Management of Entrapment Neuropathies

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Chapter 201 Management of Entrapment Neuropathies

Nerve compression is a common cause of spontaneous neurologic dysfunction. The term “entrapment neuropathy” should only be used to describe situations in which a small addition to the content of an already crowded osteomuscular channel causes compression, constriction, or distortion of peripheral nerves, or indeed causes interference with the gliding properties of the nerve.

Stewart1 defines entrapment neuropathies as “compression neuropathies that occur at specific places where nerves are confined to narrow anatomic pathways and therefore are particularly susceptible to constricting pressures.” The cause of precipitation of symptoms is always local and can be due to either internal or external factors. External factors, such as an increase in pressure in an osteomuscular tunnel (e.g., on the ulnar nerve at the elbow), can leave the gliding properties of the perineurium completely altered even when removed. Causes are either internal to the nerve itself due to systemic conditions (hereditary susceptibility to pressure, alcoholism, diabetes mellitus, uremia, carcinoma) or extraneural (presence of a mass in the osteomuscular tunnel, a particular anatomic configuration due to previous fractures or variations like anomalous muscles). The vast majority of cases operated on at our institution (Peripheral Nerve Injury Unit, Royal National Orthopaedic Hospital in London) are complications or failures referred from other centers where operations for “entrapment neuropathies” were previously performed.

Reasons for failure are normally due to error in diagnosis, inadequate decompression, or damage to the compressed nerve or its branches and adjacent vessels. Another cause can often be scarring subsequent to inadequate surgery.

Carpal tunnel syndrome provides a very good example, although it is not the topic of our chapter. It is the most common of all entrapment syndromes, and as such it is therefore possible to reveal the underlying cause of such a compression. Despite this, Rosenbaum and Ochoa2 showed that in a combined series of 2705 patients, a quarter of them had a systemic disease, 321 had rheumatoid arthritis, 166 were diabetic, and 94 had hypothyroidism. This is not to say that all these procedures should have been avoided, but that often the most common entrapment neuropathy should be considered a manifestation of systemic disease rather than a focal isolated problem.

It is also difficult to establish at which level the nerve fibers are compressed, distorted, or damaged. Consequently, considering all possibilities is worthwhile: anterior horn cell; the spinal nerve within the spinal canal and the intervertebral foramen; and the plexus at the thoracic outlet or the terminal nerves at the level of arm, elbow, wrist, and hand. In a few cases, there could also be a “double-level injury.” It is also important to remember that in the differential diagnosis, a more generalized neuropathy or musculoskeletal cause for pain, such as Parsonage-Turner syndrome or amyiotrophic lateral sclerosis, should be always be considered.

Magnetic resonance imaging (MRI) and ultrasound can easily determine whether there is a mass creating compression, such as a lipoma or intrinsic neural lesions (Fig. 201-1), or whether there is entrapment.

The Physiopathology of Chronic Nerve Compression

The process often begins with the interference of the nerve’s blood supply. Lundborg3 described the fascicular vascular unit, endoneural and perineural vascular systems linked segmentally to the mobile epineural vascular network. The integrity of this connection clearly depends on the ability with which the nerve glides in its surrounding connective tissues and the fascicles glide in the epineurium. Any restriction of excursion in either plane could interfere with blood supply. Rydevik et al.4 observed changes in both intra- and extra-fascicular microcirculation on applying a graded compression on the tibial nerve of rabbits. They found that at 20 to 30 mm Hg, there was already interference with the vascular flow, and at 60 to 80 mm Hg pressure there was no blood flow. Sunderland5 thought that the entire mechanism behind carpal tunnel syndrome was intrafascicular anoxia caused by obstruction of venous return. He stated that this produced edema and further increase in pressure.

There is, however, a peculiar anatomic lesion that characterizes chronic entrapment: the disappearance of myelin within the carpal tunnel. In 1963, Thomas and Fullerton6 analyzed a postmortem specimen of a patient with proven carpal tunnel syndrome and found that the myelin disappeared under the transverse ligament but reappeared distally. It was then clear that the focal slowing of nerve conduction was due to focal demyelination. In 1973, Ochoa and Marotte7 detected myelin changes extending also proximal and distal to the compression site. They described “resembling tadpoles, being bulbous at one end and tapered at the other” with a constant polarization (the bulb pointing away from the wrist proximally) but reversed distally (the bulb pointing away again). They also observed that with time, demyelination and remyelination occurred and eventually axons got interrupted with consequent degeneration of the distal segment. At electron microscopy they showed that “internal myelin lamellae had slipped away at the tapered ends and that these displaced lamellae had buckled at the bulbous ends.” Again Ochoa and Marotte7 stated that this phenomenon was simply a slippage of myelin lamellae followed by disintegration of the contorted myelin at the bulbs. Two years later these findings in the guinea pig were confirmed in human median nerves at the wrist and ulnar nerves at the elbow by Neary et al.8 They also found an enlargement in these nerves from increase in connective tissue. Pham and Gupta9 recently showed that Schwann cell proliferation and apoptosis in early phases of the disorder is the cellular mechanism behind the demyelination. In the area of the injury these proliferating cells downregulate myelin proteins, leading to local demyelination and remyelination. The changes occur before any axonal loss. The axons are in fact the last to be affected and the larger ones are the first to suffer, while unmyelinated fibers are more resistant until late in the course of the entrapment.

