posterior cords refer to their respective anatomic positions relative to the axillary artery. The cords constitute the longest subsections of the brachial plexus.⁶ There is some anatomic variation and communication between nerve fibers running between the different cords.^1,4 For example, some nerve fibers may exit the lateral cord and join the medial cord. Thus, the ulnar nerve may have contributions from the C7 spinal nerve.

TERMINAL NERVES

The terminal nerves arise from the brachial plexus and may be purely sensory, motor, or mixed sensorimotor (Fig. 23-3). The dorsal scapular nerve, long thoracic nerve, and a branch to the phrenic nerve arise directly from the spinal roots. The only two terminal nerves arising from the trunks are the subclavian and suprascapular nerves, and these both leave from the upper trunk. No terminal nerves come directly from the middle and lower trunk. The upper and lower subscapular and thoracodorsal nerves depart from the posterior cord, while the posterior cord terminates as the axillary and radial nerves. From the proximal aspect of the medial cord arises a single motor branch innervating the pectoral muscle, the medial pectoral nerve. The purely sensory medial brachial and medial antebrachial cutaneous nerves originate from the distal aspect of the medial cord. The medial cord terminates by sending a medial branch to the median nerve with the remnant continuing as the ulnar nerve. The lateral pectoral nerve comes off the proximal portion of the lateral cord. The lateral cord terminates as the musculocutaneous nerve and a lateral branch that joins a branch from the medial cord to form the median nerve. Individual terminal nerves are discussed in more detail below.

Spinal Accessory Nerve

Although not a nerve arising from the brachial plexus, the spinal accessory nerve or cranial nerve XI courses through the neck and shoulder region and is often affected in brachial plexus injuries. The nerve consists of a bulbar or accessory component that arises from the medulla and a spinal portion that arises from the anterior horn cells in the cervical cord down to C6. The nerves from the bulbar origin supply the soft palate and contribute to the recurrent laryngeal and possibly parasympathetic fibers, which then merge into the vagal nerve to the heart. The spinal component ascends between the ligamentum denticulatum and posterior spinal nerve roots, enters the cranium through the foramen magnum, and then exits the skull via the jugular foramen. The nerve descends posterior to the digastric and stylohyoid muscles to the sternocleidomastoid muscle, which it innervates, and terminates in the trapezius muscle, which it also supplies.

Terminal Nerves Arising from Cervical Roots

Phrenic Nerve

The phrenic nerve is derived primarily from the C4 spinal nerve, but C3 and C5 roots may also contribute (Fig. 23-3). The phrenic nerve crosses the anterior scalene and enters the thorax, where it innervates the diaphragm.

Dorsal Scapular Nerve

The dorsal scapular nerve usually arises directly from the C5 spinal nerve shortly after it exits the intervertebral foramen (Fig. 23-5). The nerve courses between the middle and posterior scalene musculature and innervates the major and minor rhomboid muscles and the levator scapulae.

Long Thoracic Nerve

Branches arising from the C5, C6, and C7 spinal nerves join forming the long thoracic nerve. The nerve descends to the lateral chest wall, where it innervates the serratus anterior muscle.

Terminal Nerves Arising from Trunks

Suprascapular Nerve

The suprascapular nerve arises from the upper trunk shortly after it is formed (Fig. 23-3). The nerve descends posteriorly between the omohyoid and the trapezius muscles. In the posterior shoulder, it courses through the suprascapular notch under the scapula’s superior transverse ligament to innervate the supraspinatus muscle, then through the spinoglenoid notch to innervate the infraspinatus muscle (Fig. 23-5).

Nerve to the Subclavius

This is a small nerve that arises from the C5 root or upper trunk, which innervates the small subclavius muscle that runs between the clavicle and first rib.

Terminal Nerves Arising from Cords

Medial Pectoral Nerves

The medial pectoral nerve arises from the medial trunk (Fig. 23-3). This nerve innervates both the pectoralis major and the pectoralis minor muscles. The major spinal contributions to this nerve are C8 and T1.

Lateral Pectoral Nerves

The lateral pectoral nerve innervates the pectoralis major. It usually comes from the lateral cord, but occasionally arises from the anterior division of the upper and middle trunks just prior to the formation of the lateral cord. This anatomic variation may explain the observation that in plexus injuries affecting the medial and lateral cords resulting in a flail arm, the strength of the pectoralis major muscle may be relatively preserved. The major spinal contributions of this nerve are C5–7.

Subscapular Nerves

The upper and lower subscapular nerves originate from the posterior cord in the axilla. The upper subscapular nerve innervates the subscapularis muscle, while the lower subscapular nerve supplies subscapularis and the teres major muscle. The major spinal contributions to this nerve are from C5 and C6.

