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.

Median Nerve in the Axilla

This can occur because of pressure secondary to improper use of crutches in the axilla or as a consequence of trauma. Spinner and Spinner¹⁰ also described infraclavicular median nerve entrapment caused by anomalous vascular perforators or vascular arches in six patients treated surgically. Subclavian dynamic arteriography was helpful in confirming the median nerve penetration. With the arm at the side, the arterial system was visualized, whereas in abduction was not.

Other cases of compression of the median nerve at the axilla have been attributed to the presence of Langer’s muscle,²⁰ which arises from the latissimus dorsi’s tendon insertion and terminates on the tendon of pectoralis major. We personally have found the presence of this muscle compressing the median nerve 6 months after shoulder dislocation, and following decompression a full resolution of the complete lesion was achieved after only 3 months.

After trauma to the shoulder, with or without dislocation, the lateral edge of the pectoralis minor tendon or the deltopectoral fascia may become thickened and therefore compress the neurovascular bundle. The median nerve here is the closest structure within the neurovascular bundle. In all these cases, decompression provides the only possibility for the nerve to recover and for the pain to subside.

Median Nerve in the Arm

Lesions at the level of the arm are very rare and normally due to trauma (Fig. 201-3) or tourniquets used for achieving a blood-free field during surgery.

FIGURE 201-3 Supracondylar fracture in 6-year-old child. Median nerve caught between post-traumatic tissue and fracture site before, and free but contused after release. No graft repair was performed and recovery was complete at 1 year.

In 1% of the population there is a supracondylar process about 5 cm proximal to the medial epicondyle. Normally detected at routine x-ray and asymptomatic, it can sometimes be connected to the medial epicondyle by the Struther’s ligament. Behind the ligament, the artery and the median nerve can be kinked.^21–25 Sensory and motor disturbances are present in different degrees. The pain is the main feature with involvement of the elbow, volar aspect of forearm, and sensory distribution of the median nerve in the hand.

Median Nerve at Pronator Arcade

This condition is very rarely due to anatomic variations but rather to repetitive physical activity with the forearm pronated. Initially pain occurs on the volar aspect of the forearm and characteristically increases during pronation against resistance, radiating also proximally. Pain and sensory disturbances are present along the territory of the nerve but motor deficits are exceptionally rare, although patients often complain about writer’s cramp. The median nerve is compressed between pronator teres and the fibrous arch of the flexor digitorum superficialis.^26–28

Electrophysiology is not very helpful because of its relative normality, although cases of slowing of velocity across the lesion have been described.²⁹ Operative findings include hypertrophy of the pronator teres muscle, passage of the median nerve under both heads of pronator teres, anomalous origin of the pronator teres, a thick fibrous band running through the muscle, or fibrous thickening of the edge of the flexor digitorum superficialis.³⁰

Anterior Interosseous Syndrome

The anterior interosseous nerve arises from the median nerve beneath the flexor digitorum superficialis and runs in an oblique and radial direction. It supplies the flexor digitorum profundus for the index and middle and the flexor pollicis longus. It was first described by Kiloh and Nevin³¹ in 1952 and is characterized by pain in the proximal forearm and weakness of flexion of the distal joint of the thumb and of the index so that the patient is unable to effectively pinch the thumb and the index together (pinch or circle sign). Sensory deficits are absent. Electrophysiology may contribute to the diagnosis by comparing the motor latencies with the normal side, and in advanced cases by showing denervation signs in the affected muscles. Paralysis of the median nerve is incomplete, and it may be misleading in localizing the site of the lesion. The most difficult differential diagnosis is brachial plexus neuropathy and, rarely, anterior interosseous neuropathy. Other than finding more diffuse neurologic involvement when the brachial plexus is involved, the key is in the history where excruciating pain in the shoulder and arm lasts for a couple of weeks always precedes the deficit if a viral infection is the cause.