As described, ischemia, either acute or chronic, can cause primary nerve damage and can obviously contribute to the pathogenesis of chronic entrapment. The vasa nervorum do suffer in fact from the same mechanical injury as the lamellae.

Management of Compressed Nerves

Initial nonoperative management includes simple measures such as avoidance of exacerbating activities, and use of splints and injections of steroids around the inflamed nerve. If these methods are unsuccessful, surgery is indicated. Surgical exposure must be adequate. Normal nerve proximal and distal to the lesion must be visualized. The dissection of the nerve must in fact be carried out from healthy tissue to the pathologic to better define the site and the nature of the lesion and therefore deal with it appropriately. All too often failures are due to insufficient decompression because of poor visualization of the nerve throughout its course. Before separating the nerve from the compressing structure, electrophysiologic evaluation may be useful. After releasing the compression, palpation of the lesion is very useful to an experienced surgeon. A nerve “woody” in texture is of course less likely to recover from simple decompression and neurolysis. Sometimes after opening or partial excision of the thickened epineurium, the texture of the nerve becomes softer (Fig. 201-2). Internal neurolysis should always be very careful and limited to the segment involved. The perineurium should rarely if ever be violated, and never when it is unscarred. Nerves in scarred beds should be placed in better positions without tension.10 Every possible attempt to restore the normal glide of the nerve is to be made at the time. To this end, in cases of previous failed decompression or recurrent symptoms it may even be necessary to consider the use of local soft tissue flaps or free flaps to achieve this. We think that as a general rule surgical decompression should aim to achieve a complete release of all the adhesions around its entire circumference to visualize the nerve throughout its course. External neurolysis should be reserved for cases where the texture of the nerve is hardened and internal neurolysis in the few cases where there is no conduction across the lesion and a “woody” nerve is present.

Postoperative care is centered on avoidance of formation of new scar and adhesions between the nerve and the surrounding tissues. Early mobilization is therefore recommended where possible. If tendons and muscles have been sectioned and repaired during the procedure the mobilization could be started very gently after 1 week.10

Ulnar Nerve at the Elbow

The possibility of many anatomic variations must be taken into account when considering ulnar nerve lesions. The Martin-Gruber anastomosis, in which motor fibers from the median reach the ulnar nerve and within it the small muscles in the hand, is reported between 10% and 44%.11 There are also possible variations in which the small muscles of the hand are completely innervated by the median nerve rather than by the ulnar nerve. For the first dorsal interosseous muscle, this possibility is reported at about 10%.11

Compressions of the ulnar nerve at the axilla or at the proximal and middle third of the upper arm are very rare. More frequent instead is the lesion at the distal third where the nerve is very close to the humerus in its course toward the cubital tunnel proper. Severe compression may occur at this site especially after supracondylar fracture in children, so that incomplete recovery after such an injury or persistence of pain always suggest a possible force still acting on the nerve. At this level, the nerve runs behind the intermuscular septum and then becomes superficial to the medial capsule of the elbow joint and deep to the Struther’s arcade joining the two origins of the flexors carpi ulnaris muscle, the so-called arcuate ligament. The clinical picture is the same as for cubital tunnel syndrome where the nerve is compressed at the level of the osteomuscular canal.

Compression, either acute or subacute, occurs with direct trauma or with long continued pressure. This is what happens in the unconscious patient, in those confined to bed or partly immobile, and in those who have lost a large amount of weight over a very short period of time. The local swelling increases the compression between the arcuate ligament and the medial aspect of the elbow joint, producing the localized mononeuropathy. The same thing can happen without external compression or trauma. Osborne12 showed how with flexion of the elbow, the “ligament’s grip” on the ulnar nerve is tightened. Marginal osteophytosis or chronic effusion in the joint with bulging of the capsule or valgus deformity may increase the liability for compression at this particular level. Campbell et al.13 showed by intraoperative electroneurography that the usual site was the retrocondylar groove followed by the cubital tunnel itself. Laxity of the arcuate ligament may contribute to recurrent subluxation of the nerve over the medial epicondyle with flexion of the elbow. There are also rare causes of compression like “snapping” of the medial head of triceps14 or the presence of an anomalous anconeus epitrochlearis.15

The absence of a sensory component of the paralysis may suggest a lesion proximal to the junction of the motor and sensory roots, either in the cord or in the canal.

