Ulnar Tunnel Syndrome

 

Dorsal sensation intact

Dorsal sensation diminished

Level of compression

Proximal or distal to wrist

Proximal to wrist




Motor symptoms are consistent with intrinsic muscle weakness. Patients may complain of muscle atrophy in the hand, cramps or fasciculations, loss of dexterity, difficulty with fine manipulative tasks, decreased grip strength, weakness specifically when applying torque to a tool or with lateral (key) pinch [4, 5]. In severe cases patients may notice Wartenberg’s sign (inability to adduct the small finger), or the development of a claw hand deformity.

Depending on the etiology, onset of symptoms may be sudden or insidious. When associated with fracture or trauma causing compression of the ulnar nerve at the wrist, symptoms develop rapidly; when associated with a degenerative process or a ganglion cyst, symptoms may be intermittent at first, then worsen and become constant.

Associated symptoms are specific to the etiology of the compression. A long history of ulnar-sided wrist pain in an older patient with the insidious onset of an ulnar tunnel syndrome suggests compression related to degenerative pisotriquetral arthritis. Patients with masses compressing the ulnar nerve sometimes complain of fullness in the ulnar aspect of the wrist. Complaints like cold intolerance, pale fingertips or splinter hemorrhages suggest vascular etiologies like hypothenar hammer syndrome or ulnar artery aneurysm. A more quantitative initial and follow-up assessment of cold intolerance is possible with the McCabe cold sensitivity severity scale [6].

A focused social history is useful since understanding the patient’s occupation, hobbies and sports can elucidate the diagnosis and direct treatment. Any activity that exposes a patient to vibration or repetitive hand trauma may cause vascular pathologies or fractures. Hypothenar hammer syndrome should be considered for carpenters or laborers, especially when there is evidence of vascular compromise. Cyclists develop compression of the ulnar nerve from prolonged direct pressure. Golfers are prone to acute hook of hamate fractures when the force of impact is transmitted through the club to the hamate hook; in addition to pain, this can lead to symptoms of ulnar neuropathy within the ulnar tunnel [7]. Racquetball and tennis players get chronic hook of hamate fractures by a similar mechanism due to repetitive trauma. The social history should also include an assessment of cigarette smoking, since smokers have an increased incidence of vascular disease, specifically Buerger’s disease, which can cause symptoms of ulnar neuropathy in the hand.


Clinical Pearl





  • Unlike carpal tunnel syndrome, ulnar tunnel syndrome is most commonly the result of compression due to mass effect from another process. Physical examination and imaging focuses on identifying this primary process.



Physical Examination


The physical examination of the hand begins at the neck. Spurling’s sign is useful in eliciting symptoms of cervical radiculopathy; Adson’s maneuver may be helpful in the diagnostic workup of a suspected thoracic outlet syndrome. The ulnar nerve is examined throughout its course; special attention is paid to the ulnar nerve at the elbow and specifically within the cubital tunnel. The relevant techniques and maneuvers are discussed further in applicable chapters. This chapter focuses on the detailed examination of the ulnar nerve at the wrist.

The wrist and hand are inspected dorsally and volarly, with attention to any masses or areas of asymmetry compared to contralateral (Fig. 15.1). The posture of the hand is observed, as advanced ulnar neuropathy may present with a claw-hand deformity (Fig. 15.2) or Wartenberg’s sign (Fig. 15.3). Skin changes, bruising, swelling and intrinsic muscular atrophy, especially of the first dorsal interosseus and the abductor digiti minimi, are noted. Splinter hemorrhages or digital pallor suggest a vascular occlusive disease like ulnar artery thrombosis. Advanced vascular insufficiency may cause digital ischemia or gangrene.

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Fig. 15.1
A large mass is demonstrated on inspection of the left palm over the ulnar tunnel in this patient with symptoms of ulnar nerve compression at the wrist. Workup revealed this to be a lipofibroma


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Fig. 15.2
Clawing of the ulnar digits is demonstrated in this preoperative photograph of a patient with long-standing symptoms of ulnar neuropathy


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Fig. 15.3
A persistent Wartenberg’s sign is demonstrated in this patient with history of ulnar neuropathy treated with decompression. Note the zig-zag incision over the ulnar tunnel

A vascular examination is very important when evaluating a suspected ulnar tunnel syndrome. In addition to simple inspection as above, the pulses are palpated, capillary refill is assessed and an Allen’s test is performed. If necessary, a handheld Doppler can be used as an extension of the physical examination to evaluate the radial, ulnar and digital arteries, as well as the superficial and deep arch. Decreased signals suggest occlusive pathology. The temperature of the digits is relevant too. Cold fingers, especially if asymmetric, suggest a vascular problem.

