Median Nerve Entrapment

The median nerve has roots in C5, C6, C7, C8, and T1. It is formed in the axilla by the lateral and medial cords of the brachial plexus, which arise on opposite sides of the axillary artery and fuse to form the median nerve anterior to the artery (see the image below).

As the nerve courses to the elbow, it lies close to the brachial artery, crossing it anteriorly to medially. After entering the cubital fossa lateral to the brachialis tendon, the median nerve passes between the two heads of the pronator teres, a possible site of compression.

As the nerve enters the forearm, it branches to the pronator teres, the flexor carpi radialis (FCR), the palmaris longus, and the flexor digitorum superficialis (FDS). The median nerve also gives off a significant branch within the pronator teres, the AIN, which supplies the flexor pollicis longus (FPL), the pronator quadratus, and the lateral half of the flexor digitorum profundus (FDP).

The median nerve continues its course in the distal forearm, under the FDS and on the FDP. The palmar cutaneous branch emerges as the median nerve becomes superficial, just above the wrist. This branch supplies the thenar eminence and central palm. After branching, the median nerve continues into the hand via the carpal tunnel. The carpal bones and the pronator quadratus compose the inferior and side borders of the carpal tunnel, and the flexor retinaculum forms the roof of the canal.

In the carpal tunnel, the median nerve runs anteriorly and laterally to the tendons of the FDS. In the hand, a muscular branch forms to supply the muscles of the thenar eminence, and the palmar digital branch forms to supply the palmar surface of the thumb, index, and middle finger and the lateral half of the ring finger, including the nail beds on the dorsal surface. The palmar nerves also give off branches to supply the two lateral lumbrical muscles.

Compression of the median nerve can occur at various sites along its course,[5]  causing specific and variable signs and symptoms.

Carpal tunnel syndrome

CTS is the most common of the median nerve entrapments. The carpal tunnel is a narrow fibro-osseous tunnel through which the median nerve passes, along with nine tendons. An increase in the volume of the tunnel contents or a decrease in the size of the tunnel can compress the median nerve.

Pronator syndrome

The ligament of Struthers (see the image below) is usually the most proximal site of compression. An anomalous bony spur, the supracondylar process, is located at the distal humerus, approximately 3-5 cm proximal to the medial epicondyle and 2-20 mm long.[6] The ligament of Struthers connects the supracondylar process to the medial epicondyle, encasing the median nerve and brachial artery. It is seen in approximately 13% of the general population and rarely causes median nerve entrapment.[7] In some cases, no bony spur can be identified; only the ligament persists.[8, 9]

The lacertus fibrosus (bicipital aponeurosis; see the image below) is the least common cause of pronator syndrome.[10, 11] The bicipital aponeurosis is the medial extension of the biceps tendon and covers the median nerve in the cubital fossa. The compression may be secondary to hypertrophy or enlargement of the aponeurosis.

Fibrous bands between the deep and superficial heads of the pronator teres (see the image below) frequently cause compression of both the median nerve and the AIN. An anatomic study proposed the determinant variations that could lead to pronator syndrome, as follows[12] :

• Short and tendinous ulnar head
• Ulnar head joined to the arch of the FDS muscle
• Ulnar head with triple origin slips
• Humeral head perforated by the median nerve

The FDS varies in origin and size, and the median nerve can be crossed and compressed by one or two aponeurotic arches (see the image below).[13, 14]

Anterior interosseous nerve syndrome (Kiloh-Nevin syndrome)

The anterior interosseous branch of the median nerve is subject to compromise near its origin. This syndrome usually occurs spontaneously, but can be caused by fracture, fibrous bands, aberrant or thrombosed vessels, and tumors. An existing anatomic abnormality, whether congenital or traumatic, can increase the predisposition to the development of AINS, especially if the area is challenged with concurrent localized edema. Known sites of compression include the following:

• Gantzer's muscle (see the image below) - This is the accessory head of the FPL and has been postulated to be a cause of AINS ^[15] ; in an anatomic study, the muscle was found in 52% of limbs and was supplied by the AIN, ^[16] and it was found to be posterior to both the median nerve and the AIN in all cases
• Fibrous arch of the FDS
• Fascial bands of the deep head of the pronator teres
• Aberrant palmaris profundus
• Aberrant flexor carpi radialis brevis (FCRB)

Increased pressure in the carpal tunnel blocks venous blood flow and axonal transport; higher pressures block intraneural blood flow and impede conduction. These pressures can be measured directly by means of catheters placed in the carpal tunnel. Normal pressures are in the range of 2-10 mm Hg. This pressure is affected by finger, wrist, and forearm position.[17] Wrist extension causes the greatest increase in carpal pressure. High pressures result in complete block of nerve conduction.