Thoracodorsal Nerve

The thoracodorsal nerve, also known as the middle subscapular nerve, comes off the posterior cord and innervates the latissimus dorsi muscle. This nerve can also arise in some cases from the radial and axillary nerves.⁴ The major spinal nerves contributing to the thoracodorsal nerve are C5–7, particularly C7.

Medial Cutaneous Nerve of the Arm

The medial cutaneous nerve of the arm (medial brachial cutaneous nerve) originates from the medial cord and supplies sensation to the medial aspect of the arm. Its primary contribution comes from the C8 and T1 spinal nerves.

Medial Cutaneous Nerve of the Forearm

The medial cutaneous nerve of the forearm (medial antebrachial cutaneous nerve) usually projects from the medial cord, but it may arise from the medial cutaneous nerve of the arm.⁴ The nerve supplies sensation from the medial forearm and also originates from the C8 and T1 spinal nerves.

Musculocutaneous Nerve

The lateral cord terminates as a bifurcation resulting in the musculocutaneous nerve and a lateral branch that combines with a branch from the medial cord to form the median nerve (Fig. 23-6). In about 5% of individuals, the musculocutaneous nerve originates from the anterior division of the upper trunk, in which case the lateral root to the median nerve arises from the middle trunk only.⁴ The major spinal nerves contributing to the musculocutaneous nerve are C5 and C6. In addition, C7 contributes to this nerve in at least half but less than two-thirds of cadavers examined.⁴ The musculocutaneous nerve innervates the coracobrachialis, biceps brachii, and brachialis muscles. It terminates as the lateral cutaneous nerve of the forearm, supplying sensation to the lateral aspect of the volar surface of the forearm.

Axillary Nerve

The axillary nerve contains portions of the spinal nerves arising from C5 and C6 and is one of the two terminal branches of the posterior cord (Fig. 23-7). The nerve usually originates near the subscapularis muscle posterior to the pectoralis minor muscle and then traverses the quadrangular or quadrilateral space formed inferiorly by teres major, laterally by the long head of the triceps brachii, medially by the humerus, and superiorly by the teres minor. Upon exiting this space, the axillary nerve innervates the teres minor and deltoid muscles. The axillary nerve also sends cutaneous branches that supply sensation to the lateral aspect of the proximal arm overlying the deltoid muscle.

Radial Nerve

The radial nerve contains contributions from mainly C5–8 (as well as T1 in approximately 10% of individuals) and, in essence, is a continuation of the posterior cord after the axillary nerve branches off (Fig. 23-8).^1,7 While still in the axillary region, a posterior cutaneous nerve branches off the radial nerve to provide sensation to the posterior aspect of the upper arm to the level of the elbow. In the proximal arm, the radial nerve travels medial to the humerus and descends between the medial and long heads of the triceps muscle along the spiral groove. In the proximal arm, the radial nerve innervates the long, medial, and lateral heads of the triceps brachii and the anconeus muscles. Upon leaving the spiral groove in the mid- to distal aspect of the arm, the radial nerve courses down to the lateral aspect of the arm and innervates the brachioradialis and extensor carpi radialis longus as well as a small branch to the brachialis muscle, the latter receiving its main contribution from the musculocutaneous nerve. An additional branch, the posterior antebrachial cutaneous nerve, separates from the radial nerve in the mid-arm region and descends to supply sensation to the posterior aspect of the forearm.

In the elbow region, the radial nerve splits to form the purely sensory superficial radial nerve and the purely motor posterior interosseous nerve. In this area is the so-called radial tunnel bound by the radius, the capsule of the radiocapitellar joint, the brachialis and biceps brachii tendons (forming the medial walls), and the brachioradialis, extensor carpi radialis, and extensor carpi ulnaris muscles (forming the lateral and anterior walls). The radial tunnel ends at the fibrous band around the superficial head of the supinator muscle, which is known as the arcade of Fröhse. The superficial radial nerve travels on the undersurface of the brachioradialis, outside the radial tunnel, into the forearm. Around the mid-forearm, the nerve moves more superficially and travels along the extensor aspect of the distal forearm. After the superficial radial nerve passes the wrist, it supplies sensation to the lateral, extensor surface of the hand and fingers, analogous to the median distribution on the palmar surface (except the distal aspects of the fingertips on the dorsal surface which are supplied by the median nerve). The posterior interosseous nerve traverses the radial tunnel and then descends under the arcade of Fröhse. The posterior interosseous nerve continues down the extensor aspect of the forearm. Along the way it innervates the supinator, extensor digitorum communis, extensor carpi radialis brevis, extensor digiti minimi, extensor carpi ulnaris, abductor pollicis longus, extensor pollicis longus and brevis, and the extensor indicis proprius.