The wrist is palpated over Guyon’s canal, and any apparent masses are characterized by their texture, mobility, tenderness to palpation, size, location and overlying skin changes. Careful palpation may reveal a pulsatile mass consistent with an ulnar artery aneurysm. The pisiform is palpated, and the pisotriquetral joint is assessed by grinding the pisiform against the triquetrum; tenderness with this maneuver suggests pathology of the pisotriquetral joint that should be considered in the workup. Another exam maneuver relies on the insertion of flexor carpi ulnaris on the pisiform – in a modified apprehension test similar to the patellar apprehension test, pressure is applied proximal to the pisiform and wrist flexion is resisted. Apprehension with this maneuver suggests pathology of the pisotriquetral joint. The hook of the hamate is palpated. Tenderness here, along with skin changes like calluses, suggests acute or chronic fracture, which may contribute to ulnar nerve symptoms [8].

The ulnar nerve is then evaluated by direct pressure and by percussion over the cubital tunnel and over the ulnar tunnel, in an attempt to elicit a Tinel’s sign. First described by Tinel in 1915, this sign is based on the proposition that “pressure on an injured nerve trunk quite often produces a tingling sensation, felt by the patient at the periphery of the nerve and localized to a very precise area of the skin” [9]. Tingling with direct pressure or percussion over the ulnar tunnel suggests pathology at that level.

Sensation in the ulnar distribution is assessed using light touch, pinprick, vibration, and static or moving 2-point discrimination. The exam is performed on the volar and the dorsal surface. If there is sensory loss involving both the volar and the dorsal aspect of the ulnar distribution, then the pathology is proximal to the dorsal cutaneous branch of the ulnar nerve which emerges 6–10 cm proximal to the wrist flexion crease [3] – in this case ulnar tunnel syndrome is considered very unlikely. The converse is not true, however; if sensation on the dorsum of the hand is spared, the pathology could be at any level.

Strength of the hand, wrist, and forearm muscles is assessed and graded on a scale of 1–5. Objective strength measurements can be obtained using a grip meter, such as a Jamar dynamometer, and a pinch meter. Since most of its motor innervation arises distal to the ulnar tunnel, the motor exam is not especially useful in determining the level of compression, however there are two exceptions. At the level of the elbow the ulnar nerve gives off motor branches to the medial half of flexor digitorum profundus (ring and small fingers) and to flexor carpi ulnaris. Asymmetric weakness in these muscles suggests pathology proximal to the motor branches innervating them; however, apparently normal strength on clinical examination could result from the compensatory effect of other muscles like flexor carpi radialis or palmaris longus, and in this case the pathology could be at any level [5].

A variety of special tests have been developed to assess motor function and strength in ulnar-innervated muscles. Froment’s sign is compensatory flexion of the thumb interphalangeal joint to compensate for adductor pollicis weakness when attempting a lateral pinch [10]. The basis for this phenomenon is substitution flexor pollicis longus (median-innervated) for adductor pollicis (ulnar-innervated) to produce a lateral pinch. Jeanne’s sign is metacarpophalangeal (MP) joint hyperextension to compensate for a weak adductor pollicis during lateral pinch [11].

Strength of the interossei can be assessed by a method described by McPherson and Meals, in which the radial aspects of the patient’s abducted index fingers are pressed against one another. If one index finger is overpowered by the other, weakness of the dorsal interosseus is suggested [12]. In the finger flexion sign described by Tsujino and Macnicol, a piece of paper is held between the patient’s middle and ring fingers. Interosseus weakness is manifested as metacarpophalangeal flexion, as flexor tendons are recruited to substitute for intrinsic weakness in a mechanism similar to that of Froment’s sign [13]. In Wartenberg’s sign (Fig. 15.3), “the position of abduction assumed by the little finger” is due to the unopposed action of extensor digiti minimi and extensor digitorum comunis to the little finger, both radially-innervated [14]. The ulnarly-innervated palmar interosseous is weak and cannot counteract the abduction moment. This posture of small finger abduction is most pronounced when the digits are held in extension. In the crossed-finger test, first volar interosseous and second dorsal interosseous weakness is manifested as inability to cross the middle finger over the index finger [15]. Duchenne’s sign is caused by weakness of the ulnar-innervated lumbricals, creating a claw deformity of the ring and small fingers due to the unopposed action of the extrinsic digital flexors and extensors [5].


Radiographic Workup and Special Imaging Studies


Unlike carpal tunnel syndrome, imaging studies are essential in the workup of a suspected ulnar tunnel syndrome, since ulnar tunnel syndrome is most commonly secondary to mass effect from another pathology. Radiographic workup begins with plain radiographs including posterior-anterior, lateral, 30° supination view to evaluate the pisotriquetral joint for degenerative or other pathology, and a carpal tunnel view to evaluate the hook of the hamate for fracture.