Median nerve compression is also associated with decreased space in the carpal canal, which can be caused by increased edema and inflammation of tenosynovium seen in systemic conditions such as diabetes,[18] arthritis, thyroid dysfunction, and renal failure. Patients with diabetes have a higher tendency to develop CTS as a consequence of their lower threshold for nerve damage.

Most of the information on chronic compressive neuropathies is based on animal models because of the paucity of biopsy studies on human nerves.

In a rare histologic study of nerves performed in a patient with CTS who died of a brain tumor, extensive demyelination and remyelination were found in the entrapped nerve.[19] Large myelinated axons were significantly decreased. Proximal nerve swelling associated with perineurial and endoneurial fibrosis was demonstrated. This correlates with the observation during surgery of thinned nerves in the zone of entrapment with proximal swelling. Animal models in which chronic neural compression is stimulated by banding of nerve with Silastic tubes have yielded similar results.[20]

Initial changes included perineurial thickening and peripheral segmental demyelination. Later changes were progressive epineurial and perineurial thickening and global demyelination. Progressive slowing of conduction velocity after an initial increase also occurred.

Both ischemic and mechanical factors have been postulated in the development of compression neuropathy. Acute and chronic compression of peripheral nerves can induce changes in intraneural microcirculation and nerve-fiber structure, increase vascular permeability with subsequent edema formation, and impair anterograde and retrograde axonal transport, which all contribute to the clinical symptoms and deterioration of nerve function.[20, 21]

According to Mackinnon,[22] "[e]xperimental studies suggest a dose-response curve such that the greater the duration and amount of pressure, the more significant is neural dysfunction." The main electrophysiologic finding in patients with symptomatic CTS is prolonged latency, indicating demyelination. However, the extent of demyelination correlates very poorly with clinical symptoms.

This poor correlation may be explained by the vascular component of the pathophysiology. Chronic mechanical trauma causes fibrosis of the perineurium and epineurium. This induces vascular proliferation, vascular hypertrophy, and vascular obstruction with wall thickening and reduction in elastin content.[23]

Although endoneurial capillaries normally constitute a blood-neural barrier (BNB) that helps to optimize the endoneurial environment, damage to the vessels may induce a miniature closed compartment syndrome by increasing the permeability, thereby contributing to increased endoneurial fluid pressure and development of an intrafascicular edema.[24]

In addition, neural gliding is prevented because of neural tethering, which decreases the excursion of the nerve fibers and results in traction. This is the basis of the tethered median nerve stress test (TMNST), which is sometimes used to diagnose chronic low-grade CTS.[25]

Upton and McComas introduced the double-crush concept of chronic nerve compression. The hypothesis suggests that compression at one site along the course of the nerve makes it more susceptible to compression at another site by compromising the axoplasmic flow in the nerve.[26]

Similarly, the reverse double-compression theory[27] states that compression of the nerve at the distal site would decrease transport of neurotrophic substances to the proximal site, thus reducing its overall production. Potential secondary sites of compression include the cervical spine, the thoracic outlet, and the cubital fossa. Animal studies have further corroborated this hypothesis.[28, 29]

The biochemical aspects of chronic compressive neuropathies have also been investigated. One study found increased expression of prostaglandin E2 and vascular endothelial growth factor (VEGF) in synovial biopsy tissues from patients with a symptomatic CTS duration history of 5-7 months and more than 12 months (but not 8-12 months).[30] The same authors found increased expression of matrix metalloprotein (MMP)-2 in small arterioles during the early painful phase of CTS.[31]

Another study involving 30 patients with variable intensity and symptom duration found a marked increase in fibroblast density, collagen fiber size and vascular proliferation, type III collagen, and increased expression of transforming growth factor (TGF)-β in fibroblasts, suggesting a response to injury to the subsynovial connective tissue.[32]