Median Nerve

The median nerve is formed by the fusion of branches from the lateral and medial cords (Fig. 23-9). The main spinal nerve contributions to the median nerve are C6–T1. Motor fibers arise from C6–T1 spinal segments, while sensory fibers are derived primarily from the C6 and C7 segments. Occasionally, C5 can also contribute to the median nerve.¹ The sensory fibers travel through the upper and middle trunks to the lateral cord into the median nerve, while the motor fibers pass through all the trunks as well as the medial and lateral cords.

The median nerve descends in the anterior compartment of the arm on the medial side to the antecubital fossa region. Past the elbow, the median nerve courses through the two heads of the pronator teres muscle and then between the flexor digitorum superficialis and profundus muscles to the wrist. In the forearm, the median nerve innervates the pronator teres, flexor carpi radialis, palmaris longus, and flexor digitorum superficialis muscles. In the upper to mid-forearm level, the anterior interosseous nerve branches from the main median nerve. This is a pure motor nerve that supplies the flexor digitorum profundus 1 and 2, flexor pollicis longus, and pronator quadratus muscle. The main median nerve trunk continues distally down the forearm to the wrist. Just before entering the carpal tunnel, the palmar cutaneous branch arises to supply sensation over the thenar eminence. The nerve then enters the carpal tunnel bounded by the carpal bones with the transverse ligament serving as the roof. Also within the carpal tunnel lie the nine flexor tendons to the fingers. Within or just distal to the carpal tunnel, the recurrent branch of the median nerve arises and innervates the abductor pollicis brevis, opponens pollicis, and the superficial head of the flexor pollicis brevis. The terminal branches of the median nerve supply the first and second lumbrical muscles, while the digital branches provide sensation to the volar aspects (and the tips of the dorsal aspects) of the thumb, index, and middle fingers, and the lateral half the ring finger.

Ulnar Nerve

The ulnar nerve arises at the termination of the medial cord distal to the medial cutaneous nerves of the arm and forearm and the medial branch of the median nerve (Fig. 23-10). The spinal nerve contributions are mainly C8 and T1, but C7 fibers may also be present in 43–92% of cases, as suggested by brachial plexus dissections.^1,4 The C7 contribution derives from a branch of the lateral cord and innervates the flexor carpi ulnaris muscle. The ulnar nerve descends anterior to the teres major and latissimus dorsi muscles into the arm. Then the nerve travels down the posterior compartment of the upper arm to the ulnar groove at the elbow. The ulnar groove is formed by the medial epicondyle of the humerus and the olecranon process of the ulna, with the ulnar collateral ligament serving as the floor. Approximately 1.0–2.5 cm distal to the ulnar groove, the nerve traverses under a fibrous aponeurotic arch connecting the humeral and ulnar heads of the flexor carpi ulnaris muscle. The area encompassing the ulnar groove and aponeurotic arch is commonly referred to as the cubital tunnel. Of note, the ulnar nerve yields no branches in the arm proximal to the elbow.

Distal to the elbow, the ulnar nerve travels between the flexor carpi ulnaris and flexor digitorum profundus muscles descending to the wrist. In the forearm, it innervates the flexor carpi ulnaris and the flexor digitorum profundus III and IV muscles. The dorsal ulnar cutaneous nerve originates in the mid or distal forearm to provide sensation to the dorsum of the medial aspect of the hand and fourth and fifth digits. Just before entering Guyon’s canal at the wrist, the palmar branch arises to provide sensation to the hypothenar eminence and motor innervation to the palmaris brevis muscle. The remaining components of the ulnar nerve travel into Guyon’s canal, formed by the hook of the hamate bone (on the radial aspect), the pisiform bone (on the ulnar aspect), the pisohamate ligament (serves as the floor), and the transverse carpal ligament (serves as the roof). Within or just distal to Guyon’s canal, the ulnar nerve splits into its terminal branches. A superficial terminal branch supplies sensation to the palmar aspect of the little finger and half of the ring finger, plus some of the distal aspects of these digits dorsally. A deep motor branch innervates the hypothenar muscles and then turns and continues across the hand to innervate the third and fourth lumbricals, interossei, adductor pollicis, and deep head of the flexor pollicis brevis muscle.

Before discussing the approach to patients with focal nerve lesions in the arm, it is important to understand the pathophysiologic basis of these neuropathies. Clinicians need to be aware of the mechanisms of nerve injury so that they can plan, time, and interpret the electrodiagnostic evaluation in order to offer the most accurate prognoses and treatment options. The pathophysiologic bases of nerve injury are limited: demyelination, conduction block, or axonal degeneration. The method by which an individual nerve is injured (e.g., gun shot wound to upper arm, prolonged hyperextension of the arm during surgery, and falling asleep on arm) often provides insight into the underlying pathophysiology.

