Background
The median nerve can be compressed at many points along its course to the wrist. Depending on the site of compression and the symptoms, the syndrome is known by various names. The most well-known and frequent form of median nerve entrapment is known as carpal tunnel syndrome (CTS). Provided in this article is a brief overview of the disorder, relevant anatomy, pathophysiology, and management.
The median nerve, colloquially known as the "eye of the hand," is one of the 3 major nerves of the forearm and hand. It courses from the brachial plexus in the axilla to innervate the intrinsic muscles of the hand. See the image below.
Anatomy of median nerve along its course in upper extremity. History of the Procedure
Cases of carpal tunnel syndrome (CTS) have been reported since the late 19th century. The first carpal tunnel release was described by Learmonth in 1933. For some years to follow, only a handful of operative reports of transverse carpal ligament release were described, presumably because the diagnosis was attributed to other proximal neuropathies. The surgical technique for CTS has remained constant, with over 95% of cases done through a small longitudinally oriented incision distal to the volar wrist crease. In recent years, an endoscopic approach has been used for the release of carpal tunnel; however, the open procedure remains the more popular operation.
Problem
Median nerve entrapment syndrome is a mononeuropathy that affects movement of or sensation in the hand. It is caused by compression of the median nerve in the elbow or distally in the forearm or wrist, with symptoms in the median nerve distribution.
The most well-known and frequent form of median nerve entrapment is known as carpal tunnel syndrome (CTS), defined as a constellation of symptoms associated with compression of the median nerve at the wrist.[1, 2] Pronator syndrome is defined as compression of the median nerve in the forearm that results in predominantly sensory alteration in the median nerve distribution of the hand and the palmar cutaneous distribution of the thenar eminence.[3, 4] Anterior interosseus nerve syndrome[5] is characterized by complete or partial loss of motor function of the muscles innervated by the anterior interosseus nerve (AIN), a motor branch of the median nerve in the forearm.
Epidemiology
Frequency
The exact prevalence of median nerve entrapment is unknown, as it encompasses various distinct syndromes.
Most of the epidemiologic studies involving median nerve compressive neuropathy have centered around carpal tunnel syndrome (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.[6] The estimated incidence of CTS in the United States is 3.4%.[7]
Another study found that 1 in 5 symptomatic subjects would be expected to have CTS based on clinical examination and electrophysiologic testing. The use of highly repetitive wrist movements, vibrating tools, awkward wrist positions, and great force seem to predispose to CTS, although the exact cause of CTS is a matter of controversy. In a study on incidence of CTS in automobile workers, the annual incidence of CTS was found to be 1%-10%.[8] Prevalence in some industries, such as fish processing, has been reported to be as high as 73%.[9]
Other conditions that are associated with a high risk for CTS include diabetes and pregnancy. People with diabetes have been known to have prevalence rates of 14% and 30% without and with diabetic neuropathy, respectively.[10] Prevalence of CTS during pregnancy has been reported to be around 2%.[11]
The exact incidence of proximal median nerve entrapment in the population is less understood than that of CTS. On average, proximal median nerve compression syndrome constitutes less than 1% of upper extremity compressive syndromes.[12] However, some studies report a very high incidence of pronator syndrome in already symptomatic workers; for example, female machine milkers have rates as high as 75%.[13] The incidence of pronator syndrome is 4 times higher in women than in men.
Etiology
Risk factors have been well studied predominantly for carpal tunnel syndrome (CTS) only, with the other types of median nerve entrapment being generally 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.
According to de Krom et al (1992) from the Netherlands,[6] 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 1,016 residents of Rochester, Minnesota, who were diagnosed with CTS from 1961-1980, 43.2% had no associated conditions.[14] 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.[15] 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,[16] the authors found risk factors associated with CTS included previous wrist fracture (OR=2.29); rheumatoid arthritis (OR=2.23); osteoarthritis of the wrist and carpus (OR=1.89); obesity (OR=2.06); diabetes (OR=1.51); and the use of insulin (OR=1.52), sulfonylureas (OR=1.45), metformin (OR=1.20), or thyroxine (OR=1.36). 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.[17]
Overall, the etiology of CTS is generally accepted as idiopathic, as the findings described above are considered to be based on unproven theories.