Risk factors have been well studied only for CTS; the other types of median nerve entrapment have generally been classified as idiopathic. The incidence of some of these risk factors differs in various studies, but most populations with CTS have somewhat similar rates of associated risk factors.[33]

According to de Krom et al,[34] associated factors include activities with a flexed wrist or with an extended wrist (exposure-related increased risk), hysterectomy without oophorectomy, height, weight, Quetelet index, slimming courses, and, in men, varicosis. However, they did not find any association between CTS and use of oral contraceptives, age at menopause, diabetes, thyroid dysfunction, rheumatism, typing, or pinch grasp.

In a retrospective study of 1016 residents of Rochester, Minnesota, who were diagnosed with CTS from 1961 through 1980, 43.2% had no associated conditions.[35] The most frequent associated conditions included Colles fracture, rheumatoid arthritis, hormonal agents or oophorectomy (or both), diabetes mellitus, and, among men, occupations that involved excessive use of the hands. Rheumatoid arthritis, diabetes mellitus, and pregnancy were significantly more frequent among the study patients with CTS than in the general population of Rochester.

These findings were supported by a retrospective case control study of 514 patients who underwent carpal tunnel release and 100 matched cases at the University of Washington.[36] The investigators of this study concluded that CTS is multifactorial, with such factors as obesity, hypothyroidism, and diabetes (but not smoking) more prevalent in the study group of patients with CTS than in the matched controls.

In a population-based case control study in Britain,[37]  risk factors associated with CTS included previous wrist fracture; rheumatoid arthritis; osteoarthritis of the wrist and carpus; obesity; diabetes; and the use of insulin, sulfonylureas, metformin, or thyroxine. No association was found between CTS and smoking, hormone replacement therapy, or combined use of oral contraceptive pill and oral corticosteroids. The results were similar when cases were restricted to those who had undergone carpal tunnel decompression.

One study found increased CTS prevalence in patients with untreated hyperthyroidism, which remitted after successful treatment of the medical condition.[38]

Overall, the etiology of CTS is generally accepted as idiopathic, in that the findings described above are considered to be based on unproven theories. More information about the etiology of idiopathic CTS is needed. This might reveal new ways of preventing or treating this condition.

Because median nerve entrapment encompasses various distinct syndromes, its exact prevalence is unknown.

Most of the epidemiologic studies involving median nerve compressive neuropathy have centered on CTS, which is the most common peripheral nerve entrapment syndrome, with a prevalence of 5.8% in women and 0.6% in men, according to a European study.[34] The estimated incidence of CTS in the United States is 3.4%.[39]

Another study found that one of five symptomatic subjects would be expected to have CTS on the basis of clinical examination and electrophysiologic testing. The use of highly repetitive wrist movements, vibrating tools, awkward wrist positions, or great force seems to predispose to CTS, though the exact cause of CTS is a matter of controversy.[33]

In a study on incidence of CTS in automobile workers, the annual incidence of CTS was found to be 1-10%.[40] Prevalence in some industries, such as fish processing, has been reported to be as high as 73%.[41]

Other conditions that are associated with a high risk for CTS include diabetes and pregnancy.[18, 42] People with diabetes have been known to have prevalence rates of 14% and 30% without and with diabetic neuropathy, respectively.[43] Prevalence of CTS during pregnancy has been reported to be around 2%.[44]

The exact incidence of proximal median nerve entrapment in the population is less well understood than that of CTS. On average, proximal median nerve compression syndrome accounts for fewer than 1% of upper-extremity compressive syndromes.[45] However, some studies report a very high incidence of PTS in already symptomatic workers; for example, female machine milkers have rates as high as 75%.[46] The incidence of PTS is four times higher in women than in men.

In 1966, Cseuz et al[47] found that duration of symptoms, presence of associated diseases, and extent of abnormality found on median nerve conduction studies were not good predictors of the outcome of carpal tunnel surgery.

Patients who obtain transient symptom relief from steroid injection of the carpal tunnel are more likely to benefit from carpal tunnel surgery than are patients who do not obtain relief from steroid injection.[48, 49]

Relief of intermittent paresthesias and pain, some improvement in the sensibility of the fingers, and improvement of nocturnal symptoms are often immediate or evident as soon as incisional pain resolves. After the initial and usually dramatic improvement in sensibility, the patient experiences some slight decrease in improvement (~1 week postoperatively). Improvement will again be realized after this transient partial relapse.

