Case 12

Published on 03/03/2015 by admin

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Case 12

EDX FINDINGS AND INTERPRETATION OF DATA

Abnormal EDX findings include:

1. A partial right radial motor conduction block across the spiral groove, as evidenced by a drop in amplitude of the compound muscle action potential (CMAP) from 5.6 mV, stimulating below the spiral groove, to 2.0 mV, stimulating above the spiral groove (Figure C12-1). This 64% amplitude decay is supported by the lack of significant CMAP dispersion and the concomitant decrease in negative CMAP area from 25.5 mV/ms to 5.65 mV/ms, respectively (78% area loss). Also, there is relative and mild focal slowing of the conducting radial motor fibers within the spiral groove (when the right radial motor nerve conduction velocity of 57 m/s is compared to the distal velocity of 66 m/s, and to the left radial motor velocities of 69 m/s proximally and 68 m/s distally). The presence of partial conduction block with relative mild focal slowing across the spiral groove is consistent with segmental demyelination at that site.

This case is consistent with a right radial mononeuropathy at the spiral groove, manifested mostly by segmental demyelination (partial conduction block within the spiral groove) with modest sensory and motor axonal loss. The presence of wristdrop and fingerdrop with weak brachioradialis but normal triceps and deltoid, along with superficial radial sensory deficit, makes the clinical diagnosis of radial nerve lesion in the region of the spiral groove very likely. Identifying a conduction block across the spiral groove localizes the lesion precisely to that segment of the radial nerve. In addition, the lesion could not be due to a posterior interosseous neuropathy because the radial sensory SNAP and brachioradialis muscle are abnormal; the motor branch to the brachioradialis (and the branch to the extensor carpi radialis longus) originates from the main trunk of the radial nerve before it divides into its terminal branches (posterior interosseous and radial cutaneous). In a posterior cord brachial plexus lesion, the deltoid, triceps, and anconeus muscles are abnormal. Finally, the SNAPs are normal in cervical radiculopathy (because the root lesion is proximal to the dorsal root ganglia), and muscles innervated by other nerves that share the same root should be affected.

In the case presented, the NCSs were done 5 weeks after the onset of the patient’s symptoms, long after the time required for wallerian degeneration (10–11 days). Thus, the conduction block seen cannot be due to early axonal loss, and the primary pathophysiologic process here is focal demyelinative block. Conduction slowing also is caused by demyelination and can accompany conduction block, although they often occur independently. Sensory and motor axonal degeneration has occurred, as confirmed by low-amplitude distal radial CMAP, low-amplitude distal radial SNAP, and fibrillation potentials in radial innervated muscles. The prognosis for this patient should be good but biphasic because it is dependent on the relatively rapid remyelination process and slower reinnervation. Reinnervation in this case should be efficient because the lesion is partial and sprouting is likely to be vigorous.

DISCUSSION

Applied Anatomy

The radial nerve is the largest nerve in the upper extremity (Figure C12-2). It is a direct extension of the posterior cord of the brachial plexus, after takeoff of the axillary nerve, and contains fibers from all the contributing roots of the plexus (i.e., C5 through T1).

image

Figure C12-2 Anatomy of the radial nerve and its branches.

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

To attain better understanding of the anatomy and innervation of this long and serpiginous nerve, its path is best dissected into multiple segments:

The “radial tunnel” is not a true bony tunnel but a potential space between the humeroradial joint to the proximal edge of the supinator muscle, called the arcade of Frohse, which is a tendinous arch in over half of the population (Figure C12-3). The tunnel is formed by the capitulum of the humerus posteriorly, the brachialis muscle medially, and the brachioradialis and extensor carpi radialis anterolaterally. The radial nerve travels over approximately 5 cm through the tunnel, innervates the extensor carpi radialis brevis and supinator and provides sensory branches to the periosteum of the lateral epicondyle and to the humeroradial joint. The radial nerve divides, about 2.5 to 3 cm distal to the lateral epicondyle and slightly proximal to the edge of the supinator muscle, into its terminal branches: the superficial radial and posterior interosseous nerves.

