Entrapment Neuropathies of the Upper Extremity

12 – Entrapment Neuropathies of the Upper Extremity

Chapter 12
Entrapment Neuropathies of the Upper Extremity
Jenny T. Bencardino
Zehava Sadka Rosenberg
Entrapment neuropathies are characterized by alteration of nerve function secondary to compression by mechanical or dynamic forces. Anatomically narrow passages predispose individual nerves to these neuropathies. The compression can be acute, chronic, or intermittent. Not infrequently compressive neuropathies are related to space-occupying lesions such as tumors, cysts, inflammatory processes (rheumatoid arthritis, tuberculosis), or posttraumatic conditions (hematoma, myositis ossificans, and fracture callous formation). In some instances, changes of the surrounding soft tissues, such as thickening of connective tissue or postoperative scarring, can produce signs and symptoms of entrapment neuropathy. Edema, caused by hormonal changes associated with pregnancy, use of oral contraceptives, menopause, and hypothyroidism, is another known cause. Dynamic changes within a narrow space or “tunnel” during repetitive daily activity can create compression of a nerve with only minimal anatomic variations.1
Clinical manifestations of entrapment neuropathy include nonspecific signs and symptoms, such as:
  • Muscle weakness, with or without associated sensory loss
  • Sharp burning pain and paresthesia along the distribution of the affected nerve (Fig. 12.1)
  • Muscle atrophy and vegetative disturbances in advanced cases
Electromyographic and nerve conduction studies may show abnormal response to nerve stimulation. However, the deep course of some nerves (e.g., the posterior interosseous nerve in the proximal forearm) may produce unreliable electromyographic analysis. In most instances, conservative measures, including immobilization, local heat, and anti-inflammatory medications, are sufficient for the treatment of compressive neuropathies. More severe cases may require percutaneous steroid injections or surgical release of the nerve.
FIGURE 12.1 ● (A) Upper extremity volar sensory innervation. (B) Upper extremity dorsal sensory innervation.


With the exception of MR imaging, most imaging techniques are insensitive for detecting compressive neuropathies. Conventional radiographs and computed tomography (CT) may show bony changes such as exostosis, osteophytes, fracture callus, and anatomic osseous variants that may produce nerve entrapment. Direct visualization of the nerve, however, is best achieved with MR imaging. Advantages of MR imaging in the diagnostic workup of neuropathy include:
  • Confirmation of the presence of nerve compression or entrapment
  • Determination of the presence of mechanical compression (e.g., soft-tissue mass)
  • Determination of the nature, site, and extent of the nerve compression
  • Exclusion of other lesions that can cause similar signs and symptoms (e.g., rotator cuff tear)
Normal peripheral nerves are seen on MR images as structures of low to intermediate signal intensity surrounded by fat, in specific anatomic locations. Mildly increased signal is a normal finding on water-sensitive sequences. Changes in signal intensity, size, and position of the involved peripheral nerve are valuable MR findings supportive of the finding of compressive neuropathy. Osseous and soft-tissue lesions can also be well depicted with MR imaging. In the subacute stage of muscle denervation, MR imaging typically shows interstitial T2 hyperintensity in the affected muscle group. In chronic cases, produced by a long-standing compressive neuropathy, muscle atrophy with fatty infiltration takes place.2,3, Increased muscle signal on fluid-sensitive images superimposed on muscle atrophy indicates an ongoing, partly reversible process.


Pathophysiology of Nerve Disorders
Nerve disorders have been classified according to the severity of injury and its potential for reversibility:
  • Neuropraxia, or first-degree nerve injury, is the least severe nerve injury with the greatest capability for recovery. There is a temporary loss of nerve conduction secondary to distortion of the myelin near the nodes of Ranvier due to ischemia, mechanical compression, or electrolyte imbalance. Also, there is a segmental block of conduction without Wallerian degeneration. Complete recovery is expected within 2 to 3 months.
  • Axonotmesis, or second-degree nerve injury, implies a more extensive injury due to interruption of the axon with secondary Wallerian degeneration distal to the site of injury. There is, however, preservation of all the supporting connective tissue structures that surround the axon and Schwann cells. The recovery period, ranging from weeks to months, depends on the distance between the site of injury and the end organs. The prognosis is relatively good, dependent on sprouting and re-innervation.
  • Neurotmesis refers to the most severe degree of injury, with no chance of regeneration. It is caused by complete disruption of the nerve and its supporting structures.
Sunderland4 further divided neurotmesis into three categories:
  • Third-degree nerve injury, in which the endoneurium is disrupted with intact perineurium and epineurium
  • Fourth-degree nerve injury, in which all neural elements are disrupted except the epineurium
  • Fifth-degree nerve injury, in which the nerve is transected, resulting in complete discontinuity of the nerve
Neurotmesis is an indication for surgical treatment with end-to-end anastomosis or nerve grafting. The surgical outcome depends primarily on the chronicity of the process.
Several categories of nerve injury may coexist in the same nerve. The double-crush theory maintains that a compressive lesion at one point along a peripheral nerve causes internal derangement of nerve cell metabolism and therefore lowers the threshold for occurrence of compression at another site.5
MR Imaging Techniques
Clinical assessment of peripheral neuropathy routinely involves nerve conduction studies and electromyography. As mentioned, however, MR imaging provides additional information to clinical neurophysiologic investigations and is, in addition, operator-independent and painless. MR examination has the further advantage of providing a lasting detailed topographical map of neuropathic involvement, avoiding localization errors of muscles in electromyography. Using electromyography as the gold standard, inversion recovery MR sequences have been shown to have a relative sensitivity of 84% and specificity of 100%.6
It remains to be determined whether nerve conduction or MR studies are the optimal diagnostic technique for entrapment neuropathies. At present, however, nerve conduction tests are more routinely used than MR. MR imaging studies are most often used to:
  • Exclude focal mass lesions or external compression
  • Identify signs of neuritis/neuropathy
  • Visualize denervation muscle injury
Acute axonal nerve lesions are manifested by T2 hyperintensity and increased girth of the nerve at and distal to the site of injury correlating with Wallerian degeneration and nerve edema. Proximal increased girth may also be encountered. Prolongation of the T2 relaxation time of denervated muscle fibers and post-gadolinium enhancement most likely reflect changes in the intramuscular vascular bed leading to capillary engorgement and increased muscular blood volume.7,8
Inversion recovery sequences have proven more sensitive than T2-weighted fast spin-echo imaging in the detection of T2 prolongation in denervated muscle. These changes can be


seen as early as 24 hours after complete transection of the sciatic nerve in rats and precede muscle atrophy.9 MR imaging has also been successfully used experimentally as an indicator of nerve healing and re-innervation following transection and repair of the posterior tibial nerve in rats. Changes in T2 relaxation, noted in the first 4 weeks following surgical intervention, completely returned to normal at 6 weeks of follow-up.10

The use of intravenous paramagnetic contrast agents might also prove to be valuable in assessing entrapment neuropathies. Sugimoto et al.11 used dynamic MR imaging to study nerve damage and suggested symptoms of carpal tunnel syndrome are produced by circulatory disturbances in the median nerve caused by chronic hypoxia rather than by compression alone. They proposed that dynamic MR imaging could be used to distinguish normal from abnormal nerves by their different patterns of enhancement. Novel contrast media, such as superparamagnetic iron oxide, may potentially be useful in detecting macrophage invasion into the degenerating nerve distal to an axonal lesion.12
The use of Gadofluoride M-enhanced MR imaging also shows promise in the assessment of nerve regrowth and regeneration. This agent selectively accumulates and persists in nerve fibers undergoing Wallerian degeneration causing T1 shortening, which is present as early as 48 hours after nerve injury. Increased T1 signal disappeared on follow-up studies, correlating with the regrowth of nerve fibers. Interestingly, Gadofluoride M enhancement persisted in nonregenerating, permanently transected nerves.13
Entrapment Neuropathies of the Shoulder
Associated Normal Anatomy
Suprascapular Nerve
The suprascapular nerve originates from the upper trunk of the brachial plexus and receives fibers from the C5 and C6 nerve roots (Fig. 12.2). The suprascapular nerve contains motor fibers that innervate the supraspinatus and infraspinatus muscles as well as sensory fibers that carry sensation from both the glenohumeral and acromioclavicular joints. The nerve traverses the supraclavicular fossa with the suprascapular vein and artery. It then enters the suprascapular notch, making a sharp turn around the scapular spine. The transverse scapular ligament bridges the scapular notch or incisura superiorly, creating a fibro-osseous tunnel. The suprascapular vessels travel above the notch. At the scapular incisura, the supra-scapular nerve branches into the supraspinatus and infraspinatus nerves. In about 50% of the population, a second ligament, the spinoglenoid ligament, produces a second more inferior and posterior tunnel traversed by the infraspinatus nerve.1,14,15
MR Appearance
The suprascapular nerve is best identified on oblique coronal T1-weighted images within the supra-scapular notch, which is located at the junction of the glenoid with the scapular neck just medial to the superior glenoid rim. Fat within the notch outlines the nerve and accompanying vessels. The nerve then takes a sharp turn inferiorly, entering the spinoglenoid notch (Fig. 12.3). At this level, the supra-scapular neurovascular bundle is best visualized on axial MR images (Fig. 12.4). Prominent suprascapular veins are not infrequently noted accompanying the nerve and in some instances are responsible for the compressive neuropathy.
Axillary Nerve
The axillary nerve, the terminal branch of the posterior cord of the brachial plexus, receives contributions from C5 and C6 nerve roots. After its formation, the nerve courses dorsal to the axillary artery, along the anterior surface of the subscapularis muscle, where it takes a sharp turn posteriorly to travel along the inferior glenohumeral joint surface.16 The axillary nerve and posterior circumflex artery then enter the quadrilateral space, which is limited by the long head of the triceps brachii muscle medially, the teres minor muscle superiorly, the teres major muscle inferiorly, and the medial aspect of the proximal humerus laterally. The axillary nerve gives off four branches in the quadrilateral space: two motor branches to the anterior and posterior portions of the deltoid muscle, a sensory branch (the superior lateral brachial cutaneous nerve), and a motor branch to the teres minor muscle.17 Price et al. found that the branch to the teres minor and the branch supplying the lateral cutaneous innervation lie closest to





the glenoid rim.17 Using statistical analysis, these investigators showed that the axillary nerve travels at a fixed distance of approximately 2.5 mm from the inferior glenohumeral ligament throughout its course. An articular branch of the axillary nerve supplies the shoulder joint capsule.