The changes in the conduction velocity seem to parallel the patient's clinical response. It has been demonstrated intraoperatively that an immediate improvement in conduction velocity can be anticipated in most cases of carpal tunnel release.[50] Patients who have no associated symptoms of thoracic outlet syndrome or physically laborious work activities are most likely to benefit from carpal tunnel release.[51]

After carpal tunnel release, swelling at the base of the palm superficial to the carpal tunnel can be expected to persist for 12-16 weeks. During this period, and probably concurrent with the swelling, the patient may experience aching pain in the thenar or hypothenar eminences, also known as "pillar pain."

In most cases, strength slowly returns after carpal tunnel release. By 6 weeks after surgical release of the deep transverse carpal ligament, patients usually have only about 50% of their preoperative grip strength. As long as patients are able to exercise and work effectively on increasing grip strength, which should begin in postoperative week 2 or 3, 75% of grip strength is usually regained by postoperative week 8-10.

Maximum grip strength and, perhaps more important, endurance of grip strength often do not return until 6 months or even longer after surgical release of the carpal tunnel. As many as 20% of patients never regain full strength after surgical release of the transverse carpal ligament.

The side effects of carpal tunnel release, their causes, and rates of resolution are debated in the literature. That the volume of the tunnel is increased is generally agreed. That grip strength decreases is also agreed, but the speed with which grip strength is recovered varies widely, ranging from 3 to 9 months. Whether the arch widens is disputed, as is the importance of that widening. Sensation generally improves rapidly after simple release.

Carpal tunnel syndrome

Symptoms of carpal tunnel syndrome (CTS) include paresthesia or numbness in the median nerve distribution of the hand (the thumb, the index finger, the middle finger, and the radial side of the ring finger). Patients may describe aching in the thenar eminence and, with severe nerve compression, weakness and atrophy of the abductor pollicis brevis (APB) and opponens pollicis.[52, 53] This leads to weakness and clumsiness of hand movements and, frequently, complaints of dropping things.

There is increased symptomatology upon active hand use, especially grasping, and the patient may have numbness in the fingers and pain in the wrist or distal forearm upon waking. Nocturnal symptoms are often alleviated by the patient's shaking of the hand or rubbing. Associated conditions and occupational and sports activities should be investigated.

Wasting of the thenar eminence is an advanced sign of CTS and usually responds poorly to surgical decompression.

Presence of the Tinel sign at the wrist—distal lancinating paresthesia in the distribution of the median nerve on light percussion—suggests CTS. It is also useful to clinically follow nerve regeneration after injury.[54, 55, 56, 57] An equally important clinical sign that is probably more specific to CTS is the Phalen sign, in which the symptoms of CTS are reproduced upon wrist flexion.[58]

In a prospective study of 1039 patients with a neurophysiologic diagnosis of CTS, Nora et al found that the most characteristic manifestation of the syndrome was paresthesia in the median nerve distribution, frequently extending to the whole hand.[59] Pain was very common but less specific, and weakness was rare. Tinel and Phalen signs were observed in 34.2% and 56.3% of the hands, respectively.

Pronator syndrome

Patients with pronator syndrome (pronator teres syndrome [PTS]) typically present with aching discomfort in the forearm, local pain over the median nerve distribution distal to the elbow, weakness in the hand, and numbness in the thumb and index finger, especially after repeated and prolonged stress.[60, 2]

Development of paresthesia in the hand after 30 seconds or less of manual compression of the median nerve at or near the pronator teres (pronator compression test) can aid in clinical diagnosis.[61, 62]

Provocation maneuvers may also indicate the possible site of entrapment in PTS.[63, 11] Reproduction of symptoms upon flexion of the elbow against resistance between 120° and 135° suggests compression of the median nerve by the ligament of Struthers. Compression by bicipital aponeurosis may be diagnosed on the basis of pain upon elbow flexion against resistance when the arm is pronated.