Clinical Features

Radial nerve lesions are usually acute and located around the spiral groove. Table C12-1 lists the common causes of radial nerve lesions in the arm. Among them, acute compression at the spiral groove, where the nerve comes in close contact with the humerus, is by far the most common. The radial nerve is compressed most often in the spiral groove after piercing the lateral intermuscular ligament, where the nerve lies unprotected by the triceps, against the humerus.

Table C12-1 Causes of Radial Mononeuropathy in the Arm

In lesions of the spiral groove, the patient usually presents with acute painless wrist drop with variable sensory loss mostly over the dorsum of the hand. On examination, there is wrist and finger drop due to weakness of all wrist and finger extensors with mild weakness of elbow flexion (along with the loss of brachioradialis reflex and belly on elbow flexion). Otherwise, elbow extension and shoulder abduction are normal. Sensory loss is limited to the territory of the radial cutaneous nerve over the dorsum of the hand. Occasionally, this extends to the dorsal aspect of the forearm because of involvement of the posterior cutaneous nerve of the forearm.

Radial nerve lesions, which often present with wrist- and finger-drop, should be distinguished from lesions of the posterior interosseus nerve and of the posterior cord of the brachial plexus, and from severe cervical radiculopathies (C7 and C8 radiculopathies). Table C12-2(A) lists the clinical findings inpatients presenting with prominent wrist and/or finger extensor weakness.

Electrodiagnosis

Acute radial nerve lesions at the spiral groove are similar to acute common peroneal nerve lesions at the fibular head (see Case 8). Both are frequently caused by compression of the nerve between an external object and an internal rigid structure, such as the humerus or fibula. Also, their EDX findings are similar, with signs of axonal loss, conduction block due to segmental demyelination, or both. Except for open trauma (such as a gunshot or knife wound), which often results in axon loss lesions, one cannot predict the prognosis of radial nerve lesions, without EDX studies and quantitation of the extent of demyelination and axonal loss.

In addition to the routine median and ulnar NCSs, radial sensory and motor NCSs are essential in the accurate diagnosis of radial nerve lesions. The distal radial CMAP (recording the extensor digitorum communis, EDC, or extensor indicis proprius, EIP) assesses the integrity of the motor axons terminating in these muscles. Because the EDC and EIP are C7-, C8-, and T1-innervated muscles through the posterior cord, the radial nerve, and the posterior interosseous nerve, a low-amplitude radial CMAP, recording EDC or EIP, by itself, is not necessarily indicative of a radial nerve lesion. In fact, lesions of any of these structures may result in a low-amplitude radial CMAP. The proximal radial CMAPs, on stimulation below and above the spiral groove are, however, important in detecting the presence or absence of conduction block (and occasionally focal slowing). The radial SNAP evaluates the integrity of postganglionic radial sensory axons.

The needle EMG examination is essential in axon-loss lesions that are not localizable by NCS and confirmatory in lesions associated with conduction block (due to segmental demyelination or early axonal loss). The branches of the radial nerve are fortunately placed strategically in the arm and forearm, spanning the nerve length in its entirety. This renders the radial nerve one of the most convenient nerves to study in the EMG laboratory. Thus, even when the pathologic process is axonal, it frequently is possible to localize the lesion to a short segment of the nerve. This contrasts with many other human peripheral nerves, wherein the nerve travels in long segments without giving off any sensory or motor branches developing. Examples include the median and ulnar nerves, which have no branches in the arm, and the common peroneal nerve, which has a single motor branch in the proximal thigh (to the short head of the biceps femoris).

The aims of the EDX examination in radial nerve lesions are to localize the lesion, gauge the extent of axonal loss or demyelination, and approximate the prognosis. The study also assists in planning surgical treatment, if necessary, and gauging the degree and progress of reinnervation.