FIGURE 12.2 ● The suprascapular nerve in the shoulder.
FIGURE 12.3 ● Normal MR anatomy of the suprascapular nerve. (A) Coronal PD-weighed image demonstrates suprascapular nerve and vessels outlined by fat within the spinoglenoid notch. The axillary nerve and vessels within the quadrilateral space are noted. (B) A more anterior coronal PD-weighed image demonstrates the suprascapular nerve and vessels outlined by fat within the suprascapular notch (or incisura).
FIGURE 12.4 ● Normal MR anatomy of the suprascapular nerve. (A) Axial PD-weighted image demonstrates the supra-scapular nerve as a linear, intermediate-signal structure at the level of the suprascapular incisura. (B) Sagittal PD-weighed image at the level of the spinoglenoid notch demonstrates the supra-scapular nerve and vessels.
FIGURE 12.5 ● Normal MR anatomy of the axillary nerve. Oblique sagittal PD-weighted image shows the axillary neurovascular bundle traveling between the teres minor muscle and the teres major muscle just medial to the humeral diaphysis in the quadrilateral space.
MR Appearance
The axillary nerve is best visualized on oblique sagittal T1-weighted images of the shoulder (Fig. 12.5). The axillary neurovascular bundle is seen below the inferior glenoid rim traversing the space between the teres minor muscle superiorly and the teres major inferiorly. Oblique coronal images oriented perpendicular to the proximal humeral shaft demonstrate the quadrilateral space adjacent to the medial humeral cortex and lateral to the long head of the triceps muscle.
Neuropathology of the Shoulder
Suprascapular Nerve Syndrome
Given its peculiar branching pattern, proximal entrapment of the suprascapular nerve at the scapular incisura results in a supraspinatus and infraspinatus muscle denervation syndrome. Distal entrapment at the spinoglenoid notch may be manifested as isolated compromise of the infraspinatus muscle.18
Common causes of compression or entrapment of the supra-scapular nerve or its branches include:19,20,21
  • Suprascapular ligament stretching from repetitive scapular motion
  • Scapular fractures or other direct trauma
  • Posttraumatic calcification of the suprascapular ligament
  • Adduction and internal rotation caused stretching of the suprascapular nerve underneath the spinoglenoid ligament14
  • Overhead activities (e.g., painters, electricians, volleyball and tennis players), which may result in chronic mechanical stretching and irritation of the suprascapular nerve
  • Rotator cuff injury (Vad et al.,19 using electrodiagnostic testing, studied patients with full-thickness tears of the rotator cuff presenting with shoulder muscle atrophy. They found a relatively high prevalence (28%) of peripheral nerve injury, including suprascapular neuropathy, axillary neuropathy, and cervical radiculopathy.)
  • Iatrogenic injury to the suprascapular nerve during rotator cuff repair
  • Soft-tissue masses, osseous tumors, and vascular malformations, which can also compress the nerve along its course (Fig. 12.6)
  • Ganglion cysts at the scapular incisura, typically associated with superior and posterior labral tears (Fig. 12.7)
FIGURE 12.6 ● Suprascapular nerve syndrome secondary to a suprascapular varix. Oblique coronal fat-suppressed T2-weighted (A) and axial PD-weighed (B) images demonstrate prominent suprascapular veins (arrow) within the suprascapular incisura and denervation edema of the infraspinatus (IS) muscle.
FIGURE 12.7 ● Suprascapular nerve syndrome secondary to a ganglion. Oblique coronal (A) and sagittal (B) fat-suppressed T2-weighted images demonstrate a large cystic lesion occupying the suprascapular incisura and spinoglenoid notch in keeping with a ganglion (arrow). Abnormal T2 hyperintensity consistent with denervation edema involving the infraspinatus muscle (IS) is noted.



Antoniou et al. studied a series of 53 patients and found that pretreatment electromyographic findings were predictive of treatment response.22 Minimal electromyographic changes in patients with suprascapular nerve impingement were associated with limited response to treatment, especially in those with nerve compression secondary to spinoglenoid notch cysts.22 In the absence of an anatomic cause, management should be nonoperative; most patients will have a good to excellent result with physical therapy. Suprascapular notch cysts and spinoglenoid notch cysts respond significantly better to operative treatment.22,23 Traumatic lesions, including traction and direct closed injuries, have an equal response to operative and nonoperative treatment. Overall, the final outcome for traumatic injuries was significantly worse than for any other etiologic processes.22
MR Appearance
MR is a useful modality for the diagnosis of suprascapular nerve entrapment. On fat-suppressed T2-weighted MR images, involved muscle displays hyperintense signal (see Figs. 12.6 and 12.7). The site of entrapment can be inferred by the location of muscle involvement.24 Isolated denervation edema of the infraspinatus muscle places the site of entrapment at the spinoglenoid notch. When increased signal of both the supraspinatus and the infraspinatus is noted, compression at the suprascapular notch is most likely.
Using electromyography as the gold standard, Ludig et al. have shown that the sensitivity and specificity of MR in detecting suprascapular nerve entrapment vary depending on the MR criteria used:25
  • Using muscular denervation edema, sensitivity and specificity were shown to be 94.5% and 100%, respectively.
  • Using fatty changes and muscle atrophy (decreased muscle bulk, best seen on sagittal oblique spin-echo T1-weighted images), sensitivity and specificity were 81% and 80%, respectively.
  • Using fatty infiltration of the supraspinatus and/or infraspinatus muscles, sensitivity and specificity were 25% and 96%, respectively.
Axillary Neuropathy
The quadrilateral space syndrome is caused by compression of the axillary nerve in the quadrilateral space. Fibrous bands are believed to be responsible for compression of the nerve and the posterior circumflex humeral artery as they travel within the quadrilateral space. Mass lesions, such as large paralabral cysts, can also damage or compress the axillary nerve within the quadrilateral space.26 Clinically, patients may have poorly localized shoulder pain, paresthesias, and discrete point tenderness in the lateral aspect of the quadrilateral space.27 In advanced cases, atrophy of the teres minor and the deltoid muscles can occur.
There may be several etiologies for post-traumatic axillary neuropathy:
  • In anterior shoulder dislocation, axillary nerve injury results from traction and compression of the nerve and the subscapularis muscle by the dislocated humeral head (Fig. 12.8). The shoulder is the most common joint dislocation seen in the emergency department and has an overall incidence of 1.7% in the population.28 Nerve injury complicates shoulder dislocation in up to 45% of cases,29 and the axillary nerve is the most commonly involved because of its relatively tethered course through the quadrilateral space.
  • The risk for axillary nerve and brachial plexus injury is greater if the shoulder is not reduced within 12 hours. Although neurologic injury is well known to orthopaedists who treat shoulder dislocation, few reports in the radiologic literature stress the association of teres minor atrophy with prior shoulder dislocation.30,31,32 Axillary nerve injury may develop after manipulative reduction in which traction with rotation or abduction is simultaneously applied.33
  • Posttraumatic injury to the axillary nerve can also be secondary to proximal humeral fractures34 and rarely as a result of a direct blow to the deltoid muscle.
The vast majority of patients recover with nonoperative treatment.35 Surgical débridement of fibrous bands has been reported to be successful in alleviating symptoms in patients with quadrilateral space syndrome who do not respond to conservative measures.36 In the management of posttraumatic axillary neuropathy, baseline electromyographic studies should be obtained within 4 weeks of the injury, with a follow-up evaluation at 12 weeks.35 If no clinical or electromyographic improvement is noted, surgery may be appropriate. The results of operative repair are best if surgery is performed within 3 to 6 months of the injury. The monofascicular composition of the nerve and the relatively short distance between the zone of injury and the motor endplate both contribute to the generally good outcome of axillary nerve repair.35
MR Appearance
Anatomically, the lateral cutaneous branch and the branch to the teres minor are closest to the glenoid rim and are therefore the most vulnerable.16 Clinical signs of axillary neuropathy are often vague. Wong and Williams found sensory deficits only in 182 of 196 patients with postoperative axillary neuropathy.37 Damage to the teres minor branch, however, may be difficult to assess on clinical grounds. MR evaluation of vague clinical symptoms may demonstrate signs suggestive of teres minor denervation injury (Figs. 12.9 and 12.10). Unlike electromyography, which directly evaluates nerve function, MR imaging provides indirect indicators of nerve injury by detection of changes in the fat and water composition of muscle. Changes in T1 and T2



prolongation can be appreciated within 15 days of the injury.36 The following MR findings are helpful in evaluating axillary neuropathy:

  • Denervation muscle edema, not observed as often as fatty infiltration and atrophy
  • Teres minor fatty infiltration and decreased muscle bulk with or without involvement of portions of the deltoid.36 The incidence of atrophy or abnormal signal in the teres minor muscle has been reported to be as low as 0.8%.36
  • Associated abnormal MR findings such as labral tear, rotator cuff tear, subacromial subdeltoid bursitis, and acromioclavicular joint degenerative osteoarthritis
  • The identification of teres minor atrophy in the absence of quadrilateral space lesions should prompt careful evaluation for signs of posttraumatic glenohumeral instability and prior dislocation.30,31
FIGURE 12.8 ● The axillary nerve. (A) The axillary nerve is seen coursing within the quadrilateral space in close relationship to the inferior glenoid rim. (B) Traction on the axillary nerve by a dislocated humeral head.
FIGURE 12.9 ● Quadrilateral space syndrome. Axial (A) and oblique coronal (B) PD-weighted images demonstrate selective atrophy and fatty infiltration of the teres minor muscle (asterisk).
Parsonage-Turner Syndrome
Parsonage-Turner syndrome, also referred to as acute brachial neuritis, is clinically characterized by sudden onset of severe atraumatic pain in the shoulder girdle. The pain typically decreases spontaneously in 1 to 3 weeks and is followed by weakness of at least one of the muscles about the shoulder. The exact etiology has not been established, but viral and immunologic causes have been considered.38,39 The age range at presentation is quite wide, and there is typically a male predominance (male-to-female ratio of 2:1 to 11.5:1).40,41
In the early descriptions by Parsonage and Turner,40,41,42 the long thoracic nerve was reported to be the most frequently compromised nerve. However, later studies have shown a higher rate of isolated suprascapular nerve disease.39 The axillary, radial, and phrenic nerves,40 as well as the entire brachial plexus,41 may also be affected. Bilateral involvement is found in as many as one third of the patients.39 An abnormal electromyographic pattern with fibrillation potentials and positive waves may be seen.41
Parsonage-Turner syndrome can resemble a variety of other clinical entities, including rotator cuff pathology, cervical radiculopathy, spinal cord tumor, and peripheral nerve compression. The most confusing differential diagnosis is compressive neuropathy of the suprascapular or axillary nerve. The more insidious onset of pain and lack of spontaneous resolution of symptoms can help to distinguish compressive neuropathy from Parsonage-Turner syndrome. MR imaging can be useful in solving this diagnostic dilemma by displaying involvement of multiple muscles in more than one nerve distribution, characteristic of Parsonage-Turner syndrome.36 MR imaging (see below) also helps to exclude suprascapular or axillary nerve entrapment related to paralabral ganglions or other impinging mass lesions.43 Rotator cuff pathology can also be readily excluded using MR imaging.
No specific treatment has yet been proven effective in Parsonage-Turner syndrome. In the early stages, analgesics may be required. Steroids have proven ineffective for pain relief and do not improve muscle function. Rest is recommended, and immobilization of the affected upper extremity


may be helpful in pain relief and in preventing stretching of the affected muscles. Once the pain subsides, physical therapy is recommended. The overall prognosis is good, with almost 75% of patients experiencing complete recovery within 2 years. However, the period of time for complete recovery is variable, ranging from 6 months to 5 years.

FIGURE 12.10 ● Posttraumatic axillary neuropathy secondary to a paralabral cyst. Oblique coronal fast spin-echo T2-weighted (A) and axial fat-suppressed post-gadolinium T1-weighted (B) images demonstrate a large multiloculated paralabral cyst (asterisk) in association with posterior labral tearing (arrow). (C) Oblique sagittal T1-weighted image shows selective fatty infiltration and atrophy of the teres minor muscle (Tmi) associated with remodeling of the posterior glenoid rim (arrow) and posteroinferior paralabral cyst (asterisk).
MRI Appearance
MR imaging findings in the acute stage of Parsonage-Turner syndrome include diffuse increased signal intensity on fluid-sensitive sequences consistent with interstitial muscle denervation edema.43 The most commonly affected muscles are those innervated by the suprascapular nerve, including the supraspinatus and infraspinatus (Fig. 12.11). The deltoid muscle can also be compromised in cases of axillary nerve involvement. Later in the course of the disease, muscle atrophy manifested by decreased muscle bulk may be visualized (see Fig. 12.11). Whole-body MR examination has been proposed as a potentially useful noninvasive diagnostic tool for Parsonage-Turner syndrome, allowing identification of a specific pattern of altered muscle signal confined to the shoulder girdle or a specific nerve distribution.44
FIGURE 12.11 ● Parsonage-Turner syndrome. Oblique sagittal T1-weighted (A) and fat-suppressed T2-weighted (B) images show denervation edema and atrophy of the infraspinatus (IS) and teres minor (arrow) muscles.


Entrapment Neuropathies of the Arm and Elbow
Associated Normal Anatomy
Ulnar Nerve
The ulnar nerve is the direct continuation of the medial cord of the brachial plexus. It contains motor and sensory fibers arising from the C8 and T1 nerve roots. At mid-arm level, the ulnar nerve crosses from the anterior compartment to the posterior compartment, piercing the intermuscular septum. Approximately 8 cm proximal to the medial epicondyle, the ulnar nerve may pass under the arcade of Struthers, which is present in 70% of individuals (Fig. 12.12).45 The arcade of Struthers is made up of fibers from the deep fascia of the distal arm connecting the medial intermuscular septum to the medial head of the triceps muscle.46
At the elbow, the ulnar nerve is located superficially as it descends posterior to the medial epicondyle within the cubital tunnel. The elbow capsule and portions of the ulnar collateral ligament form the floor of the cubital tunnel. Superficially, the roof of the tunnel is formed by the arcuate ligament (Osborne ligament or the cubital tunnel retinaculum), which extends from the medial epicondyle to the medial olecranon process (Fig. 12.13). O'Driscoll et al. postulated that the cubital tunnel retinaculum is likely a remnant of the anconeus epitrochlearis muscle.47 Normal anatomic variants range from no band at all to a well-defined muscle.
The ulnar nerve enters the anterior compartment of the forearm between the humeral and ulnar heads of the flexor carpi ulnaris. It then travels between the flexor carpi ulnaris




and the flexor digitorum profundus muscles in the forearm. It splits into superficial and deep branches at the wrist.

FIGURE 12.12 ● The ulnar nerve: anterior (A), medial (B), and axial (C) views. In the distal arm the ulnar nerve descends within the arcade of Struthers, then runs posterior to the medial epicondyle and deep to the cubital tunnel retinaculum and arcuate ligament within the cubital tunnel before entering the forearm between the two heads of the flexor carpi ulnaris muscle.
FIGURE 12.13 ● Normal MR anatomy of the ulnar nerve. Axial PD-weighted image demonstrates the ulnar nerve posterior to the medial epicondyle and medial to the posterior recurrent vessels.
FIGURE 12.14 ● Normal MR anatomy of the ulnar nerve. Axial PD-weighted image depicts the ulnar nerve surrounded by fat as it courses between the ulnar and humeral heads of the flexor carpi ulnaris muscle.
The ulnar nerve proper supplies the following structures:
  • The elbow joint
  • The flexor carpi ulnaris muscle and the ulnar half of the flexor digitorum profundus to the fourth and fifth fingers
  • The palmaris brevis (the superficial motor branch of the ulnar nerve)
  • The hypothenar muscles, the third and fourth lumbricals, all interossei, the adductor pollicis, the deep head of the flexor pollicis brevis, the flexor digiti minimi, the abductor digiti minimi, and the opponens digiti minimi (the deep motor branch of the ulnar nerve)
  • The medial palm
  • The palmar and distal dorsal skin of the fifth finger
  • The medial half of the fourth finger
MR Appearance
In most individuals, the ulnar nerve is clearly highlighted by fat throughout its course in the elbow and proximal forearm.48 Axial MR images depict the nerve traversing the cubital tunnel behind the medial epicondyle, roofed by the arcuate ligament (see Fig. 12.13). The accompanying vessels are usually located lateral to the nerve (see Fig. 12.13).49 In cases where the elbow has to be imaged in 90° of flexion, the size of the cubital tunnel is compromised, rendering identification of the ulnar nerve more difficult.49,50 Distal to the elbow joint, the ulnar nerve is commonly highlighted by fat as it travels between the ulnar and humeral heads of the flexor carpi ulnaris muscle and posterior to the flexor digitorum superficialis muscle (Fig. 12.14). The normal nerve is low in signal on T1-weighted images but typically demonstrates a mild increase in signal on fluid-sensitive sequences.
Median Nerve
The median nerve is formed by the blending of the lateral and medial cords of the brachial plexus, and it is the nerve to the radial side of the flexor portion of the forearm and hand (Fig. 12.15). It contains both motor and sensory fibers from the C5, C6, C7, C8, and T1 nerve roots. The median nerve descends in the arm, first lateral, then ventral, and finally medial to the brachial artery. It has no branches at the level of the arm. At the elbow, the median nerve is found medial and parallel to the brachial artery. It passes between the bicipital aponeurosis


(lacertus fibrosus) and the brachialis muscle, traveling deep to the pronator teres as it courses into the forearm (Fig. 12.16). In the elbow region, the median nerve supplies all the superficial muscles of the ventral forearm (the pronator teres, the flexor carpi radialis, the palmaris longus, and the flexor digitorum superficialis) except the flexor carpi ulnaris muscle.