Compression by the pronator teres is suggested by symptoms upon resisted pronation of the forearm with wrist flexion (to relax the flexor digitorum superficialis [FDS]) or direct pressure on the leading edge of the pronator while the forearm is in maximum supination with the wrist in a neutral position. Compression may be at the FDS proximal arch if symptoms are aggravated by resisted flexion of the FDS to the middle finger.

Anterior interosseus nerve syndrome

Typical symptoms of anterior interosseus nerve (AIN) syndrome (AINS) include inability to flex the terminal phalanges of the thumb and index finger (eg, loss of pinch and fine motor skills such as writing) and inability to pronate the forearm when the elbow is flexed.[64, 3] This results from motor loss of the flexor pollicis longus (FPL), the flexor digitorum profundus (FDP) of the index finger, and the pronator quadratus.[65] Absence of sensory symptoms is typical; the AIN is a pure motor nerve.

AINS should be differentiated from flexor tendon rupture or other tendon pathologies. This can be accomplished by observing passive flexion of the interphalangeal (IP) joints in AINS when the wrist and metacarpophalangeal (MCP) joints are hyperflexed.

Parsonage-Turner syndrome presents with symptoms that are similar to those observed in AINS.[66] It is preceded by severe pain for weeks. Treatment consists of high-dose corticosteroids and acyclovir. Decompression typically does not help.

Some evidence suggests that there is a higher prevalence of concurrent conditions, such as diabetes mellitus and rheumatoid arthritis, in patients with carpal tunnel syndrome (CTS). At present, however, there is not enough evidence to warrant routine laboratory screening for such conditions in all patients with newly diagnosed CTS.[67]

Low-value preoperative testing remains relatively common in patients undergoing carpal tunnel release and should be reduced.[68]

Both ultrasonography (US) and magnetic resonance imaging (MRI) may be useful in the evaluation of patients with upper-extremity neuropathies.[69, 70] Atrophy can be appreciated in the involved muscles. Signal changes can also point to the affected muscles.

US can similarly identify the affected muscles by looking at the muscle mass, perfusion on Doppler US, and active contraction of affected muscles.[71, 72]  For diagnosis of CTS, peripheral nerve US may be particularly useful in combination with electrodiagnostic studies (see Procedures).[73, 74]

Sonoelastography also appears to be potentially useful for the diagnosis of CTS, in that the median nerve in CTS patients has been found to be substantially stiffer than in healthy volunteers.[75]  Ultrasound elastography may also be useful for determining the severity of CTS.[76]

Electrodiagnostic examination

Major limitations are associated with electrodiagnostic examination. False-positive and false-negative results are common. Patients with a positive clinical diagnosis of CTS and negative findings on electrodiagnostic studies improve with carpal tunnel release.[77]

Although electrodiagnostic studies provide quantifiable values, they are particularly dependent on the proficiency of the examiner.[78]  These studies should only complement the clinical evaluation by helping to localize the level and severity of the injury and to monitor the progression of the disease when it is being managed conservatively. Electrodiagnostic studies are not generally helpful in confirming a diagnosis of more proximal lesions.

The American Association of Neuromuscular and Electrodiagnostic Medicine (AANEM) has development a quality measurement set for the electrodiagnosis of CTS.[79]

Needle electromyography

Needle electrodes are placed into muscle to record fibrillation potentials; sharp waves and increased insertional activity indicate advanced nerve compression. However, electromyography (EMG) cannot differentiate a median nerve lesion at the pronator teres from a more proximal lesion.[80]  In addition, proximal median neuropathy is frequently normal preoperatively.[60]

Measurement of nerve conduction velocity

The velocity of motor and sensory nerve conduction is measured across definite landmarks. Latency greater than 3.5 ms or asymmetry of conduction velocity greater than 0.5 ms as compared with that of the opposite hand indicates possible entrapment neuropathy. Each segment of the upper extremity can be isolated for specific measurement.

Generally, an increase in sensory latency is observed first, and upon progression of the disease, an increase in the latency of motor fibers is seen. These studies assess only the large myelinated fibers, not the small ones that mediate pain. Nerve conduction studies may be less dependable when there is multiple levels of damage or when a systemic polyneuropathy is present.

