Ulnar tunnel syndrome could be broadly defined as a compressive neuropathy of the ulnar nerve at the level of the wrist. The ulnar tunnel, or Guyon’s canal, has a complex and variable anatomy. Various factors may precipitate the onset of ulnar tunnel syndrome. Patient presentation depends on the anatomic zone of ulnar nerve compression: zone I compression, motor and sensory signs and symptoms; zone II compression, isolated motor deficits; and zone III compression; purely sensory deficits. Conservative treatment such as activity modification may be helpful, but often, surgical exploration of the ulnar tunnel with subsequent ulnar nerve decompression is indicated.
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A zone I compression elicits motor and sensory signs and symptoms, a zone II compression results in isolated motor deficits, and a zone III compression causes purely sensory deficits.
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In select cases, conservative treatment such as activity modification may be helpful, but often, surgical exploration of the ulnar tunnel with subsequent ulnar nerve decompression is indicated.
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The anatomy of the ulnar tunnel is complex, but numerous anatomic studies have described the tunnel in significant detail. Because organic lesions are often implicated in the cause, surgical exploration and decompression of the ulnar tunnel represent a common treatment modality.
Introduction
Ulnar tunnel syndrome (UTS) is broadly defined as a compressive neuropathy of the ulnar nerve at the level of the wrist. The term “ulnar tunnel syndrome” was coined by DuPont and colleagues in 1965 to describe the condition of 4 patients with acquired ulnar neuritis. The ulnar tunnel proper, also known as “Guyon’s canal,” is one potential but not exclusive site of ulnar nerve compression at the wrist. The eponym comes from Guyon’s description in 1861 of a space at the base of the hypothenar eminence at which the ulnar nerve bifurcates and that is vulnerable to compression from surrounding structures. Numerous factors may precipitate the onset of UTS, including space-occupying lesions, vascular lesions, and repetitive trauma. Patient presentation depends on the anatomic zone of ulnar nerve compression and therefore may be purely motor, purely sensory, or a combination of both. In select cases, conservative treatment such as activity modification may be helpful, but often, surgical exploration of the ulnar tunnel with subsequent ulnar nerve decompression is indicated.
Anatomy
As with all nerve-related disease, a thorough understanding of anatomy and potential sites of compression is critical. The ulnar nerve emerges from the medial cord (C8–T1) of the brachial plexus and passes through the axilla into the anterior compartment of the arm, before piercing the intermuscular septum and traveling in the posterior compartment medially. It then courses superficially and passes posterior to the medial epicondyle, into the anatomic cubital tunnel. The nerve then continues deep along the flexor digitorum profundus in the forearm. Before its entrance to the ulnar tunnel, approximately 3.4 cm proximal to the ulnar styloid, the ulnar nerve gives off the dorsal cutaneous branch, which innervates the ulnar and dorsal side of the hand. The main nerve resurfaces at the level of the wrist where it passes through the ulnar tunnel, which is a fibro-osseous structure. The anatomy of the tunnel is complex, and variations in the nomenclature and structures surrounding the tunnel have previously been a source of confusion and misinterpretation. For example, the terms pisohamate tunnel, pisohamate hiatus, and pisohamate arcade have been used variably and interchangeably to describe the ulnar tunnel in part or whole. The entrance of the tunnel is triangular and begins at the proximal edge of the palmar carpal ligament. It extends distally to the fibrous arch of the hypothenar muscles at the level of the hook of the hamate and is approximately 40 to 45 mm in length. The boundaries of the tunnel vary along its length. Generally, the roof of the canal consists of the palmar carpal ligament, palmaris brevis, and hypothenar connective tissue. The floor of the canal consists of the transverse carpal ligament, pisohamate ligament, pisometacarpal ligament, and the tendons of the flexor digitorum profundus and opponens digiti minimi. The medial wall of the canal is formed by the pisiform, the abductor digiti minimi, and the tendon of the flexor carpi ulnaris. The lateral wall is formed by the hook of the hamate, the transverse carpal ligament, and the flexor tendons.
Within the boundaries of the canal lie the ulnar nerve, ulnar artery, accompanying veins, and connective fatty tissue. The ulnar nerve lies slightly deep and ulnar to the ulnar artery. During its course in Guyon’s canal, the ulnar nerve bifurcates into a superficial and a deep branch approximately 6 mm distal to the distal pole of the pisiform. The superficial branch innervates the palmaris brevis and provides the sensory fibers over the hypothenar eminence and small and ring fingers. The motor branch of the nerve exits deep in the canal and courses around the ulnar edge of the hamulus and then runs radially between the abductor digiti minimi and flexor digit minimi and dorsal to the flexor tendons of the small finger ( Fig. 1 ).
Compression of the ulnar nerve at the wrist is not limited to the confines of the ulnar tunnel. Shea and McClain and, later, Gross and Gelberman studied the relationship between the symptoms of ulnar neuropathy and the anatomic location of nerve compression about the wrist. They classified compressive ulnar neuropathy at the wrist into 3 types ( Fig. 2 ). Type I syndrome, or a zone I compression, occurs as a result of nerve compression proximal to or within Guyon’s canal, before any nerve bifurcation, and manifests as motor weakness of all the ulnar innervated intrinsic muscles and sensory deficits over the hypothenar eminence and the small and ring digits. Type II syndrome, or a zone II compression, manifests exclusively as motor weakness of the hand. The sensory branch is spared and therefore sensation along the ulnar nerve distribution remains intact. Compression of the deep ulnar branch may occur as it exits Guyon’s canal at the level of the hamulus. Type III syndrome, or a zone III compression, occurs secondary to compression of the superficial sensory branch of the ulnar nerve and manifests as isolated sensory loss.