FIGURE 12.15 ● The median nerve. The four potential sites of compression are the supracondylar process and ligament of Struthers; the ulnar and humeral heads of the pronator teres; the lacertus fibrosus; and the fibrous edge of the flexor digitorum superficialis.
FIGURE 12.16 ● Normal MR anatomy of the median nerve. Axial PD-weighted image demonstrates the median nerve between the pronator and the brachialis muscles.
The anterior interosseous nerve branches off the median nerve in close proximity to the bifurcation of the brachial artery into the radial and ulnar arteries, approximately 2 to 5 cm below the level of the medial epicondyle. The anterior interosseous nerve courses over the flexor digitorum profundus and along the interosseous membrane toward the wrist joint. It supplies all the ventral deep muscles of the forearm, including the radial half of the flexor digitorum profundus, the flexor pollicis longus, and the pronator quadratus muscles. The ulnar half of the flexor digitorum profundus is supplied by the ulnar nerve.
The most common nerve variation of the median and ulnar nerves is the Martin Gruber anastomosis, occurring in 22% to 39% of the population.51,52 The anastomosis presents in two patterns:
  • A motor branch from the median nerve in the proximal forearm to the ulnar nerve in the middle to distal third of the forearm
  • A motor branch from the anterior interosseous nerve to the ulnar nerve
In patients with a Martin Gruber anastomosis, the median nerve supplies all the hand intrinsic musculature, which may produce confusing findings on clinical examination.
MR Appearance
The median nerve is frequently difficult to visualize on MR images at the level of the elbow due to the prominent muscles in this region. The median nerve travels within a narrow, relatively fat-deprived perifascial plane between the pronator teres and brachialis muscles (see Fig. 12.16). The median nerve is more easily demonstrated where it courses between the superficial humeral head and deep ulnar head of the pronator teres muscles and underneath the lacertus fibrosus.
Radial Nerve
The radial nerve arises from the posterior cord of the brachial plexus and supplies the extensor muscles of the arm and forearm as well as the overlying skin. It contains motor and sensory branches from the C5, C6, C7, C8, and T1 nerve roots. In the proximal arm, the radial nerve descends between the medial and long heads of the triceps muscle. It then runs within the spiral groove of the humeral shaft in direct contact with the bone. Approximately 10 cm above the lateral epicondyle, the radial nerve pierces the lateral intermuscular septum, running between the brachioradialis and brachialis muscles. Motor branches, accompanied by branches of the profunda brachii artery and vein, innervate the lateral head of the triceps near the elbow.
The radial tunnel is a defined anatomic space that begins at and is bounded posteriorly by the capitellum and ends at the proximal, or as some believe, the distal aspect of the supinator muscle (Fig. 12.17).46,53 The brachioradialis and more distally the extensor carpi radialis longus and brevis


muscles form the anterolateral margin of the tunnel, whereas the brachialis muscle bounds the tunnel medially. In the region of the radiocapitellar joint, the radial nerve divides into the motor branch, the posterior interosseous nerve, and the superficial sensory branch. The superficial sensory branch passes into the forearm deep to the brachioradialis. The posterior interosseous nerve passes into the posterior compartment between the superficial and deep heads of the supinator muscle to supply nine muscles on the extensor aspect of the forearm. The nerve then passes under the arcade of Frohse, the proximal edge of the superficial head of the supinator muscle. Fibrous or tendinous thickening of the arcade has been described in 32% to 65% of the population. The posterior interosseous nerve innervates the supinator, the extensor carpi ulnaris, the extensor digitorum communis, the extensor digiti quinti, the abductor pollicis longus, the extensor indicis proprius, and the extensor pollicis longus and brevis muscles.

FIGURE 12.17 ● The radial nerve. The radial nerve splits into the superficial radial nerve and the posterior interosseous nerve at the radiocapitellar joint. The posterior interosseous branch courses between the deep and superficial heads of the supinator muscle.
MR Appearance
The radial nerve is best visualized on axial images around the elbow joint as it courses in the perifascial fat plane between the brachialis, brachioradialis, and extensor carpi radialis longus and brevis muscles. The division of the radial nerve at the level of the radiocapitellar joint can be identified as the nerve splits into the superficial branch and the deep posterior interosseous nerve. Distinguishing between the radial nerve and its branches and the accompanying vessels is sometimes difficult. The arcade of Frohse is occasionally depicted as a low-signal-intensity band at the proximal edge of the superficial head of the supinator muscle (Fig. 12.18). The posterior interosseous nerve is frequently seen sandwiched between the superficial and deep heads of the supinator.
Neuropathology of the Arm and Elbow
Ulnar Neuropathy
Ulnar nerve compression is the most common neuropathy at the elbow and the second most common neuropathy in the upper extremity, exceeded only by carpal tunnel syndrome.53 There are several potential sites of ulnar nerve injury or compression at the distal arm and elbow. The most common is at the cubital tunnel. In this location, the ulnar nerve is quite superficial and can be easily injured by direct trauma. The cubital tunnel undergoes dynamic changes with flexion and extension of the elbow.54,55 During elbow flexion, the tunnel is reduced in size as the overlying arcuate ligament becomes progressively taut. The arcuate ligament is tightest at 90° of elbow flexion. Medial bulging of the ulnar collateral ligament and the medial head of the triceps contributes to a further decrease in the volume of the cubital tunnel and medial displacement of the ulnar nerve. In addition, increased cubital tunnel pressure with flexion has also been described.


Other sites of ulnar nerve compression include:56
FIGURE 12.18 ● Normal MR anatomy of the radial nerve. Axial PD-weighted image of the proximal forearm shows the posterior interosseous nerve between the arcade of Frohse and the deep head of the supinator muscle.
  • The arcade of Struthers
  • The edge of the medial intermuscular septum
  • The ligament of Struthers
  • The thickened arcuate ligament
  • The deep flexor pronator aponeurosis (4 cm distal to the medial epicondyle)
Cubital Tunnel Syndrome
The cubital tunnel syndrome can be classified into physiologic and compressive syndromes, and the latter can be subdivided into acute, subacute, and chronic presentations:
  • Physiologic cubital tunnel syndrome occurs secondary to the normal loss in volume and increase in pressure within the tunnel during elbow flexion. This is the mechanism seen in sleep palsy, when the arm is held in flexion for a prolonged period of time.
  • Acute external compression syndrome typically follows a single episode of blunt trauma to the cubital tunnel. The sensory fibers of the ulnar nerve are located superficially under the arcuate ligament, making them most vulnerable to external compressive forces.
  • Subacute compression syndrome has been described in bed-ridden or wheelchair-bound patients and following surgery. Avoidance of prolonged pronation and flexion of the arm should decrease the risk of cubital tunnel external compression syndrome.
  • Chronic cubital tunnel syndrome may be caused by masses such as tumors, distended bursae, ganglions, hematoma, inflammatory pannus, gouty tophi, loose bodies, osteophytes, and scarring (Figs. 12.19 and 12.20)
The anconeus epitrochlearis muscle, an accessory muscle that traverses the cubital tunnel, has also been implicated as a cause of ulnar neuropathy and external compression syndrome (Fig. 12.21).57 Other causes include:
  • Callus formation from distal humeral and supracondylar fractures
  • Elbow dislocation
  • Avulsion of the medial epicondylar apophysis (Fig. 12.22)
Lateral shift of the ulna, commonly associated with chronic laxity of the ulnar collateral ligament, is a frequent cause of chronic cubital tunnel syndrome in athletes (Fig. 12.23). Tardy ulnar palsy refers to a delayed neuropathy presenting 15 to 20 years after a childhood capitellar epiphyseal injury and secondary cubitus valgus.58 Congenital hypoplasia of the capitellum may also cause lateral shift of the ulna with traction on the ulnar nerve.
Subluxation or dislocation of the ulnar nerve at the level of the cubital tunnel can lead to secondary friction neuritis and compressive neuropathy (Fig. 12.24). Ulnar nerve subluxation can be seen in up to 16% of individuals. The condition is often asymptomatic. Medial shift of the ulnar nerve is



accentuated by elbow flexion. Congenital absence (Fig. 12.25), laxity or tear of the arcuate ligament, trochlear hypoplasia, and posttraumatic cubitus valgus deformity are all postulated etiologic factors of ulnar nerve instability. Snapping triceps syndrome, dislocation of the medial head of the triceps muscle over the medial epicondyle, has been implicated as an additional cause of ulnar nerve dislocation (Fig. 12.26).59,60

FIGURE 12.19 ● Ulnar neuropathy secondary to compression by hemangioma. An axial post-gadolinium fat-suppressed T1-weighted image shows an avidly enhancing soft-tissue mass encasing (arrowhead) the ulnar nerve (solid arrow) in the medial aspect of the distal arm, consistent with a hemangioma (asterisk). Note invasion of the medial humerus by the mass (open arrow).
FIGURE 12.20 ● Ulnar neurop-athy secondary to scar. Axial T1-weighted (A) and fat-suppressed T2-weighted (B) images demonstrate encasement of the ulnar nerve (arrowhead) by scar tissue (arrows). Selective denervation edema of the flexor carpi ulnaris (fcu) muscle in the proximal forearm is noted.
FIGURE 12.21 ● Anconeus epitrochlearis muscle. Axial T1-weighted image demonstrates the accessory muscle (white arrows) effacing the fat within the cubital tunnel. The ulnar nerve (black arrow) is normal. O, olecranon.
FIGURE 12.22 ● Compressive ulnar neuropathy caused by a displaced fracture fragment. Axial fast spin-echo T2-weighted image shows an old, displaced, non-united avulsion fragment (asterisk) of the medial humeral epicondyle resulting in mass effect and secondary subluxation of the ulnar nerve (arrow).
Clinically, ulnar neuropathy is characterized by nocturnal paresthesias involving the fourth and fifth fingers, elbow pain radiating to the hand, and sensory symptoms related to prolonged flexion of the elbow. If weakness occurs, it may affect finger abduction, thumb abduction, pinching of the thumb and forefinger, and eventually power grip. The differential diagnosis includes compressive ulnar neuropathy at the wrist, lower cervical radiculopathy, thoracic outlet syndrome, amyotrophic lateral sclerosis, and other cord lesions.
Initial treatment for acute and subacute ulnar neuropathy at the elbow is nonsurgical. Rest and avoidance of pressure on the nerve may suffice. If symptoms persist, splint immobilization


is warranted. For chronic neuropathy associated with muscle weakness, or for neuropathy that does not respond to conservative measures, surgery, including medial epicondylectomy and anterior ulnar nerve transposition, is usually necessary.61

FIGURE 12.23 ● Ulnar neuritis. Axial fat-suppressed T2-weighted image shows thickening and increased signal within the ulnar nerve (arrowhead). Note associated edema and partial tear of the common flexor tendon (arrow).
FIGURE 12.24 ● Ulnar nerve subluxation. Axial fat-suppressed T2-weighted image shows an anteriorly subluxed, thickened, and edematous ulnar nerve (arrowhead). The arcuate ligament is absent.
Medial epicondylectomy, a form of decompression in situ, has a very high rate of complications and recurrence and provides relief of symptoms in only 50% of patients.53 Therefore, ulnar nerve transposition is often necessary. There are three types of anterior ulnar nerve transposition. Subcutaneous transposition is the easiest to perform technically and is an effective procedure, particularly in the elderly and in patients with a generous layer of adipose tissue in the arm. It is the procedure of choice for repositioning the nerve following surgical reductions of acute fractures and elbow arthroplasty.53 Intramuscular and submuscular transpositions are more technically complicated procedures and can result in severe postoperative perineural scarring. Nonetheless, submuscular transposition has a high degree of success and is the preferred method in contact sports athletes and when prior surgery has been unsuccessful.53
FIGURE 12.25 ● Absent arcuate ligament. Axial T1-weighted image demonstrates absence of the arcuate ligament incidentally noted in this asymptomatic patient. The ulnar nerve is normal (arrow).
FIGURE 12.26 ● Medial head of triceps. Axial T1-weighed images depict a prominent medial head of triceps muscle (arrowheads) and tendon (arrow) at the level of the cubital tunnel (open arrow). Note blending of the medial head tendon with the main triceps tendon (t) on a more distal image, a feature distinguishing it from the anconeus epitrochlearis muscle.