TYPES OF NERVE FIBER DAMAGE

Neuropraxia

The term “neuropraxia,” also known as first-degree injury, refers to neuronal dysfunction due to transient conduction block.^1,8–10 In regard to focal peripheral nerve lesions, neuropraxia may arise from ischemia or demyelination. Compression of a nerve can result in segmental ischemia, which if of only short duration, results in a rapidly reversible physiologic conduction block lasting minutes or perhaps a few hours. However, experimental studies suggest that pressure related to compression on the nerve can result in distortion of the underlying nerve segment with paranodal and then segmental demyelination.¹¹ Neuropraxia due to demyelination may resolve after several weeks following remyelination of the nerve segment. Thus, prognosis in lesions associated with only conduction block resulting from mechanical (as opposed to immune-mediated or radiation) mechanisms without secondary axonal loss is excellent.

Axonotmesis

Axonotmesis or second-degree injury refers to nerve injuries in which the axon is interrupted but the epineurium is intact.^1,8–10 Following this type of nerve injury, the axon distal to the lesion, now separated from its cell body, will degenerate over the next 7–10 days. Subsequently, regenerating nerve sprouts emerge from the proximal stump of the sectioned nerve to attempt reinnervation of previously denervated tissues (e.g., muscle or cutaneous skin). Because the endoneurium is preserved, there is a greater likelihood that the regenerating axons can grow back and reinnervate denervated tissues than in neurotmesis described below. Axons grow back at a rate of 1 mm/d, so restoration of function can take many months to over a year, depending on the site of the lesion and length of the nerve.

Neurotmesis

Neurotmesis refers to severe, often penetrating nerve injuries, in which the axon and the supporting epineurium are interrupted (i.e., nerve transaction).^1,8–10 Present technology precludes distinction between axonotmesis and neurotmesis without exploratory surgery and direct inspection of the nerve. Because the endoneurium is also interrupted, it is more difficult for regenerating nerve sprouts to reinnervate the target tissues. Scarring secondary to the disruption of the overlying connective tissue can also impede reinnervation. Regenerating nerves may become entwined with the scar tissue creating a neuroma. Thus, the prognosis for spontaneous recovery following this type of lesion is poor.

As with other neuromuscular disorders, the most important step is trying to localize the site of the lesion based on the history and physical examination. Following this, electrodiagnostic studies are performed to confirm the localization or try to localize the exact site of the lesion more accurately, if not apparent by the clinical examination. Often radiologic studies are done to further assist in identifying the site of the lesion and the possible cause. We begin the discussion of the approach of such patients with a review of electrodiagnostic studies that can be helpful.

ELECTRODIAGNOSTIC STUDIES

The evaluation of the arm for possible cervical radiculopathy, brachial plexopathy, or mononeuropathy(ies) requires performing sensory, motor, and mixed sensorimotor nerve conduction studies (NCS) along with electromyography (EMG) (Table 23-2). This text is not meant to be a “how-to book” on EMG and NCS, and for this we refer the reader to several excellent reference books regarding electrodiagnostic medicine (more details can also be obtained in Chapter 2 of this book).^6,12–15 However, clinicians taking care of patients with neuromuscular disorders need to be aware of the utility and limitations of these studies. The electrodiagnostic studies also need to be tailored to the individual patients depending on their symptoms and signs and as the results of the ongoing EMG and NCS are being analyzed.

Sensory NCS

Evaluating the sensory nerve action potentials (SNAPs) is important in distinguishing a radiculopathy from a more distal process. The lesion in most radiculopathies is proximal to the dorsal root ganglia (DRG). Because the cell bodies and distal axons are intact in cervical radiculopathies, the SNAPs should be normal. In contrast, in brachial plexopathies and mononeuropathies (in nerves with sensory fibers), in which the lesion is distal to the dorsal root ganglion, one would expect to see reduced amplitudes of SNAPs in the distribution of the affected nerve, provided there is significant axonal injury. In cases of a demyelinating lesion or conduction block (as the case in neuropraxic injuries), the SNAP distal to the site of the lesion is usually normal. When the injury to the plexus or peripheral nerve is axonal in nature, one also needs to remember that it takes several days from the time of the injury for Wallerian degeneration of the axons to occur distally. Thus, it takes approximately 7–10 days for the SNAPs to disappear, even if the nerve is completely severed. After this period of time there is sufficient degeneration of axons to begin to distinguish postganglionic axonal loss from conduction block/demyelination or a preganglionic lesion. However, an abnormal SNAP does not imply that the spinal root is normal. For example, in traumatic brachial plexopathies, avulsion of nerve root may occur concurrently with injury to nerve distal to the DRG.

It is very important to compare the SNAPs in the affected arm to the analogous nerves in the contralateral arm. It is possible that the SNAP amplitude(s) in an affected arm may still fall “within normal limits” for that electrodiagnostic laboratory even if injured. An asymptomatic limb provides better normative data for that individual than does normative data derived from populations. We, like most electrodiagnosticians, consider SNAP amplitude(s) less than half of that obtained from the analogous nerve in an asymptomatic limb to be abnormal. This of course is not helpful if the symptoms are bilateral.