The extension of the motor paralysis to the median innervated thenar muscles suggests an involvement of the lower trunk of the brachial plexus rather than ulnar nerve.

The absence of a sensory involvement combined with involvement of the ulnar nerve–supplied small muscles of the hand but preservation of the forearm ulnar nerve muscle suggest a lesion at the wrist, distal to the separation between motor and sensory branches.

Presentation of the apparent bilateral lesion, even if possible, should always alert on possible more proximal lesion.

Slowing of conduction of the nerve at the elbow suggests a lesion at that level but the possibility of a polyneuropathy must always be remembered.

Pressure on the nerve (percussion test) determines paresthesia. There is numbness in the ulnar fingers, including the dorsal branch, and weakness or complete palsy of the ulnar supplied muscles, but classic-claw hand sign is seen only in the very severe cases. Because the ulnar nerve does not supply the sensation of the forearm, there is no lack of sensation in the ulnar aspect of the forearm.

Surgical Techniques

The methods are simple decompression, anterior transposition (subcutaneous or submuscular), and medial epincondylectomy.

During simple decompression,16 which is adequate in most cases, the exposure of the nerve and its decompression by release of the arcade of the flexor carpi ulnaris are performed. The ulnar nerve is traced out through either an anterior semicircular incision centered on the medial epicondyle (author’s preference) or a rather linear incision basically on the course of the nerve. The nerve is identified proximal to the elbow behind the intermuscular septum and then followed distally. It is checked for any form of compression or tether along its course until the entrance in the flexor carpi ulnaris tunnel. Great attention is required to avoid damage to the branch to flexor carpi ulnaris at this point. In cases of severe deformity, the presence of significant osteophystosis, or recurrent subluxation or persistent symptoms following simple decompression exists, and then transposition is required. This will require a longer incision because of the necessity of releasing the intermuscular septum proximally, and the arcuate ligament distally, thus preventing a tether to the nerve once transposed. An incomplete release of these two structures is in fact one of the most frequent causes of failure and the need for reintervention following transposition. We recommend subcutaneous transposition, putting two or three sutures between the subcutaneous fat and the underlying aponeurosis of the flexor origin in order to retain the nerve in its new course. Immediate mobilization of the arm is recommended to avoid formation of scarring and tethering once transposed.

The submuscular transposition requires division of the superficial flexor muscles about 2 to 3 cm distal to the medial epicondyle, and any tendinous connections are divided to provide a straight bed for the nerve. The aponeurosis over the flexor origin is repaired with interrupted sutures, and immobilization is guaranteed with a right angle plaster for 2 weeks. Although previously advised by Seddon17 and more recently Janjua et al.,18 we do not advise submuscular transposition, having seen constriction, adhesion, and distortion of the nerve in the submuscular and intramuscular bed.

When bony compression on the nerve is due to a very large medial epicondyle, an osteotomy may be a sensible approach. After incising of the periosteum the bony work is performed smoothing the surface in contact with the nerve and then the periosteum closed. The advantage of this procedure is that the vascularity of the nerve is not interfered with as much as in anterior transposition.

Possible complications include devascularization of the nerve, which may lead to pain of a causalgic nature or even complete deficit of the nerve. Hematomas are also not infrequent, which can lead to more postoperative scarring and consequent retethering of the nerve.

Ulnar Nerve at the Wrist

A complete ulnar nerve lesion at the pisiform leads to a mixed lesion with a clawed ring and little fingers with associated sensory loss. The dorsum and ulna aspect of the hand, however, is spared, as this is supplied by the dorsal branch of the nerve, which is given off 4 to 5 cm proximal to Guyon’s canal.

In some cases the compression can be at the level of the hook of the hamate, and sensation is normal throughout the fingers. Intrinsic motor paralysis is usually complete but hypothenar muscles can be spared. In pure motor involvement, pain is not a consistent feature. When the whole nerve is compressed, pain is localized at the wrist and radiates down to the ulna via two fingers. These lesions are more frequently the results of ganglia19 or of occupational compression. Other causes can be previous trauma with or without alteration of the anatomy at the level of the Guyon’s canal or even external compressions by crutches.

Electrophysiology confirms the diagnosis by measuring the distal motor latency to the hypothenar and to the first dorsal interosseous and the sensory conduction velocity across the wrist.

Conservative treatment can be effective in the early phases by avoiding precipitating activities. If the deficit has occurred after a fracture at the wrist, then a decision must be made of whether to decompress the nerve or wait for spontaneous recovery. If spontaneous recovery does occur, partial recovery should initially be seen within a matter of weeks.

Surgical Techniques

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