MR Appearance
Enlargement of the ulnar nerve and intraneural T2 hyperintensity are MR features compatible with cubital tunnel syndrome. The larger size and more superficial location of the ulnar nerve, as compared to the median and radial nerves, account for the more frequent detection of signal hyperintensity in the former.62 Additional MR findings include the following:
  • Ganglion cysts, soft-tissue tumors (see Fig. 12.19), degenerative spurs, and anomalous muscles such as the anconeus epitrochlearis (see Fig. 12.21) may be responsible for compressive ulnar neuropathy and can be easily depicted on MR images.
  • Selective denervation edema and atrophy of the flexor carpi ulnaris and flexor digitorum profundus muscles, best appreciated on axial forearm images, are additional contributory features in the MR diagnosis of ulnar neuropathy (see Fig. 12.20).62
  • The arcuate ligament should always be evaluated for thickening, tearing, or congenital absence.
  • Subluxation of the ulnar nerve may be seen on standard axial MR images performed with full extension of the elbow (see Fig. 12.24). However, when a history of ulnar nerve subluxation is available, MR imaging in elbow flexion is preferable for eliciting the subluxation.63 MR diagnosis of snapping triceps syndrome also can be enhanced by imaging in elbow flexion.64
  • On MR examinations obtained after anterior ulnar nerve transposition, T2 hyperintensity equalize within the ulnar nerve may persist long after the surgery (Fig. 12.27). Intense increased signal, however, is more likely to reflect persistent neuritis. Ulnar nerve thickening can be seen in the first postoperative year in up to 50% of patients following transposition.65 Tethering of the nerve and engulfing scar can also be identified. Other causes


    for persistent pain after anterior ulnar nerve transposition include extensive scarring or retearing at the resection site of the pronator–flexor muscle group.

FIGURE 12.27 ● Failed anterior ulnar nerve transposition. Axial post-contrast fat-suppressed T1-weighted image (A) and oblique sagittal fat-suppressed T2-weighted image (B) demonstrate increased signal and thickening of the transferred ulnar nerve (arrowheads). m, medial epicondyle.
Median Nerve Entrapment
The most common cause of median nerve entrapment at the elbow is the pronator syndrome. Other causes, however, have been described, and compressive neuropathy of the median nerve may be associated with:
  • Elbow fractures and dislocations66
  • Accessory muscles such as the Gantzer muscle (the accessory head of the flexor pollicis longus muscle)
  • Soft-tissue masses (Fig. 12.28)
  • Dynamic forces at the elbow
  • Prolonged pressure on the forearm (honeymooner's paralysis refers to median neuropathy secondary to pressure from a lover's head against a partner's forearm)
Clinical signs of median neuropathy include weak pronation of the forearm, weak flexion and radial deviation of the wrist associated with thenar atrophy, and inability to oppose or flex the thumb.
Pronator Syndrome
The pronator syndrome is the most common neuropathy of the median nerve at the elbow. Patients with pronator teres syndrome have numbness in the median nerve distribution with repetitive pronation/supination of the forearm, but not with flexion and extension of the elbow. On physical examination, resistance to pronation and/or resistance to isolated flexion of the third proximal interphalangeal joints elicit pain in the forearm. Electromyographic studies may show only mildly reduced conduction velocities.
From proximal to distal, the four potential sites of compression in the pronator syndrome are:
  • The supracondylar process/ligament of Struthers
  • The lacertus fibrosus
  • The pronator teres muscle
  • The proximal arch of the flexor digitorum superficialis muscle
The supracondylar process syndrome is the least common compression neuropathy of the median nerve at the elbow. The supracondylar process (or avian spur) is found in 3% of humans. It arises from the distal humerus, about 5 to 7 cm above the elbow joint (Fig. 12.29).67 The absence of a supracondylar process on plain films does not rule out the possibility of compression caused by the ligament of Struthers. The ligament of Struthers is a fibrous bridge that may arise from the supracondylar process68 and attach to the medial epicondyle, forming a fibro-osseous tunnel within which the median nerve, and occasionally the ulnar nerve, may become entrapped. The compression is worsened with extension and supination. The presence of pronator muscle weakness indicates high median nerve compression, as is seen in patients



with supracondylar process syndrome. An unusual musculo-aponeurotic band that originates as the ligament of Struthers but terminates as the brachiofascialis muscle of Wood, resulting in high median nerve entrapment, has recently been described.69

FIGURE 12.28 ● Cystic schwannoma of the median nerve. (A) Coronal T1-weighted image demonstrates ovoid mass arising from the median nerve. A comet sign is noted proximally (arrow). (B) Axial fast spin-echo T2-weighted image shows marked homogeneous hyperintensity in keeping with a cystic variant of schwannoma.
FIGURE 12.29 ● Supracondylar process. Lateral radiograph of the elbow depicts osseous excrescence arising from the anterior aspect of the distal humerus and pointing toward the elbow joint.
At the level of the elbow joint, the median nerve lies underneath the bicipital aponeurosis or lacertus fibrosus. The lacertus fibrosus arises from the distal bicipital tendon and courses obliquely over the pronator–flexor group of muscles to insert on the antebrachial fascia. A thickened lacertus fibrosus can produce compression of the pronator muscle and median nerve. The lacertus fibrosus is tightened during pronation of the forearm as the bicipital tuberosity of the radius and the distal biceps tendon rotate posteriorly.
The pronator syndrome is most frequently caused by dynamic compression of the median nerve between the superficial (humeral) and deep (ulnar) heads of the pronator teres muscle, just 2 to 4 cm distal to the medial epicondyle (Fig. 12.30).70,71,72 Fibrous bands can be found in up to 50% of anatomic specimens located dorsal to the humeral head or to the nerve itself. These bands can produce nerve compression, particularly in pronation and elbow extension, when the distance between the two heads of the pronator teres is decreased.
The most distal, as well as second most common, site of median nerve compression is at the fibrous arch of the origin of the flexor digitorum superficialis muscle. This fibrous arch is located about 2 cm distal to the ulnar head of the pronator teres. The median nerve is susceptible to compression if the arch has a large sharp edge and if the adjacent muscles are hypertrophied.
MR Appearance
When median neuropathy at the elbow is clinically suspected, MR imaging should span the distal third of the arm to the level of the flexor digitorum superficialis muscle in the proximal forearm.62 The following findings are characteristic:
  • When the ligament of Struthers is the culprit for median nerve compression, a linear low-signal-intensity structure emanating from the supracondylar process can be seen.73
  • The pronator syndrome may lead to signal abnormalities or atrophy in the pronator–flexor muscle group, including the pronator teres, the flexor carpi radialis, the palmaris longus, and the flexor digitorum superficialis muscles (Fig. 12.31).
  • P.1960

  • Fatty replacement with atrophy indicates irreversible loss of muscle fibers and is seen with chronic denervation over the course of several months.
  • MR imaging to assess median nerve entrapment may be indicated in patients following posterior elbow dislocation who present with difficulty in reduction, median nerve symptoms, pain more severe than usual, and an increase in medial joint space on radiographs. In a patient with median nerve entrapment secondary to elbow dislocation, areas of normal muscle signal within the pronator–flexor group may be correlated with electromyographic findings of re-innervation after nerve release.66
  • MR imaging can depict displacement or engulfment of the median nerve by space-occupying lesions, ganglions, or a distended bicipitoradial bursa.60
FIGURE 12.30 ● Median nerve in supination and pronation of the elbow. The nerve may become trapped between the two heads of the pronator teres in forearm pronation. This is the most common compression site in pronator syndrome. (Adapted from

Pecina MM, Drmpotic-Nemanic J, Markiewitz AD. Tunnel syndromes in the upper extremities. In: Pecina MM, Krmpotic-Nemanic J, Markiewicz AD, ed. Tunnel syndromes. New York: CRC Press, 1991:29-53

, with permission.)