The specific sensory studies performed are again dependent on the possibilities for the site of the lesion (Table 23-3).¹⁶ If one is evaluating a patient with sensory symptoms affecting the thumb, the possibilities include a C6 radiculopathy, upper trunk, lateral cord, median or radial mononeuropathies, or injury to the digital branches of these nerves. The sensory studies most helpful would be a median SNAP from the thumb or index finger and the superficial radial SNAP, and perhaps the lateral antebrachial cutaneous SNAP. In addition, the median and ulnar mixed nerve palmar studies are helpful to look for carpal tunnel syndrome. As with all electrodiagnostic evaluations, it is important to define the boundaries of abnormality by identifying a normal response in a nerve that is not felt to be clinically affected (e.g., an ulnar SNAP in this situation). If the patient has symptoms involving little finger, then the investigator needs to conduct studies to differentiate a C8/T1 radiculopathy, lower trunk, medial cord, and ulnar neuropathy from one another.

Motor NCS

Evaluation of a motor nerve is performed by stimulating the nerves at several locations and recording the compound muscle action potential (CMAP) from accessible muscle bellies, as discussed in Chapter 2 (Table 23-3).¹⁶ As with sensory studies, the majority of accessible motor stimulation sites are remote from the proximally located lesions associated with a radiculopathy or plexopathy. Thus, it is technically very difficult to assess for a demyelinating/conduction block lesion in these proximal sites. Further, most electrodiagnostic laboratories routinely perform median, ulnar, and radial motor conductions recording from muscles that innervated primarily by the C8–T1 segments. These motor studies are most useful in lower trunk and medial cord injuries as well as median, ulnar, or radial neuropathies. They are of limited value in pathology affecting the C5–7 segments or the elements of the brachial plexus through which these fibers descend. Motor conduction studies can assist in localizing the site and nature of the lesion (e.g., axonal or demyelinating/conduction block) involving testable nerves. Again, following an axonal lesion, one needs to wait about 7–10 days until Wallerian degeneration has occurred and CMAP amplitudes become reliably reduced. Furthermore, in demyelination/conduction block, one could identify this type of lesion only by stimulating the nerve proximal and distal to the site of the lesion. Axillary CMAPs recorded from the deltoid or musculocutaneous CMAPs recorded from the biceps brachii are technically more difficult to perform and interpret and are limited by patient tolerance of the intensity of stimulus often required to achieve a supramaximal CMAP in deeply positioned nerves. In such cases, it would be important to study the contralateral asymptomatic side as a comparison. Radiculopathies are not usually associated with an abnormal CMAP, unless there has been severe end-stage neurogenic atrophy of the muscle. This is a product of most muscles being innervated by more than one nerve root, and by the difficulty of identifying conduction block at the root level. Thus, detecting reduced CMAP amplitudes in cervical radiculopathies is uncommon unless it is severe or there are multiple roots affected.

F-Waves

F-wave studies have limited value in the evaluation of most radiculopathies and entrapment neuropathies. The reason for this is clear if one understands the pathogenesis of most of these focal neuropathies and the limitations inherent in F-wave assessment. The length of a possible compressive/demyelinating lesion is small in most radiculopathies and even mononeuropathies due to entrapment/compression (e.g., ulnar neuropathy at the elbow or median neuropathy at the wrist). Remember, the F-wave latency takes into account the time for the stimulus to travel antegrade through the motor nerve, stimulate a pool of anterior horn cells, and then travel back down the motor axon to stimulate the muscle. Thus, even if there were focal slowing across a small site of demyelination, this may be obscured by the normal conduction to and from the spine across the majority of the nerve. Further, most criteria regarding F-waves use the shortest latencies of multiple responses to define if the study is abnormal. Thus, one only needs to have one normal axon for the F-wave study to be deemed normal. Finally, amplitude measurement, the most important parameter obtained in NCS, cannot be reliably assessed in F-wave studies. However, if one is looking for a large proximal demyelinating lesion, as can be seen in some focal forms of chronic inflammatory demyelinating neuropathy, then F-waves are of some value.

H-Reflex

The only reliable H-reflex in the arm is from the flexor carpi radialis muscle following median nerve stimulation at the antecubital fossa.¹⁷ This study is not routinely performed, as it usually does not assist in localizing the lesion apart from what is gained from the clinical examination, routine motor and sensory NCS, and the EMG. Nevertheless, the H-reflex for the flexor carpi radialis muscle may be abnormal in C6 or C7 radiculopathies, upper or middle trunk plexopathies, lateral cord lesions, or proximal median neuropathies. The major value of the H-reflex in the upper extremities occurs when H-reflexes are recognized during routine NCS. This implicates the presence of pyramidal tract pathology affecting that limb and may shift the investigation of the patient’s complaints from the peripheral to central nervous system.