Sensibility testing

Sensibility tests can be used to identify compressive neuropathies associated with sensory loss. These include two-point discrimination, Semmes-Weinstein monofilament (SWM) testing, and Strauch's ten test. The SWM test is more reliable, but it is time-consuming.[81]

No specific conditions contraindicate the surgical treatment of median nerve compression, other than general contraindications for minor outpatient surgery. Some would prefer the patient to be off anticoagulant medications (eg, warfarin and clopidogrel), especially when an axillary block is used. Individuals with severe median nerve compression should be cautioned that some of their symptoms may persist after surgery.

There has been controversy over whether any of the various surgical techniques commonly used to treat carpal tunnel syndrome (CTS) is superior to any of the others in terms of final patient outcomes. (See Orthopedic Surgery for Carpal Tunnel Syndrome.) The techniques most commonly used at present include the following:

• Traditional surgical open release
• Limited-incision open release
• Limited-incision device-assisted release
• Single- or dual-port endoscopic release

Endoscopic carpal tunnel release offers the advantages of decreased scar formation, less scar sensitivity, and avoidance of an incision directly over the carpal tunnel between the thenar and hypothenar muscles. A number of studies comparing the two basic techniques (endoscopic and open) suggested that endoscopic techniques are superior to open techniques in terms of earlier functional recovery and earlier return to work. Various multicenter studies did not find endoscopic carpal tunnel release to be associated with a higher complication rate than open release.

In an evidence-based review by Shores and Lee, endoscopic release provided no demonstrable added benefit as compared with open carpal tunnel release,[82] though review of current literature suggests that the operative technique chosen should ultimately be based on patient and surgeon preference. This analysis included an updated systematic review by the Cochrane Collaboration in 2007, as well as a 5-year follow-up of patient outcomes by Atroshi et al in 2009.

A 2014 Cochrane review (admittedly based on low-quality evidence only) found that open and endoscopic approaches to carpal tunnel release were approximately equally effective with respect to symptomatic relief and functional improvement.[83] Endoscopic release appeared to yield better improvement in grip strength and to have a lower rate of minor complications (though there was no difference in the rate of major complications); it was also associated with quicker return to work. The applicability of these conclusions is limited by the flaws of the studies included.

In a 2020 systematic review that included 27 studies, Orhurhu et al compared open with endoscopic carpal tunnel release.[84]  They noted that whereas both approaches were satisfactory in terms of pain relief, symptom resolution, patient satisfaction, time to return to work, and adverse events, there was growing evidence in favor of the endoscopic approach with respect to pain relief, functional outcomes, and satisfaction, at least in the early postoperative period (though the difference might disappear over time).

A learning curve should be anticipated with endoscopic carpal tunnel release, and prior cadaveric practice would be advisable. The fear of catastrophic nerve injuries and the absence of any clear increase in overall benefits of endoscopic release have prompted many surgeons to continue using the traditional approach, with or without modifications of the incision to reduce postoperative discomfort.

Minimally invasive percutaneous ultrasonography (US)-guided approaches to carpal tunnel release has been described as alternatives to the open and endoscopic approaches now in use.[4, 85, 86, 87]

Carpal tunnel syndrome

Most cases of median nerve entrapment neuropathy improve after several weeks of conservative therapy. A change in lifestyle and work activities is necessary. Patients should be advised to decrease or avoid weightbearing repetitive hand movements and the use of vibrating tools. Wrist splinting is frequently suggested for nonoperative treatment of CTS. Wrist splinting in a neutral position at night is recommended. Avoiding wrist extension in splints minimizes intratunnel pressure.[88]

If significant lifestyle changes or financial burden would be inflicted by avoiding activities, a more aggressive treatment should be considered. Operative treatment is recommended for physically active patients and those with severe or long-standing symptoms.

Oral anti-inflammatory medications and corticosteroid injections can be used for transient relief or in high-risk patients. Improvement of symptoms confirms the diagnosis and may be a predictor of satisfactory surgical outcome, if necessary.[89]

A 1-mL combination of 0.5 mL of lidocaine 1% and 0.5 mL of triamcinolone is a common choice for injection in the area around the median nerve at the proximal wrist crease. US has been employed to guide injection.[90] Side effects include irritation and postinjection flare, which may last for a couple of days, and skin discoloration around the injection site. Infection and tendon rupture are rare complications.