FIGURE 12.31 ● Pronator syndrome. Oblique coronal (A) and axial (B) fat-suppressed T2-weighted images show diffuse denervation edema of the pronator teres muscle (arrowheads).
Anterior Interosseous Syndrome (Kiloh-Nevin Syndrome)
This compressive neuropathy is rare compared with the pronator syndrome. Compression is confined to the anterior interosseous nerve, which is a purely motor branch of the median nerve, and may occur at any place along the course of the nerve. Most commonly, however, it occurs where the anterior interosseous diverges from the median nerve. Common etiologic factors include:1,45,48
  • Trauma, such as supracondylar fractures
  • Posttraumatic thrombosis of the ulnar artery
  • An aberrant or thrombosed radial artery in the mid-forearm
  • A fascial band at the origin of the flexor digitorum superficialis
  • A tendinous origin of the ulnar head of the pronator teres
  • Anomalous muscles such as Gantzer's muscle or the palmaris profundus muscle
  • An enlarged bicipital bursa
Clinically, the anterior interosseous syndrome can be distinguished from the pronator syndrome by the complete absence of sensory deficit in the former. Motor weakness and paralysis are confined to the flexor pollicis longus, the flexor digitorum profundus to the index and middle fingers, and the pronator quadratus.1,45 A characteristic pinch is noted owing to inability to flex the distal joints of the thumb and index fingers. Advanced cases may show electromyographic abnormalities.
MR evaluation of the anterior interosseous nerve syndrome requires imaging the forearm as well as the elbow region. A common MR finding is edema and atrophy of the muscle groups innervated by the nerve, including the flexor pollicis longus muscle, the pronator quadratus muscle, and the radial half of the flexor digitorum profundus.74 The nerve may be difficult to detect due to its small size and encroachment by surrounding muscle mass.75 Treatment is initially conservative. Surgery is indicated if there is no improvement in 6 to 8 weeks.
Radial Nerve Injury
Radial nerve compression at the elbow occurs infrequently and is often misdiagnosed.76 It is frequently associated with trauma, and causes include:
  • Displaced humeral shaft fracture77
  • Inappropriate use of axillary crutches
  • Proximal prolonged tourniquet application
  • Lateral or posterior arm intramuscular injection
FIGURE 12.32 ● High radial nerve entrapment secondary to intramuscular lipoma. (A) Axial T2-weighted and (B) post-contrast fat-suppressed T1-weighted images at the level of the distal arm demonstrate a large intramuscular lipoma (asterisk) obliterating the fat planes in the location of the radial nerve. Triceps muscle denervation edema is noted (arrow).


Nontraumatic radial nerve compression is much less common, including compression by mass lesions (Fig. 12.32). In weightlifters, compression of the radial nerve beneath the lateral head of the triceps muscle can occur 10 cm proximal to the elbow joint during extension against resistance.
Radial nerve compression at the elbow has been subdivided into two major categories, both involving compression of the posterior interosseous nerve. In radial tunnel syndrome pain is present without motor deficits. Posterior interosseous nerve syndrome is a purely motor neuropathy. In a study of 71 patients by Rinker et al., the most consistent symptoms were deep forearm pain, pain radiating to the neck and shoulder, and a “heavy” sensation of the affected arm.76 The most common physical findings included tenderness over the radial nerve at the supinator muscle level, pain on resisted supination, and a positive Tinel sign over the radial forearm. Electrophysiologic studies are of limited value in diagnosis, since 90% of patients have normal findings. Upon surgical exploration, posterior interosseous nerve pathology was found in 46% of patients. Surgery is effective, and Rinker et al. found that of 79 surgical decompressions, 77% had excellent recovery and 20% were judged to have good outcome.76
Radial Tunnel Syndrome
Radial tunnel syndrome refers to compression of the posterior interosseous nerve within the radial tunnel without motor deficit.78 The entity is somewhat controversial since the main manifestation is pain at the radial tunnel without muscle weakness.79 The clinical entity may mimic and coexist with lateral epicondylitis. Electromyographic studies are frequently unrevealing due to the deep location of the posterior interosseous nerve. Thus, the clinical diagnosis of radial tunnel syndrome is often confounding. From proximal to distal, potential compression sites of the posterior interosseous nerve within the radial tunnel include:
  • Fibrous bands extending from the radiocapitellar joint
  • The tendinous edge of the extensor carpi radialis brevis muscle
  • The radial recurrent artery and branches (leash of Henry)
  • The arcade of Frohse at the proximal edge of the supinator muscle80
  • A fibrous band at the distal end of the supinator muscle81
The most common compression site is at the arcade of Frohse (see Fig. 12.18), followed by the tendinous edge of the extensor carpi radialis brevis muscle (Fig. 12.33).
Dynamic compression within the radial tunnel may occur as a result of repeated pronation and supination or forceful extension. Tennis players,82 swimmers, housewives, welders, conductors, and violinists are frequently affected by this disorder. Patients present with protracted elbow and forearm pain without motor deficit.83 Radial tunnel syndrome most frequently affects individuals in the fourth to sixth decade of life, with an equal male-to-female ratio. Surgical release of the arcade of Frohse often provides symptom relief.84,85,86
Posterior Interosseous Nerve Syndrome
The posterior interosseous nerve syndrome is defined as a motor neuropathy. The compression sites are the same as those for the radial tunnel syndrome (see above). Compression of the posterior interosseous nerve may also be secondary to trauma or surgery, space-occupying lesions, and inflammatory processes.87 Mass lesions such as ganglia and the bicipitoradial


bursa may also result in compressive neuropathy of the radial nerve at the tunnel (Fig. 12.34).88

FIGURE 12.33 ● Free edge of the thickened extensor carpi radialis brevis. (A) Axial T1-weighted image depicts a low-signal free edge of the extensor carpi radialis brevis in an asymptomatic individual. (B) The thickened free edge (arrow) is shown in close proximity to the posterior interosseous nerve (arrowhead) in a patient with radial tunnel syndrome. Associated mild fatty infiltration of the supinator muscle (S) is noted.
Insidious, deep forearm pain and weakness of the muscles innervated by the posterior interosseous nerve result in loss of extension of all digits and decrease of wrist extension. The extensor carpi radialis longus is never affected and the extensor carpi radialis brevis is frequently spared, as their innervation often originates proximal to the branching of the posterior interosseous nerve (Fig. 12.35).89 In contrast, the extensor carpi ulnaris longus is always affected. The unopposed pull of the extensor carpi radialis longus results in radial deviation of the wrist. In the absence of masses, fractures, or dislocation, the initial management is conservative. If there are no signs of improvement after 6 to 8 weeks, surgical decompression may be warranted.
MR Appearance
MR findings of radial tunnel syndrome and posterior interosseous nerve syndrome are similar and include signs of denervation muscle injury such as increased T2 signal and/or atrophy of the muscles supplied by the posterior interosseous nerve. In one study, denervation muscle edema was found in 52% of 25 patients with a clinical diagnosis of radial tunnel syndrome.90 Isolated supinator involvement was the most common finding, followed by concomitant increased signal within the supinator and extensor muscles (see Fig. 12.35). Isolated involvement of the extensor muscles was also reported.
Identification of mass effect with compression of the posterior interosseous nerve is another important diagnostic MR feature of radial tunnel syndrome and posterior interosseous nerve syndrome. In 16% of patients with radial tunnel syndrome, a thickened free edge of the extensor carpi radialis brevis was identified (see Fig. 12.33B).90 Other causes included prominent recurrent radial vessels (4%), posterior interosseous schwannoma (4%), and distended bicipitoradial bursa (4%).90 Intrinsic signal alteration of the posterior interosseous nerve was not recorded in any of these cases.
FIGURE 12.34 ● Posterior interosseous nerve syndrome secondary to bicipitoradial bursitis. (A) Axial PD-weighted image shows a markedly distended bicipital radial bursa (arrows) adjacent to the posterior interosseous nerve (arrowhead). (B) Axial fat-suppressed T2-weighted image demonstrates denervation edema and mild atrophy of the supinator (s), extensor carpi ulnaris (ecu), and extensor digitorum communis (edc) muscles in the proximal forearm.
FIGURE 12.35 ● Posterior interosseous nerve syndrome. Axial T1-weighted (A) and fat-suppressed T2-weighted (B) images at the proximal forearm show atrophy and edema of the supinator and extensor musculature. The extensor carpi radialis longus, which is not innervated by the posterior interosseous nerve, is not involved. s, supinator; edc, extensor digitorum communis; ecrb, extensor carpi radialis brevis; ecrl, extensor carpi radialis longus.



Entrapment Neuropathies of the Wrist
Associated Normal Anatomy
Median Nerve
The median nerve travels between the flexor digitorum superficialis and flexor carpi radialis muscles just proximal to the wrist joint. It then passes through the carpal tunnel along with the flexor tendons of the fingers and thumb (Fig. 12.36). The carpal tunnel is a fibro-osseous canal bordered at its medial margin by the pisiform bone and the hook of the hamate. The scaphoid and trapezium form its lateral margin and the carpal bones its dorsal margin. The volar border is formed by the flexor retinaculum. The flexor retinaculum can be divided into three parts from proximal to distal:91
  • The antebrachial fascia proximal to the wrist (Fig. 12.37A)
  • The transverse carpal ligament proper (Fig. 12.37B)
  • The palmar aponeurosis between the thenar and hypothenar muscles (Fig. 12.37C)
The transverse carpal ligament proper inserts into the scaphoid and trapezium radially and the pisiform and the hook of the hamate ulnarly. The narrowest point of the tunnel is located between the hook of the hamate and the trapezial ridge.
On cross-section, the carpal tunnel is a tightly packed space containing the median nerve, synovium, and the nine extrinsic flexor tendons of the thumb and fingers (the flexor pollicis longus tendon, four flexor digitorum superficialis tendons, and four flexor digitorum profundus tendons). The median nerve supplies the thenar eminence muscles, including the abductor pollicis brevis, the opponens pollicis, and the superficial head of the flexor pollicis brevis. It also supplies the first and second lumbricals and provides sensation to the



palmar and distal dorsal aspects of the radial three-and-a-half fingers.