Pathophysiology
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 catheters placed in the carpal tunnel. Normal pressures range from 2-10 mm Hg. This pressure is affected by finger, wrist, and forearm position.[18] 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, arthritis, thyroid dysfunction, and renal failure. Patients with diabetes have a higher tendency to develop carpal tunnel syndrome (CTS) due to a 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, the authors found extensive demyelination and remyelination 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 (2002),[22] "Experimental 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 and clinical symptoms correlate very poorly. This 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 (1973) 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]
Investigators are also looking into the biochemical aspects of chronic compressive neuropathies. 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 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 TGF-beta in fibroblasts, suggesting a response to injury to the subsynovial connective tissue.[32]
Presentation
Pronator syndrome
Patients with pronator syndrome 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.[4, 33]
Development of paresthesia in the hand after 30 seconds or less of manual compression of the median nerve at or near the pronator muscle (pronator compression test) can aid in clinical diagnosis.[34, 35]
Provocation maneuvers may also indicate the possible site of entrapment in pronator syndrome.[36, 37] Reproduction of symptoms upon flexion of the elbow against resistance between 120° and 135° suggests ligament of Struthers compression of the median nerve. Compression by bicipital aponeurosis may be diagnosed based on pain upon elbow flexion against resistance when the arm is pronated. Compression by 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 anterior interosseus nerve syndrome (AINS) symptoms 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 the inability to pronate the forearm when the elbow is flexed.[5, 38] This results from motor loss of the flexor pollicis longus, the flexor digitorum profundus of the index finger, and pronator quadratus.[39] Absence of sensory symptoms is typical, as the anterior interosseus nerve 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.[40] It is preceded by severe pain for weeks. Treatment consists of high-dose corticosteroids and acyclovir. Decompression typically does not help.
Carpal tunnel syndrome
Symptoms of carpal tunnel syndrome (CTS) include paresthesia and/or numbness in the median nerve distribution of the hand (thumb, index, 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 and opponens pollicis.[41, 42] 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 and/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 median nerve on light percussion—suggests CTS. It is also useful to clinically follow nerve regeneration after injury.[43, 44, 45, 46] 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.[47]
In a prospective study of 1039 patients with a neurophysiologic diagnosis of CTS, Nora et al (2000) found that the most characteristic manifestation of the syndrome was paresthesia in the median nerve distribution, frequently extending to the whole hand. Pain was very common but less specific, and weakness was rare.[48] Tinel and Phalen signs were observed in 34.2% and 56.3% of the hands, respectively.
Indications
See Surgical therapy.
Relevant Anatomy
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. The illustration below depicts the course of the median nerve in the upper extremity.
Anatomy of median nerve along its course in upper extremity. 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, flexor carpi radialis, palmaris longus, and flexor digitorum superficialis (FDS). The median nerve also gives off a significant branch within the pronator teres, the anterior interosseous nerve, which supplies the flexor pollicis longus, the pronator quadratus, and the lateral half of the flexor digitorum profundus muscles.
The median nerve continues its course in the distal forearm, under the FDS and on the flexor digitorum profundus. 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 pronator quadratus muscle 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,[49, 50, 51] causing specific and variable signs and symptoms.
Pronator syndrome
Ligament of Struthers (see image below): This 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 in length.[52] 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.[53] In some cases, no bony spur can be identified; only the ligament persists.[54, 55]
Ligament of Struthers. Lacertus fibrosus (bicipital aponeurosis; see image below): This is the least common cause of pronator syndrome.[56, 37] 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.
Lacertus fibrosus. Pronator teres (see image below): Fibrous bands between the deep and superficial head of the pronator teres frequently cause compression of both the median nerve and the anterior interosseous nerve. An anatomical study proposed the determinant variations that can lead to pronator syndrome: a short and tendinous ulnar head, an ulnar head joined to the arch of the FDS muscle, an ulnar head with triple origin slips, and a humeral head perforated by the median nerve.[57]
Pronator teres. FDS arch (see image below): The FDS varies in origin and size, and the median nerve can be crossed and compressed by 1 or 2 aponeurotic arches.[58, 59]
Fibrous arch of flexor digitorum superficialis. 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 anatomical abnormality, whether congenital or traumatic, can increase the predisposition to the development of anterior interosseous nerve syndrome (AINS), especially if the area is challenged with concurrent localized edema. Known sites of compression include the following:
- Gantzer's muscle (see image below): This is the accessory head of the flexor pollicis longus. It has been postulated to be a cause of AINS.[60] In an anatomical study, the muscle was found in 52% of limbs and was supplied by the anterior interosseous nerve.[61] It was found to be posterior to both the median and anterior interosseous nerves in all cases.
Gantzer's muscle. - Fibrous arch of FDS
- Fascial bands of deep head of pronator teres
- Aberrant palmaris profundus
- Aberrant flexor carpi radialis brevis
Carpal tunnel syndrome
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 9 tendons. An increase in the volume of the tunnel contents or a decrease in the size of the tunnel can compress the median nerve.
Contraindications
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 anticoagulative medicines, such as warfarin (Coumadin) and clopidogrel (Plavix), 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.
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