Radial Nerve at the Arm

Spontaneous radial nerve compression at this level may occur at the level of the lateral head of triceps.^32,33 A common characteristic in the history is strenuous muscular exercise. Other causes, such as previous trauma, mass lesions, and external compression (Saturday night palsy), can be responsible. Spinner and Spinner¹⁰ described 12 cases of compression of the radial nerve in the axilla due to vascular penetration. Deficits are wrist drop with lack of extension of all fingers and sensory deficit in the dorsal ulna aspect of the thumb and first web space. If the lesion is at the level of the humeral groove, there will also be a lack of sensation in the dorsal aspect of the forearm due to the involvement of the posterior cutaneous nerve of the forearm. If the triceps is involved as well, then the lesion will be even higher.

Posterior Interosseous Nerve

The posterior interosseous nerve has been described as compressed by a fibrous band at the radiocapitellar joint³⁴ by a portion of Henry’s vascular leash or by the proximal edge of extensor carpi radialis brevis. However, the most frequent site for compression is Frohse’s arcade, that is, the proximal edge of supinator.^35–37 Entrapment may occur spontaneously, but the cause is often to be found in masses compressing the nerve or related to trauma.³⁸

Involvement of the posterior interosseous nerve can vary from weakness of its supplied muscles to complete palsy. The brachioradialis, the extensor carpi radialis brevis and longus, and the sensory branch of the nerve are not affected as these branches arise more proximal to the lesion. This results in lack of dorsiflexion of all fingers; however, wrist extension is still present but with radial deviation due to the absence of activity in extensor carpi ulnaris. Pain is very rarely present in the proximal forearm.

Superficial Radial Nerve

The superficial radial nerve can be compressed at two levels. The first site is at the fascial edge of brachioradialis.⁴¹ The second is about 8 cm proximal to the radial styloid⁴² or at the styloid itself where it is superficial and very vulnerable to any sort of external compression (tight surgical gloves, watches, any constrictive band).

Patients complain of paresthetic symptoms in the territory of the nerve and sometimes pain. When the symptoms persist even after removal of the external pressure, the operation aims at removing any sort of tether on the course of the nerve through a longitudinal incision centered over it.

Lateral Cutaneous Nerve of Thigh

This nerve may become entrapped where it passes under the inguinal ligament in its course to exit from the pelvic cavity (meralgia paresthetica). At this level the nerve is medial to the tendon of the sartorius muscle before giving off its terminal branches, which distributes to anterior and lateral aspect of the thigh as far as the distal third.

The entrapment’s causes are external compression, which may be derived from tight belts but also may be secondary to obesity. The nerve can also be compressed inside the pelvis by masses or as a result of previous trauma. Due to its wide anatomic variations, it is possible to be injured during the harvesting of iliac crest bone graft.

The symptoms are paresthesia in the anterolateral aspect of the thigh but very often pain of severe intensity and burning characteristics in the same area with associated sensory deficit. If they do not disappear spontaneously in a few weeks or months, then surgical release is indicated.⁴³

Common Peroneal Nerve

After its origin from the sciatic nerve at the apex of the popliteal fossa, the common peroneal nerve passes around the neck of the fibula through the origin of the superficial head of the peroneous longus muscle. It then gives origin to its divisions: the superficial peroneal nerve, which supplies the peroneal muscles and the lateral aspect of the leg and the dorsum of the foot, and the deep peroneal nerve, which goes to tibialis anterior and the dorsiflexor of all toes and the skin between the first and second toe.

The nerve may be affected by external compression as in cases of prolonged bedrest, anesthesia, coma, tight plaster casts, or generally any sort of compression applied at this level. The deficit also may be caused by internal compression, such as entrapment after fractures of the fibular neck or ganglion of the tibiofibular joint (Fig. 201-4), which finds its way into the nerve through the articular branch of nerve.^47,48 Other less common causes are post-traumatic false and true aneurysms or sometimes also Baker’s cysts.^49,50 Foot drop is the key feature in the symptoms with associated sensory deficit of various degrees in the territory of the nerve.