FIGURE 12.36 ● The median and ulnar nerves in the wrist and hand.
FIGURE 12.37 ● Normal MR anatomy of the median nerve. (A) Axial T1-weighted image at the level of the distal radioulnar joint demonstrates the antebrachial fascia overlying the median nerve. (B) Axial T1-weighted image at the level of the distal carpal tunnel shows the flexor retinaculum extending between the hook of the hamate and the tubercle of the trapezium. (C) Axial T1-weighted image at the level of the proximal metacarpals shows the palmar aponeurosis and the proximal digital branches of the median nerve.
The palmar cutaneous branch, supplying the skin over the lateral part of the palm, arises from the radial aspect of the median nerve, proximal to the wrist. It then travels in close proximity to the flexor carpi radialis tendon outside the carpal tunnel.
MR Appearance
The carpal tunnel is best demonstrated on axial images. The median nerve typically shows intermediate signal intensity on all pulse sequences, although mild hyperintensity may be noted on fast spin-echo T2-weighted images. High-resolution imaging may allow discrimination of individual nerve fascicles.92
The morphology of the median nerve changes as it travels from the distal radioulnar joint to the metacarpal region.93 At the level of the distal radioulnar joint, the normal median nerve is seen as a round to oval structure (see Fig. 12.37A) lying deep to the palmaris longus tendon, medial and superficial to the flexor carpi radialis and flexor pollicis longus tendons, and lateral and superficial to the flexor digitorum superficialis tendons. The median nerve is slightly flat in the proximal carpal tunnel at the level of the pisiform and scaphoid bones. In this location, the nerve is usually superficially located, immediately deep to the flexor retinaculum and atop the flexor pollicis longus and flexor digitorum superficialis tendons. In the distal carpal tunnel, at the level of the hook of the hamate and tubercle of the trapezium, the median nerve remains flattened and maintains its relationship with the nearby tendons (see Fig. 12.37B). The median nerve divides into digital branches at the level of the metacarpal bases (see Fig. 12.37C).
The position of the median nerve is subject to wrist motion. The nerve is usually in a shallow position against the flexor retinaculum with wrist extension. With wrist flexion, the nerve may migrate deep within the flexor tendons.94 A reversed palmaris longus muscle may decrease the available space for the median nerve and result in mechanical compression.95
Ulnar Nerve
The ulnar nerve at the level of the wrist passes through Guyon's canal, a triangular fibro-osseous tunnel lodged between the pisiform bone medially, the hook of the hamate laterally, and the palmar carpal ligament volarly (Fig. 12.38). The floor of the tunnel is formed by the tendons of the flexor digitorum profundus, the transverse carpal ligament, the pisohamate and pisometacarpal ligament, and the opponens digiti minimi muscle. Guyon's canal is also known as the pisohamate tunnel or the distal ulnar tunnel. 96
FIGURE 12.38 ● Guyon's canal. This coronal PD image demonstrates the ulnar nerve as it travels within Guyon's canal.


Proximal to Guyon's canal, the ulnar nerve supplies sensory branches to the dorsal ulnar hand and a palmar branch to the skin over the hypothenar eminence. Within Guyon's canal, the ulnar nerve gives off superficial sensory and deep motor branches (see Fig. 12.36). The superficial branch supplies a branch of the palmaris brevis muscle and provides sensation to the fifth finger and the ulnar half of the fourth finger. The deep motor branch travels along with the ulnar artery and takes an acute lateral turn at the hook of the hamate. In this location, it goes through the pisohamate hiatus. This is the most vulnerable site for compression of the deep motor branch of the ulnar nerve. The deep motor branch innervates the hypothenar muscles, including the abductor digiti minimi, flexor digiti minimi, and opponens digiti minimi, as well as the adductor pollicis, the third and fourth lumbricals, and all the interossei muscles.
MR Appearance
Guyon's canal, located lateral and superficial to the flexor retinaculum, is best depicted on axial MR images but may also be appreciated on coronal MR images. Within the canal, the ulnar nerve is easily seen as a small, low-signal structure highlighted by fat (see Fig. 12.38). The average transverse dimension of the ulnar nerve at the level of the pisiform is 3 mm.97 The nerve lies closer to the bony landmarks and medial and deep to the ulnar artery. Using high-resolution techniques, the bifurcation into superficial and deep motor branches can be seen. The mean distance between the proximal edge of the pisiform bone and the ulnar nerve bifurcation is 12 mm.97 Only a short segment (approximately 10 mm) of the deep motor nerve is visible before it blends with the hypothenar muscles. The superficial ulnar nerve can be consistently visualized beyond the ulnar tunnel. The fibrous arch of the flexor digiti minimi brevis muscle can be depicted as a thin, low-signal-intensity band attaching to the hamulus and splitting Guyon's canal into superficial and deep compartments.
Anatomic Variants
Anatomic variants are frequently found both at the carpal tunnel (41%) and Guyon's canal (21%).98,99 Lanz defined four categories of variation found in the median nerve within the carpal tunnel:
  • Variations in the course of the thenar branch
  • Accessory branches at the distal carpal tunnel
  • A bifid median nerve or high division of the distal median nerve (Fig. 12.39)
  • Accessory branches proximal to the carpal tunnel
In addition, the motor branch may arise in the forearm or may be split by a persistent median artery or an aberrant muscle only to join distal to the transverse carpal ligament.97 Anomalous muscles, such as a reversed palmaris longus muscle, an accessory palmaris profundus, and an accessory flexor digitorum superficialis (Fig. 12.40), can occasionally be found in the carpal tunnel region, as can aberrant origins of the thenar and lumbrical muscles.100,101,102
Neuropathology of the Wrist
Carpal Tunnel Syndrome
The carpal tunnel syndrome is the most common neuropathy of the upper extremity. It is also one of the most common orthopaedic conditions, with an estimated incidence of nearly 1% annually, or almost 2.8 million new cases per year.103 Its prevalence varies between 0.125% and 5.8% of the population.104,105,106 Carpal tunnel syndrome is most often found in patients between 30 and 60 years of age. It has a male-to-female ratio of 1:5. Up to 50% of patients present with bilateral symptoms. Typical clinical findings include pain and paresthesia in the median nerve distribution. The symptoms can be transient and reversible.
FIGURE 12.39 ● Bifid median nerve. Axial fat-suppressed T2-weighted image shows high bifurcation of the median nerve (arrows) at the level of the carpal tunnel.
FIGURE 12.40 ● Accessory flexor digitorum superficialis muscle. Axial T1-weighted image shows anomalous muscle (asterisk) deep to the lateral flexor tendons at the level of the metacarpals.


Repeated compression of the median nerve with subsequent ischemia, subendoneurial edema, synovitis, and eventually fibrosis is considered a likely etiology for carpal tunnel syndrome.107 Several mechanisms for median nerve compression have been suggested:
  • It has been hypothesized that median nerve compression most likely occurs during wrist flexion at the proximal edge of the transverse carpal ligament.56
  • Alternatively, the median nerve can be compressed where the carpal tunnel is narrowest, at the level of the hook of the hamate, by either synovial hypertrophy or a mass lesion.
  • In asymptomatic individuals, dynamic MR imaging has demonstrated that in wrist flexion the median nerve moves radially and posteriorly and becomes interposed between the flexor tendons.94 In patients with carpal tunnel syndrome, the median nerve is more likely to remain adjacent to the flexor retinaculum during wrist flexion, perhaps predisposing it to compression and subsequent carpal tunnel syndrome.
  • Increased pressure within the carpal tunnel has also been noted following repeated flexion and extension movements.
Tethering of the nerve due to scar tissue, leading to reduced nerve gliding, is another proposed theory for the development of carpal tunnel syndrome.108
The incidence of carpal tunnel syndrome has been reported to be increased in a variety of systemic diseases, such as diabetes, pregnancy, rheumatoid arthritis (Fig. 12.41), and hypothyroidism. Musicians, dental hygienists, meat packers, and frozen food processors are also predisposed to carpal tunnel syndrome,109 probably related to occupational repetitive wrist motion. Nonspecific flexor tenosynovitis is one of the most common etiologies for carpal tunnel syndrome (Fig. 12.42).
A variety of space-occupying lesions within the carpal tunnel may manifest as median compressive neuropathy. Masses can be classified as neurogenic or non-neurogenic. Peripheral nerve tumors include schwannomas, neurofibromas, fibrolipomatous hamartoma of the median nerve (Fig. 12.43), and neurofibrosarcomas. Other mass lesions include anomalous muscles, ganglion cysts (Fig. 12.44), fracture fragments, bony spurs, inflammatory synovial pannus, amyloid deposits, and rice bodies.
Evaluation for carpal tunnel syndrome includes clinical assessment as well as electrodiagnostic testing. Clinical assessment includes Phalen's test (worsened paresthesia following 1 minute of maximal passive wrist flexion) and Tinel's sign (paresthesia in the median nerve territory elicited by gentle tapping over the carpal tunnel). Phalen's test has a sensitivity of 75% and a specificity of 47%; the corresponding values for Tinel's sign are 60% and 67%.110,111 Electrodiagnostic testing is appropriate in most cases. In addition, MR evaluation of selected patients may be important, since some symptomatic patients fail to show decreased median nerve conduction velocity.112 MR examination can also depict space-occupying lesions within the carpal tunnel, including anomalous muscles, persistent median artery, carpal tunnel lipomatosis, ganglion cysts, and synovial hypertrophy.
Conservative treatment includes limiting wrist motion by day, nighttime splinting in neutral position, and anti-inflammatory medications. Local steroid injections into the carpal tunnel have been reported to produce improvements in nerve conduction parameters.113 Surgical intervention is recommended for patients who have either failed conservative management or who have intolerable pain, constant numbness, or muscle weakness. The surgical treatment consists of either open or endoscopic release of the flexor retinaculum. The complication and success rates are similar for both approaches, but patients appear to return to work sooner with less pain and debilitation after endoscopic procedures.114,115




Complications of carpal tunnel release include incomplete release, injury to the median or ulnar nerves, and injury to the digital nerves, the ulnar artery, or the superficial palmar arch.114