The first step in the diagnosis of a radial nerve lesion is to establish that the lesion involves the main trunk of the radial nerve; this is done by excluding restricted lesions of the posterior interosseus nerve, the posterior cord of the brachial plexus, and the C7 and C8 roots (Table C12-2(B)). A radial nerve lesion at the spiral groove, studied after the potential time to complete wallerian degeneration, is characterized by the following:

Another aim of the EDX examination is to prognosticate the radial nerve lesion based on the primary pathologic process. This is achieved by studying the radial CMAP amplitude and area after 10–11 days, the time needed to complete wallerian degeneration. To better assess the distal radial CMAP and SNAP, radial motor and sensory NCS should be performed on the affected and asymptomatic limbs, for comparison purposes. In axonal lesions where the radial CMAPs are uniformly low in amplitudes, the distal radial CMAP, stimulating at the elbow, and the distal radial SNAP estimates the degree of motor and sensory axonal loss, respectively. However, in demyelinating lesions in which conduction block is present, comparison between the distal and the proximal radial CMAP on the symptomatic side, stimulating above the spiral groove estimates the number of fibers that underwent segmental demyelination across the spiral groove. In mixed (axonal and demyelinating) lesions, as in this patient, one must compare the distal radial CMAP and SNAP amplitudes to their contralateral counterparts as well as contrast the distal to the proximal radial CMAPs.

Radial Tunnel Syndrome

Radial tunnel syndrome (RTS) is a term coined by Roles and Maudsley in 1972 to describe patients with lateral forearm pain and “persistent tennis elbow” who improved after surgical decompression of the posterior interosseous nerve within the radial tunnel. This syndrome continues to be debated by many physicians, while many orthopedic and hand surgeons continue to decompress the nerve within the radial tunnel.

According to its proponents, the patient with RTS complains of lateral forearm pain and tenderness in the region of the radial tunnel, which may radiate to the arm and/or wrist. The pain is worse with resisted extension of the middle finger with the elbow extended or resisted supination with the elbow extended. These maneuvers contract the extensor carpi radialis or the supinator muscles. On examination, there are either no findings or subtle abnormalities. Tenderness in the proximal arm that is usually maximal near the supinator is common. Apart from these findings, there is usually no other weakness, sensory loss, or reflex changes. In almost all cases of RTS, the EDX studies (NCS and needle EMG) are normal. Rarely, there are mild chronic denervation and reinnervation changes of posterior interosseous-innervated muscles on needle EMG, often with normal radial sensory and motor NCS. Perineural injection of local anesthetic and corticosteroid around the radial nerve within the tunnel as a diagnostic test for radial nerve entrapment. Advocated treatment of this syndrome is decompression of the posterior interosseous and radial nerves by severing the arcade of Frohse and any other compressive elements within the radial tunnel.

Despite its popularity among orthopedic and hand surgeons, there are many opponents to the existence of this syndrome. These physicians argue that (1) the symptoms of the RTS are seldom substantiated by clinical or electrophysiologic findings, (2) the tender points correlate with the “trigger points” described in regional myofascial pain syndromes, (3) the pain relief from corticosteroid injection is not a proof that the radial nerve is compressed, since patients with local musculoskeletal complaints, such as lateral epicondylitis or trigger points often get pain relief by blocks, and (4) cases of true compression of the posterior interosseous nerve are often due to mass lesions (e.g., ganglion), trauma, and, occasionally, entrapment at the arcade of Frohse and have definite neurological and EDX abnormalities that are consistent with axon-loss (Table C12-3). Many opponents believe that most patients with this alleged syndrome have actually a lateral epicondylitis (“tennis elbow”) that is resistant to treatment or have a regional myofascial syndrome rather than true nerve compression.

Table C12-3 Differences Between a “True” Posterior Interosseous Neuropathy and a “Presumed” Posterior Interosseous Nerve Entrapment in Radial Tunnel Syndrome

  Posterior Interosseous Neuropathy Radial Tunnel Syndrome
Pathophysiology Nerve compression, usually by mass (e.g., ganglion), acute trauma, and, rarely, by the tendinous arch at the arcade of Frohse Presumed nerve entrapment at the radial tunnel, mostly, by the tendinous arch at the arcade of Frohse
Clinical manifestations Objective and subjective weakness of PIN muscles*; rarely painful Pain is always present with finger extension or supination; often with tenderness on palpation over the proximal lateral forearm with distal and/or proximal radiation; rarely weakness
Electrodiagnostic findings Denervation in PIN muscles*; radial motor CMAP may be low; radial SNAP is normal Usually normal

* See Figure C12-2.