Somatosensory-Evoked Potentials

Somatosensory-evoked potentials have limited utility in radiculopathies and most neuropathies for much the same reason as discussed with F-waves. However, somatosensory-evoked potentials may be of value in assessment of brachial plexopathies because routine sensory NCS will not pick up a demyelination or conduction in the plexus.^18–20,21

Needle EMG

The EMG examination is essential in the evaluation of patients for radiculopathy, plexopathy, and mononeuropathy. In combination with the clinical examination and carefully performed motor and sensory NCS, EMG of muscles supplied by different spinal roots, trunks, divisions, and cords of the brachial plexus, and different terminal nerves solidifies the localization of the site of the lesion. As discussed in Chapter 2, with EMG we assess the presence of abnormal insertional and spontaneous activity, the morphology of motor unit action potentials (MUAPs), and the recruitment properties of these units. Abnormal insertional or spontaneous activity in the form of positive sharp waves or fibrillation potentials implies membrane instability, which in neurogenic processes is typically due to axonal degeneration. Irritation of the nerve with or without axonal degeneration may result in fasciculation potentials, complex repetitive discharges, or myokymic discharges. The detection of myokymic discharges in a patient with history of cancer and radiation, who is now presenting with focal deficits in an arm, would strongly suggest radiation-induced injury to the roots or plexus as opposed to tumor infiltration. The demonstration of abnormal spontaneous activity in the paraspinal muscles suggests that there is at least some injury to the anterior horn cells or spinal nerves but also does not exclude an injury more distally (e.g., double crush).

Importantly, fibrillation potentials and positive sharp waves may not be present for up to 1 week in a paraspinal muscle and 3 weeks in limb muscles following axonal injury to a nerve root. However, voluntary recruitment of MUAPs is affected immediately. Thus, any injury to the nerve that results in a significant loss of muscle strength should be accompanied by reduced recruitment (e.g., fast-firing) of MUAPs. In neuropraxic injuries in which there is demyelination or conduction block without axonal degeneration, fibrillation potentials and positive sharp waves are not seen and the only abnormality apparent on the EMG is reduced recruitment of MUAPs. Reduced recruitment in the absence of abnormal spontaneous activity, NCS abnormalities, and morphological change in MUAPs more than 3 weeks subsequent to symptom onset implicates conduction block.

Following an axonal injury and muscle fiber reinnervation, fibrillation potentials and positive sharp waves are no longer evident. Reinnervation is more complete in muscles closer to the site of axonal injury (e.g., paraspinal muscles in a radiculopathy). If reinnervation occurs by successful axonal regrowth, then reestablishment of a near-normal number of motor units and innervation ratio, motor unit number and morphology may appear normal. In contrast, if reinnervation takes place via collateral sprouting, the motor units of an effected muscle will remain chronically reduced in number and increased in size, even if strength is reestablished. Muscle groups more distal to the site of the lesion (e.g., hand intrinsic muscles in a cervical radiculopathy) may be less likely to be completely reinnervated, and thus fibrillation potentials and positive sharp waves may persist indefinitely.

Another important point is that because of fascicular arrangement of axons running through various segments of the nerve trunk from the spine to the target muscle, an incomplete nerve injury may not necessarily demonstrate an abnormality in every muscle innervated by an affected spinal nerve root, trunk, cord, or terminal nerve.

RADIOLOGICAL STUDIES

Imaging studies such as a myelogram or magnetic resonance imaging (MRI) of the cervical spinal and brachial plexus are extremely valuable and complement the clinical examination and electrodiagnostic medicine study. MRI has, for the most part, replaced myelogram and computerized axial tomographic (CT) scans except in individuals in whom MRI is contraindicated (e.g., those with magnetic implants) for evaluation of radiculopathies. CT scans, particularly with contrast within the subarachnoid space can be useful²² but high-resolution MRI is much more sensitive for radiculopathies, plexopathies, and focal neuropathies (Figs. 23-11,23-12 and 23-13).^23–29 Several studies have investigated the utility of ultrasound in focal neuropathies.^30–36

CERVICAL RADICULOPATHIES

Recall the disparity between the number of cervical vertebrae (seven) and nerve roots (eight) (Fig. 23-2). As a result, each numbered cervical nerve root is related to the bony level immediately inferior to it. For example, the C5 spinal root exits the spinal column between the fourth and fifth cervical vertebra, and it is vulnerable to compression from a herniated disc (herniated nucleus pulposus or HNP) between C4 and C5. The C6 spinal root exits the spinal column between the fifth and the sixth cervical vertebrae and may be injured from an HNP between C5 and C6. In the same manner, an HNP between C6 and C7 levels may damage the C7 root, while an HNP at the C7 and C8 vertebrae may impinge the C8 nerve root. The T1 spinal nerve exists between the eighth cervical and first thoracic vertebrae and may be damaged by an HNP at this level.