FIGURE 201-4 Ganglion of the common peroneal nerve. Note the nerve enlarged by the intra-articular fluid on the left. The articular branch was isolated and the nerve decompressed in the middle, and the articular branch ligated and resected to avoid recurrence on the bottom. No recurrence and normal neurology were found at 3 years.

Tibial Nerve at the Ankle

The tibial nerve originates in the popliteal fossa and then passes deep through the gastrocnemius muscle. Above the ankle it becomes fairly superficial, running just under the flexor retinaculum to reach the sole of the foot. Here it gives off its two terminal divisions, the medial and lateral plantar nerves.

Compression of the nerve in its course before the tarsal tunnel is mainly due to the presence of masses that may be intra- or extra-neural (Fig. 201-1). This is a very challenging diagnostic problem.⁵¹ In its course within the tarsal tunnel, the nerve may be compressed due to post-traumatic fibrosis or a cyst arising from the adjacent tendons. The condition may also be spontaneous and slowly progressive. In these cases, it is most often associated with obesity, decreased elasticity of collagen, or a progressive acquired flat foot deformity in adults.⁵²

Symptoms may include pain in the sole of the foot, positivity at percussion test behind the medial malleolus, and sensory deficit in the sole of the foot. Only rarely can weakness in the intrinsic muscles of the foot be detected.⁵³

Sciatic Nerve

The sciatic nerve leaves the pelvis through the sciatic notch behind the piriformis muscle. The nerve is vulnerable to fractures of the ilium and sacrum as soon as it exits the sciatic notch. Posterior dislocation of the femur or fracture dislocation of the hip may contuse or compress it, masses displace it (Fig. 201-5), and endometrial implant⁵⁶ can cyclically irritate it. Potential spontaneous entrapment at the piriformis level is still debated. Solheim et al.⁵⁷ credited Yeoman⁵⁸ with the first suggestion that the piriformis muscle had a role in the production of sciatica. Robinson⁵⁹ described two cases of sciatica apparently caused by hypertrophy of the piriformis and relieved by the surgical release of the muscle. Stewart⁶⁰ clarified the diagnosis criteria. A clinical picture of focal lesion of the sciatic nerve with electrophysiologic confirmation of a focal lesion, radiologic exclusion of other compression along the course of the nerve, appropriate findings at operation and resolution of the symptoms after the surgery were needed for the diagnosis. Compression of the sciatic nerve in the buttock by varicose gluteal veins have been identified by Bendszuz et al.⁶¹ Two of three patients found relief with surgery, and the third with carbamazepine. We concur with Tiel, who asked for renaming of the condition to “nonlocalizing sciatica” and restriction of surgical resection of the piriformis to cases where all other treatments have failed.⁶²

FIGURE 201-5 Large lipoma creating compression of the sciatic nerve at the notch. The patient suffered from sciatica. On the right, the sciatic nerve appears flattened after removal of the large lesion. Surgery resolved symptoms.

The symptoms present are pain, and sensory disturbances within the territory of the whole sciatic nerve and motor involvement is only present in post-traumatic cases or in cases of compression due to masses.

Pain may be relieved after injections of local anesthetics and corticosteroids or botulinum as described by Childers et al.⁶³ and Fishman et al.,⁶⁴ and lately as introduced by Huerto and colleagues,⁶⁵ using ultrasonography and electric stimulation.

“Iatropathic Entrapments”

Any nerve can become “entrapped” following trauma. Therefore, in any case where previous surgery has been performed, the possibility of iatropathic entrapment should be considered (Fig. 201-6). The symptoms may vary from paresthesia without motor involvement to excruciating pain with no motor function present. In any of these situations, and particularly when pain is present, surgical decompression gives the only possibility of abolishing pain and restoring function.

FIGURE 201-6 Radial nerve compressed by plating of fractured clavicle (revision, shortening, and fixation with straight plate). Nerve damaged by wire around fractured humerus (top left). Brachial plexus (top right). Femoral nerve injured in the thigh by a plastic clip blindly positioned during bleeding in course of gynecologic intrapelvic procedure (bottom left). Ulnar nerve transfixed by wire after treatment of supracondylar fracture (bottom right).