If bony pathology is suspected or visualized on plain films, CT is useful in better characterizing the bony anatomy. If no bony pathology is suspected, or if soft tissue pathology is suspected or detected on physical examination, MRI is the most useful imaging study after plain films.

If vascular pathology is suspected, a variety of special studies may be considered. Handheld Doppler ultrasound is an extension of the physical examination as described above. Color duplex is useful in distinguishing vascular structures from adjacent masses, and in this way ganglia are distinguished from the adjacent artery, and aneurysms or pseudoaneurysms of the artery can be identified as such. Segmental arterial pressure measurements (expressed as digital brachial index or DBI) and pulse volume recordings are other noninvasive vascular tests used in initial workup. To evaluate a known vascular lesion of the ulnar artery, however, contrast arteriography is the gold standard especially for preoperative planning purposes [16].

Other imaging studies are useful as well. Imaging of the elbow or cervical spine may be indicated in the workup of compressive neuropathies suspected to originate at higher levels. If the patient’s presentation includes shoulder pain and a history of smoking, a chest radiograph should be obtained to rule out Pancoast tumor [4].

Electrodiagnostic studies are useful to confirm the diagnosis, to exclude compression at the level of the cervical spine or the cubital tunnel, and to characterize involvement of ulnar nerve motor branches, sensory branches, or both. If muscle wasting is obvious, an EMG should also be done. Increased latencies or decreased nerve conduction velocities across the ulnar tunnel point to pathology at that level.


Clinical Pearl























Bony pathology suspected

CT in addition to plain films

Vascular pathology suspected

Ultrasound exam or contrast arteriography

Soft tissue mass suspected

MRI

Proximal pathology suspected

Elbow XR, chest radiograph or cervical spine imaging

Obvious muscle wasting

EMG


Anatomy: (Figs. 15.4, 15.5, 15.6, and 15.7)




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Fig. 15.4
Schematic depiction of the cross-sectional relationship between the ulnar and carpal tunnels in the wrist


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Fig. 15.5
Schematic depiction of the roof of the ulnar tunnel


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Fig. 15.6
With superficial structures reflected, this illustration depicts the relationship of the ulnar artery and nerve as they bifurcate within the ulnar tunnel


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Fig. 15.7
With most soft tissue structures removed, this diagram depicts the floor of the ulnar tunnel and the relationship of the neurovascular structures to the carpus

The ulnar nerve arises from the C8 and T1 nerve roots, and emerges as a terminal branch of the medial cord of the brachial plexus. Within the cubital tunnel at the elbow it gives off branches to flexor carpi ulnaris, and to the ulnar half of flexor digitorum profundus. Within the forearm, the dorsal cutaneous branch arises about 6–10 cm proximal to the wrist flexion crease and supplies sensation to the dorso-ulnar hand and fingers. The nerve then passes through the ulnar tunnel where it divides into a sensory branch and a motor branch, as described below. The motor branch then divides to innervate all dorsal interossei, volar interossei, the medial two lumbricals, abductor digiti minimi, flexor digiti minimi brevis, opponens digiti minimi, adductor pollicis, and flexor pollicis brevis – all the small muscles of the hand not innervated by the median nerve [3, 17].

The ulnar tunnel is the space through which the ulnar neurovascular bundle passes at the wrist, and within this confined space the nerve is susceptible to compression. The ulnar tunnel is 4–4.5 cm in length, and unlike the carpal tunnel, the anatomic borders change from proximal to distal. It extends from the proximal edge of the palmar carpal ligament to the fibrous arch of the hypothenar muscles [18]. Within it the ulnar nerve divides into deep and superficial branches. Gross and Gelberman published a landmark anatomical study of this region in 1985, subdividing it into three zones which have since become the standard nomenclature [18].

Zone I begins at the proximal edge of the palmar carpal ligament and ends where the ulnar nerve bifurcates. The floor of Zone I is the transverse carpal ligament proximally and the pisohamate and pisometacarpal ligaments distally; the roof is the palmar carpal ligament proximally and the palmaris brevis distally. Compression of the nerve within Zone I usually presents with combined motor and sensory symptoms, although isolated motor or sensory loss is possible [18].

It is worthwhile noting that the hook of the hamate does not constitute the radial border of the ulnar tunnel, but instead forms part of the floor. Thus the neurovascular structures are not constrained radially by the hook of the hamate [19]. However, pathology of the hamate can still cause compression in the ulnar tunnel [18].

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May 22, 2017 | Posted by in ORTHOPEDIC | Comments Off on Ulnar Tunnel Syndrome

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