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.

Clinical Features

Rarely, nerve entrapment neuropathies are related to disturbances of the autonomic function. More often motor and sensory symptoms are evident. If the affected nerve is mostly carrying fibers mediating cutaneous sensibility, then sensory symptoms such as pain, paresthesia, and hypoesthesia predominate. If the entrapment is of a “purely motor nerve,” the classic motor involvement is characterized by weakness, wasting, fasciculations, and occasional spasms. Sensory symptoms such as pain, however, can still be present due to the presence of the afferent fibers from the spindles and Golgi organs. Electrophysiologic evaluation reveals the presence of fibrillation potentials in the affected muscles.

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.

FIGURE 201-2 Median nerve compressed after supracondylar fracture in a 7-year-old child. The patient was referred because of lack of recovery after 3 months from the trauma. Note the shape of the median nerve immediately after the release of the constriction and then at end of the procedure 15 minutes later. The nerve has already regained a more normal shape and the indentation was no longer 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.

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.