Addition of oral vitamin B6[91] has also been reported as a nonoperative treatment for CTS.

Nerve gliding exercises have been used to improve symptoms.[92] Aerobic exercise without wrist strain that results in weight reduction could help alleviate CTS.[93]

In addition to assessing clinical symptoms, some hand surgeons follow the improvements resulting from carpal tunnel therapy by conducting routine nerve conduction studies. Deterioration of nerve conduction in some cases prompts surgical intervention to avoid axonal loss.

Pronator syndrome and anterior interosseous nerve syndrome

Initial treatment of pronator syndrome (pronator teres syndrome [PTS]) and anterior interosseous nerve (AIN) syndrome (AINS) is typically nonsurgical and includes rest, activity modification, anti-inflammatory medications, and splints for at least several months, unless a motor deficit is noted. Patients who do not respond to conservative treatment or who experience motor deficits require decompressive surgery.

The results of decompressive surgery may vary. Before treating PTS, the authors ensure that any carpal tunnel pathology is addressed. If symptoms persist, any proximal nerve compression should be examined, and if signs of thoracic outlet compression are present, the patient is referred for physical therapy.

Surgical treatment of PTS is offered if the above measures yield no improvement.

Carpal tunnel syndrome

When a regimen of conservative treatment fails to relieve patient symptoms of CTS or signs of thenar muscle weakness and atrophy are present, surgical decompression of the median nerve is usually recommended. The following are some of the predictors of nonoperative treatment failure[94] :

• Age greater than 50 years
• Symptom duration exceeding 10 months
• Constant paresthesia
• Stenosing flexor tenosynovitis
• Positive Phalen test result in less than 30 seconds

The traditional exposure (see the image below) remains more common, though minimally invasive approaches confer the advantage of less postoperative discomfort. (See Orthopedic Surgery for Carpal Tunnel Syndrome.) A minimally invasive percutaneous US-guided approach has been described.[4, 85, 86, 87]

The surgeon should choose the method that offers the best visualization of the median nerve so as to avoid injury to the nerve and its branches. A curved longitudinal incision is made paralleling the thenar crease and crossing the wrist crease obliquely in an ulnar direction to a point in line with the long axis of the flexed ring finger. The distal end stops before or beyond the proximal wrist crease in order to afford good visualization of the scissor cut on the retinaculum.

Postoperative wrist pain is somewhat proportional to the length of the incision. Accordingly, some surgeons use minimally invasive incisions, sparing the extended proximal incision with special retractors (see the first image below) and/or using blade guide instruments (see the second image below) to visualize and divide the retinaculum. The ulnar cutaneous branch, which is sometimes found in the distal portion of the incision, should be avoided.

The incision in the retinaculum should follow the course of the nerve as it is exposed gradually by the advancing cut, preferably with visualization of the thenar motor and sensory branches. Care should be taken not to injure the superficial palmar arch.[95] The completeness of the distal cut is confirmed by checking for remaining cross bands and the yellow fat at the end of the carpal tunnel.

Endoscopic retinaculotomy with various techniques, including either the two-portal or the single-portal technique, has been advocated to decrease the length of the incision and thus potentially decrease postoperative incisional discomfort. Numerous endoscopic systems have been described,[96, 97] but the risk of complications, including iatrogenic nerve injury,[98] poor visualization, inability to identify anatomic variations, incomplete release, and apparent beneficial cost savings, remains to be defined.[99, 98]  (See the images below.)

The following is a brief description of the endoscopic technique used by the authors’ group. After a longitudinal palmar skin incision, the palmar fascia is split longitudinally, and a self-retaining retractor is applied. The distal edge of the carpal ligament is exposed and partially divided. Similarly, a transverse proximal incision is made in the wrist, exposing the carpal ligament. (See the image below.)

With the wrist in hyperextended position, an elevator is passed from proximal to distal under the transverse carpal ligament. A cannula is then passed through the same path, and the endoscope is applied. Under endoscopic observation, a meniscus knife is pushed forward along the groove (positioned superiorly) in the cannula to release the flexor retinaculum. (See the images below.)

After all instruments have been removed, a custom-made glass or plastic tube is inserted. The clear tube allows a view of pathology in the carpal tunnel and confirmation of release of the flexor retinaculum.