Most cervical radiculopathies involve the C5–8 spinal nerve roots (C7 occurring in 31–81%, C6 in 19–25%, C8 in 4–10%, and C5 in 2–10%).^13,37–41 Causes of cervical radiculopathy are multiple (Table 23-3), and most commonly involve compression of nerve root by an HNP or osteophytes in the case of degenerative spine disease. Individuals with a cervical radiculopathy typically present with neck or posterior shoulder pain in the scapular region that radiates down the affected arm. Turning the head toward the painful arm, particularly with neck extension, can narrow the neural foramen further compressing the nerve root and thus exacerbating the pain, as can downward pressure on the affected individual’s head. The patient may have weakness in the distribution of the affected myotome and sensory loss in the dermatome that is involved. The deep tendon reflexes of affected segment may also be reduced. Because there is much overlap in the territories supplied by individual spinal roots, symptoms and signs can be similar to a plexopathy or focal neuropathy. Therefore, as previously discussed, EMG and NCS combined with imaging studies are extremely valuable in localization. Imaging studies are also important to assess structural etiology (e.g., HNP, osteophyte impinging on root, tumor of the nerve or extrinsic tumor/mass compression of the nerve, or inflammatory process). Further, nerve root avulsion may accompany nearly 80% of severe brachial plexopathies due to trauma.

C5 Radiculopathy

People with a C5 radiculopathy may have weakness of shoulder abduction, external rotation, elbow flexion, and supination of the wrist along with sensory loss in the shoulder region although sensory signs and symptoms may be absent in many cases. The biceps brachii and brachioradialis deep tendon reflexes may be asymmetrically reduced compared to the unaffected limb. Routine median and ulnar motor and sensory NCS are normal, as these do not carry any fibers emanating from the C5 spinal root. Electrodiagnostic localization is dependent on the EMG examination (Table 23-1). Abnormalities in the mid-cervical paraspinal, supraspinatus, infraspinatus, deltoid, biceps brachii, supinator, and brachioradialis muscles are seen in C5 radiculopathies. However, these muscles are also innervated by C6. The rhomboids are primarily innervated by C5, so abnormalities in this group strongly support a C5 radiculopathy. Further, if one sees membrane instability in the triceps brachii, pronator teres, extensor carpi radialis, or flexor carpi radialis that are innervated by C6, but not by C5, the above findings are more consistent with a C6 nerve root lesion or multiple root involvement.

A common differential diagnostic consideration in a patient with C5 radiculopathy is rotator cuff injury, which may also produce shoulder pain and weakness in arm abduction and external rotation. Clinical distinction can be made be reproduction of discomfort by passive movement of the shoulder, rather than at the neck, and by the preservation of biceps strength and reflex in most rotator cuff injuries. Other differential diagnostic considerations not related to trauma or degenerative spine disease include brachial plexopathy, diseases that may present as multifocal neuropathies, and in the absence of pain or paresthesia, motor neuron disease.

C6 Radiculopathy

Individuals with a C6 radiculopathy can present in a similar manner to that described above with a C5 radiculopathy. However, weakness may also involve extension of the elbow (triceps), pronation, and extension of the wrist (extensor carpi radialis). Patients often complain of paresthesia localized to the thumb. In a patient with suspected C6 radiculopathy, one needs to consider an upper trunk or lateral cord lesion, median neuropathy, or radial neuropathy. Therefore, at the very least, we usually perform median and radial SNAPs and a median CMAP. In addition, we obtain lateral antebrachial cutaneous SNAPs, if we are suspicious of a brachial plexopathy affecting the upper trunk. As discussed, these NCS should be normal in a C6 radiculopathy, but the flexor carpi radialis H-reflex may be abnormal. However, localization hinges on the EMG study (Table 23-1). There is significant overlapping of findings in C6 and C5 as well as C7 radiculopathies. Needle EMG may demonstrate abnormalities in the mid to low cervical paraspinals, supraspinatus, infraspinatus, deltoid, biceps brachii, triceps brachii, pronator teres, brachioradialis, supinator, extensor carpi radialis, and flexor carpi radialis muscles. Rotator cuff injury, multifocal neuropathies, and brachial plexus neuritis are likely to be the most common differential diagnostic considerations unrelated to trauma or degenerative joint disease of the cervical spine.