FIGURE 12.41 ● Carpal tunnel syndrome and rheumatoid arthritis. (A) Axial fat-suppressed T2-weighted image at the level of the proximal carpal row shows swelling and edema of the median nerve (white arrow) associated with flexor tendinosis (arrowheads), erosive changes (black arrow), and extensive inflammatory pannus (asterisks). (B) Axial fat-suppressed T2-weighted image at the level of the hook of the hamate demonstrates denervation edema of the thenar muscles (asterisk).
FIGURE 12.42 ● Carpal tunnel syndrome and flexor tenosynovitis. Axial fat-suppressed T2-weighted image demonstrates marked peritendinous inflammatory edema of the flexor tendons within the carpal tunnel consistent with tenosynovitis (open arrows). Note flattening and edema of the median nerve (arrow) and associated synovitis in this patient with rheumatoid arthritis (asterisk).
FIGURE 12.43 ● Fibrolipomatous hamartoma of the median nerve. (A) Sagittal T1-weighted image shows a fat-containing fusiform mass with typical spaghetti-like appearance (arrowheads). (B) Axial PD-weighted image demonstrates pathognomonic coaxial-cable–like appearance of the nerve (arrowheads) at the level of the carpal tunnel. Denervation edema of the thenar musculature (asterisk) is noted.
FIGURE 12.44 ● Ganglion cyst. Coronal (A) and axial (B) PD-weighted images show a volar ganglion cyst (arrowheads) displacing the median nerve (arrows).
MR Appearance
MR findings of carpal tunnel syndrome can be divided into four categories: increased size of the nerve, nerve flattening, bowing of the flexor retinaculum, and increased T2 signal within the median nerve (Fig. 12.45):
  • Size of the nerve. The cross-sectional area of the median nerve is significantly larger in patients with carpal tunnel syndrome than in asymptomatic individuals.116 However, the cutoff size of the cross-sectional area between a normal and a pathologic median nerve is unclear. To evaluate proximal enlargement of the median nerve on axial MR images, comparison of the cross-sectional area of the nerve at the level of the radioulnar joint and at the level of the pisiform bone should be obtained. In patients with carpal tunnel syndrome, the median nerve at the level of the pisiform may be twice or three times as large as at the level of the radioulnar joint.117
  • Nerve flattening. Flattening of the nerve can be evaluated using flattening ratios, defined as the ratio between the major and minor axes of the nerve both at the level of the distal radioulnar joint and at the level of the hook of the hamate.117 A flattening ratio greater than 3 at the level of the hook of the hamate may indicate median nerve pathology.
  • Flexor retinaculum bowing. Bowing of the flexor retinaculum likely reflects increased pressure or volume within the carpal tunnel. In normal individuals, the flexor retinaculum at the level of the hook of the hamate should be flat or slightly convex. The degree of bowing is determined by dividing the distance of palmar displacement of the retinaculum by the distance between the hook of the hamate and the tubercle of the trapezium. In normal patients, the ratio varies from 0 to 0.15 (mean 0.05). In carpal tunnel syndrome, however, the ratio varies from 0.14 to 0.26 (mean 0.18).117
  • Signal hyperintensity. Increased T2 signal within the median nerve may be real or spurious. The median nerve may reveal slightly increased signal on fat-suppressed


    T2-weighted fast spin-echo images that should not be misinterpreted as abnormal.117

FIGURE 12.45 ● Carpal tunnel syndrome. (A) Axial fat-suppressed T2-weighted image through the distal carpal tunnel demonstrates enlargement of the median nerve with bowing of the flexor retinaculum. The bowing ratio of the flexor retinaculum, determined by dividing its palmar displacement by the distance between the hook of the hamate to the tubercle of the trapezium, was 0.18 (normal ratio, 0 to 0.15). (B) Axial T2-weighted image through the proximal metacarpal region shows a swollen and hyperintense median nerve (arrow).
At present there is no consensus about the diagnostic accuracy of MR signs of carpal tunnel syndrome, and there is disagreement as to the specificity of nerve swelling and flattening in the literature. In general, although MR findings may suggest carpal tunnel syndrome, they should be reviewed in light of clinical history, physical examination, and electrodiagnostic studies. Nevertheless, in many instances MR imaging can provide useful information regarding the presence of tenosynovitis, masses, or alignment abnormalities as the causative factors of clinical symptoms.
MR imaging may also be useful in postoperative evaluation. Recovery of distal flattening of the median nerve and partial reversal of intraneural T2 hyperintensity have been found on MR examinations performed in asymptomatic postoperative patients.118 Interruption of the flexor retinaculum, associated with palmar migration of the carpal tunnel contents, represents MR evidence of successful carpal tunnel decompression. In the absence of these findings, incomplete retinacular release and/or postoperative scarring should be considered (Fig. 12.46). Other signs of incomplete retinacular release include persistent proximal enlargement of the median nerve and refractory distal flattening of the median nerve. In a recent study of 41 postoperative wrists by Wu et al., proximal enlargement of the median nerve, tenosynovitis, excessive palmar migration of the median nerve, and the presence of a mass within the carpal tunnel were found to be useful features in the MR diagnosis of recurrent carpal tunnel syndrome.119
Ulnar Tunnel Syndrome
Compression of the ulnar nerve is more commonly seen at the elbow but occasionally occurs in Guyon's canal at the wrist. Ulnar compressive neuropathy proximal to the wrist results in loss of sensation on the dorsal ulnar hand. This is in contrast to the ulnar tunnel syndrome, in which there is spared sensation in this territory. There are three potential sites of ulnar nerve compression at Guyon's canal:
  • Zone 1 extends from the proximal edge of the palmar carpal ligament to the bifurcation of the ulnar nerve into the deep motor and superficial sensory branches.
  • P.1973

  • Zone 2 extends from the bifurcation of the ulnar nerve just distal to the fibrous arch of the hypothenar muscles and contains the deep motor branch of the ulnar nerve.
  • Zone 3, which is parallel to zone 2, extends to the distal end of Guyon's canal and contains the superficial sensory branch of the ulnar nerve.
FIGURE 12.46 ● Failed surgical release of the flexor retinaculum. Resection of the flexor retinaculum (arrow) with palmar displacement of the median nerve and flexor tendons is seen at the proximal (A) and distal (B) carpal tunnel. Note the surgical scar effacing the median nerve (arrowheads).
FIGURE 12.47 ● Ulnar neuropathy secondary to fracture of the hook of the hamate. Axial fat-suppressed T2-weighted image demonstrates a non-displaced fracture (arrow) of the hook of the hamate (h) associated with edema within Guyon's canal (arrowhead).
Clinical presentation correlates with the zone in which the ulnar nerve compression occurs:
  • Zone 1 lesions present as combined motor and sensory deficits.
  • Zone 2 lesions are characterized by pure motor deficits.
  • Zone 3 lesions present with isolated sensory deficits.
In a study by Murata et al.,120 most patients were found to have compression of the ulnar nerve at zones 1 and 3. In 55% of cases the compression occurred in more than one zone.120
The two leading causes of ulnar tunnel syndrome are idiopathic conditions (45%) and trauma (26%).120 Ulnar nerve compression by a displaced fracture or enlargement of the hook of the hamate (Fig. 12.47) has been reported. Handlebar palsy is characterized by isolated compressive neuropathy of the deep terminal motor branch of the ulnar nerve in bikers.121 Because no sensory fibers are affected, patients are not aware of the ongoing nerve compression until a severe nerve lesion develops. Space-occupying lesions are responsible for ulnar tunnel syndrome in the remainder of the cases and include tumors (Figs. 12.48 and 12.49), musculotendinous variants, aberrant fibrous bands, enlarged bursae, and ulnar artery aneurysm and thrombosis.122
MR Appearance
The size and signal intensity of the ulnar nerve within the Guyon's canal should be assessed.62 Denervation edema and/or atrophy of the hypothenar, the third and fourth lumbricals, and the interossei muscles are indicative of ulnar nerve injury.121,123 MR can depict the presence of space-occupying lesions within or about the Guyon's canal, including:
  • Accessory muscles such as an anomalous abductor digiti minimi, an anomalous flexor digiti minimi brevis, or a reversed palmaris longus124,125,126
  • Ulnar nerve schwannoma
  • Ganglion cyst127
  • Lipoma96
FIGURE 12.48 ● Ulnar nerve schwannoma. Axial fast spin-echo T2-weighted image demonstrates a high-signal fusiform mass arising from the superficial branch of the ulnar nerve (arrow).
FIGURE 12.49 ● Ganglion cyst compressing the ulnar nerve. Axial (A) and oblique coronal (B) fat-suppressed T2-weighted images demonstrate a ganglion cyst (arrows) within Guyon's canal.
FIGURE 12.50 ● Ganglion cyst compressing the superficial radial nerve. Axial fast spin-echo T2-weighted image (A) and coronal T1-weighted image (B) show a bilobed ganglion cyst (arrows) compressing the superficial radial nerve and radial artery (arrowheads).



Postoperative MR imaging may also be useful in demonstrating compression of the ulnar nerve by translocated carpal contents as a complication of open carpal tunnel release.128
Superficial Radial Nerve Syndrome (Wartenberg Syndrome)
Wartenberg syndrome refers to entrapment of the sensory branch of the radial nerve in the distal forearm. Other descriptive terms for the syndrome are handcuff neuropathy or watchstrap nerve compression. The superficial radial nerve emerges from a deep to a superficial position between the brachioradialis and the extensor carpi radialis longus tendons at the junction of the proximal two thirds to distal one third of the forearm. The superficial radial nerve then courses in a superficial subcutaneous plane to provide sensation to the dorsal aspect of the radial half of the hand, including the thumb, index finger, and lateral aspect of the long finger. Sensation to the digits is provided up to the level of the proximal interphalangeal joint. Potential sites of compression include:
  • Fascial bands in the subcutaneous plane at the nerve's exit point
  • The tendon of the brachioradialis
  • The tendon of the extensor carpi ulnaris longus
  • Ganglion cysts arising from the radiocarpal joint
The most common etiology is trauma, including watchstrap compression, a tight plaster or dressing, and postoperative scar. Other associated conditions include De Quervain's disease (up to 50%), carpal tunnel syndrome, ganglia of the first extensor compartment, and flexor carpi radialis tenosynovitis/tendinopathy.129,130
Patients report decreased sensation, paresthesia, and tingling in the distribution of the superficial radial nerve.131 The symptoms are often provoked by extreme pronation of the wrist. MR imaging may identify a mass effect along the course of the superficial radial nerve (Fig. 12.50). In the early stages, conservative treatment, including wrist splinting and anti-inflammatory medication, can be effective. Partial resection of the brachioradialis tendon allows for an easy glide motion of the superficial radial nerve at its exit point.
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