Pronator syndrome and anterior interosseous nerve syndrome

Before surgical treatment of PTS or AINS, compression points are determined by physical examination, either with stress on a particular tendon or muscle unit or with the elicitation of pain with direct palpation.

The incision to explore the median nerve in the proximal forearm begins a few centimeters above the elbow crease at the antecubital fossa and continues distally in an S or zigzag fashion (see the image below).

The bicipital aponeurosis (lacertus fibrosus) should always be divided. The median nerve is then exposed by dividing the superficial fibers of the pronator teres where the areas of compression are addressed individually.

For exposing the AIN, division or retraction of the superficial head of the pronator teres is usually necessary. The fibrous tissue arch of the flexor digitorum superficialis (FDS) should also be addressed as a potential site of compression, and the deep head of the pronator teres is often divided. If a ligament of Struthers is identified, the incision is extended above the elbow crease to divide this structure.

Vascular abnormalities can also be a cause of constriction that must be addressed. A compression site can usually be identified by noting a discoloration at a narrowing of the nerve after the area of constriction.

Another favorite approach for PTS and AINS is to use two transverse skin incisions that allow adequate exploration and decompression distally and proximally. This approach is thought to be associated with less postoperative discomfort and scarring.[100] (See the image below.)

After carpal tunnel decompression, volar wrist splints are used to restrict range of motion in the wrist during the first 2 weeks after the procedure. Movement of the metacarpophalangeal (MCP) and interphalangeal (IP) joints is encouraged.

Some prefer early movement of the wrist within 24-48 hours after surgery, when the splint and dressings are removed and early physical therapy is initiated.[101] Some have reported that earlier mobilization decreases the risk of flexor tendon “bowstringing” (see Complications) and hastens the process of returning to work and engaging in daily activities, unlike with long-term immobilization.

The sutures are removed 12-14 days after carpal tunnel release. Within 2 weeks, patients are allowed to return to work with one-handed duty. At 1 month after surgery, patients are allowed to work with weight restriction, and at 6-8 weeks after surgery, they are allowed full activity without restrictions.

Most surgeons use soft dressing postoperatively for proximal median nerve entrapment. Splinting, however, is done by keeping the elbow slightly flexed and the wrist in a neutral position.

Recurrent symptoms after surgical decompression of the carpal tunnel usually result from incomplete sectioning of the anterior carpal ligament, flexor tendon synovitis, and scarring in the carpal tunnel.[102] Further surgery, in particular to deal with scarring, leads to relief in only 50% of this minority group of patients.

Injury to both the ulnar and the median nerve has been reported for all carpal tunnel release techniques. Most of these are self-limited problems with paresthesias that resolve.

Scar tenderness at the incision site in the wrist occurs in nearly all patients, but a small number of patients find the sensitivity disabling, especially with the open carpal tunnel release technique. Cseuz et al found that 36% of their patients reported unpleasant scar sensitivity when queried months or years postoperatively.[47] Most patients with scar symptoms reported "minor discomfort which did not interfere with their daily activities."

The median nerve proper, the recurrent thenar motor branch, the median palmar cutaneous nerve branch, the ulnar palmar cutaneous nerve branch, the superficial radial nerve, and digital nerve branches are all vulnerable to injury at the time of carpal tunnel surgery.

Reflex sympathetic dystrophy (RSD) can occur, presumably from irritation of the median nerve. The hand may be swollen, warm, and dry. Later, the skin may become cool, pale, or shiny with trophic changes. The patient may describe hyperalgesia and hyperesthesia.

The transverse carpal ligament is the stabilizing structure for the origin of the abductor pollicis brevis (APB) and the abductor digiti minimi (ADM). Patients frequently note "pillar" pain for several months near these muscle origins, weakening their grip until stable scar tissue forms.

In rare cases, after division of the flexor retinaculum, the flexor tendons move anteriorly with wrist flexion (ie, "bowstringing" of the flexor tendons).[103] When these patients flex their wrists, they may experience pain, a snapping sensation, and paresthesias in a median distribution.

Rarely, patients describe increased stiffness in finger joints after carpal tunnel surgery.

The risk of deep postoperative wound infection after carpal tunnel surgery is small. At the Mayo Clinic, the incidence of infection was 0.5% in 3600 patients.[104]