C7 Radiculopathy

People with a C7 radiculopathy often have pain or sensory symptoms radiating down the arm into the middle digit. Weakness of elbow extension and wrist flexion or finger extension may be evident along with a diminished triceps reflex. In patients with suspected C7 radiculopathy, a median CMAP, median SNAP to the third digit, and radial SNAP can be done to assess for a more distal lesion. But again, one should expect routine NCS to be normal in a C7 radiculopathy except for perhaps the flexor carpi radialis H-reflex. On EMG, abnormalities may be detected particularly in the triceps brachii, anconeus, pronator teres, flexor carpi radialis, extensor digitorum communis, and less commonly the extensor digitorum indicis, extensor pollicis longus and brevis, and flexor pollicis longus muscles (Table 23-1). The differential diagnosis of C7 radiculopathy is limited and is probably mimicked most closely by radial mononeuropathies. Most radial neuropathies occur at or distal to the spiral groove, thus resulting in sparing of triceps and prominent weakness of wrist extension. C7 root lesions, on the other hand, typically affect the triceps but rarely produce severe weakness of wrist extension.

C8/T1 Radiculopathy

It is often very difficult to distinguish a C8 from a T1 radiculopathy, so these are discussed together. Individuals who are affected have sensory disturbance affecting the medial aspect of the hand and forearm along with hand weakness. The differential diagnosis included a lower trunk plexopathy such as neurogenic thoracic outlet syndrome, a medial cord lesion, an ulnar neuropathy, and in the absence of pain and sensory symptoms, motor neuron disease. In cases of ulnar neuropathy, the site of the lesion may be at the wrist, elbow, or elsewhere. The NCS are very helpful in terms of localization. It is important to perform ulnar and median CMAPs and SNAPs as well as a medial antebrachial cutaneous SNAP to exclude a plexus or root lesion unless unequivocal focal abnormalities of the ulnar motor conduction studies can be demonstrated (Table 23-3). The SNAPs should be normal in a radiculopathy, but in a lower trunk or medial cord injury the ulnar and medial antebrachial cutaneous SNAP amplitude may be reduced. A reduction in the median CMAP amplitude with a normal median SNAP would further support a lower trunk or medial cord injury (Table 23-2). On EMG, one may see abnormalities in any of the median- or ulnar-innervated muscles innervated by C8 and T1 spinal roots (Table 23-1). The thenar eminence may be predominantly innervated by T1, so the median CMAP amplitude may be disproportionately reduced compared to the ulnar CMAP in a T1 radiculopathy. Most of the radial-innervated muscles supplying the fingers originate from the C7 and C8 spinal segments but not T1. Therefore, EMG of these muscle groups can help distinguish a C8 from a T1 radiculopathy. In the case of a lower trunk lesion, muscles innervating radial muscles via the C8 nerve root will be affected as well as intrinsic hand muscles, whereas this will not be the case in medial cord lesions.

Multiple Cervical Radiculopathies

Most cervical radiculopathies involve only one root, but approximately 12–30% may involve multiple levels.^38,40 If this is the case, CMAP amplitudes are more likely to be reduced although SNAPS will remain spared. The presence of EMG abnormalities suggesting a polyradiculopathy must raise the suspicion of other diseases, particularly motor neuron disease. In such cases, it is important to study the lower extremity, thoracic paraspinals, and even selected cranial nerves (e.g., the tongue and sternocleidomastoid).

THORACIC RADICULOPATHIES

For the sake of completeness, we will briefly discuss thoracic radiculopathies although these are relatively uncommon. HNPs in the thoracic region account for only 0.22–5.3% of all disc protrusions.^42–45 Approximately 75% of symptomatic thoracic radiculopathies occur between T8 and T12, with most occurring between T11 and T12. Central and centrolateral HNPs can compress the spinal cord, leading to symptoms and signs of a myelopathy. Patients may present circumferential chest or abdominal pain and/or paresthesias, leg pain or weakness, or bowel or bladder difficulties (e.g., constipation, urinary retention, and incontinence). At the T11–12 region, the conus medullaris or cauda equina may be affected with ensuing bowel/bladder and lower extremity deficits.

Trauma is the most common cause of a herniated thoracic disc accounting for 14–63% of cases.^46,47 Degenerative changes of the spine account for a minority of cases. Other structural causes for thoracic radiculopathies that need to be considered include compression due to metastatic disease, vertebral collapse, Pott’s disease, and primary nerve tumors. Perhaps, the most common etiology of thoracic radiculopathy is diabetes mellitus (e.g., diabetic radiculoneuropathy). Additional nonstructural causes of thoracic radiculopathies include Lyme disease, herpes zoster, cytomegalovirus, sarcoidosis, and carcinomatous meningitis. Of note, thoracic disc herniations on imaging are far more common than causally related clinical syndromes, and clinicians need to be cautious before attributing nonspecific clinical symptoms to an imaging abnormality.

The electrodiagnostic evaluation of thoracic radiculopathies is limited. NCS are not helpful. EMG may demonstrate abnormal insertional and spontaneous activity in the thoracic paraspinal muscles. Care must be taken not to insert the needle too far so as to avoid a pneumothorax. EMG of abdominal muscles may be of value, as one can also assess for MUAP morphology and recruitment abnormalities.

TREATMENT OF RADICULOPATHIES