Anatomy
As with all nerve-related disease, a thorough understanding of anatomy and potential sites of compression is critical. The ulnar nerve emerges from the medial cord (C8–T1) of the brachial plexus and passes through the axilla into the anterior compartment of the arm, before piercing the intermuscular septum and traveling in the posterior compartment medially. It then courses superficially and passes posterior to the medial epicondyle, into the anatomic cubital tunnel. The nerve then continues deep along the flexor digitorum profundus in the forearm. Before its entrance to the ulnar tunnel, approximately 3.4 cm proximal to the ulnar styloid, the ulnar nerve gives off the dorsal cutaneous branch, which innervates the ulnar and dorsal side of the hand. The main nerve resurfaces at the level of the wrist where it passes through the ulnar tunnel, which is a fibro-osseous structure. The anatomy of the tunnel is complex, and variations in the nomenclature and structures surrounding the tunnel have previously been a source of confusion and misinterpretation. For example, the terms pisohamate tunnel, pisohamate hiatus, and pisohamate arcade have been used variably and interchangeably to describe the ulnar tunnel in part or whole. The entrance of the tunnel is triangular and begins at the proximal edge of the palmar carpal ligament. It extends distally to the fibrous arch of the hypothenar muscles at the level of the hook of the hamate and is approximately 40 to 45 mm in length. The boundaries of the tunnel vary along its length. Generally, the roof of the canal consists of the palmar carpal ligament, palmaris brevis, and hypothenar connective tissue. The floor of the canal consists of the transverse carpal ligament, pisohamate ligament, pisometacarpal ligament, and the tendons of the flexor digitorum profundus and opponens digiti minimi. The medial wall of the canal is formed by the pisiform, the abductor digiti minimi, and the tendon of the flexor carpi ulnaris. The lateral wall is formed by the hook of the hamate, the transverse carpal ligament, and the flexor tendons.
Within the boundaries of the canal lie the ulnar nerve, ulnar artery, accompanying veins, and connective fatty tissue. The ulnar nerve lies slightly deep and ulnar to the ulnar artery. During its course in Guyon’s canal, the ulnar nerve bifurcates into a superficial and a deep branch approximately 6 mm distal to the distal pole of the pisiform. The superficial branch innervates the palmaris brevis and provides the sensory fibers over the hypothenar eminence and small and ring fingers. The motor branch of the nerve exits deep in the canal and courses around the ulnar edge of the hamulus and then runs radially between the abductor digiti minimi and flexor digit minimi and dorsal to the flexor tendons of the small finger ( Fig. 1 ).
Compression of the ulnar nerve at the wrist is not limited to the confines of the ulnar tunnel. Shea and McClain and, later, Gross and Gelberman studied the relationship between the symptoms of ulnar neuropathy and the anatomic location of nerve compression about the wrist. They classified compressive ulnar neuropathy at the wrist into 3 types ( Fig. 2 ). Type I syndrome, or a zone I compression, occurs as a result of nerve compression proximal to or within Guyon’s canal, before any nerve bifurcation, and manifests as motor weakness of all the ulnar innervated intrinsic muscles and sensory deficits over the hypothenar eminence and the small and ring digits. Type II syndrome, or a zone II compression, manifests exclusively as motor weakness of the hand. The sensory branch is spared and therefore sensation along the ulnar nerve distribution remains intact. Compression of the deep ulnar branch may occur as it exits Guyon’s canal at the level of the hamulus. Type III syndrome, or a zone III compression, occurs secondary to compression of the superficial sensory branch of the ulnar nerve and manifests as isolated sensory loss.
Common pathway of compressive peripheral neuropathies
The details of nerve degeneration and regeneration as a result of compression loading have been studied extensively over the past few decades and have yielded a tremendous amount of information regarding the pathophysiology of nerve compression. In general, these studies have demonstrated that nerve injury correlates to both the degree and duration of compression, with both mechanical and ischemic factors contributing to neurologic dysfunction. Situations such as trauma or sustained compression will induce the accumulation of edema into the endoneurial space of the nerve trunk. Because of the diffusion barrier created by the perineurium and the lack of lymphatic vessels in the endoneurial space, the fluid may not easily escape. The result is an increase in endoneurial fluid pressure and encroachment of the normal endoneurial microcirculation. A study by Lundborg and colleagues showed that after 2 to 8 hours of experimental compression-induced ischemia (80 mm Hg) in nerves of animals, the endoneurial fluid pressure may increase rapidly and persist for 24 hours or longer. Another example of metabolic conduction block is the sensory loss and motor paralysis that can occur after deflating the tourniquet around the upper arm. This type of metabolic block, caused by local arrest of intraneural microcirculation, is immediately reversible when the compression is removed. With extended compression, however, edema within the fascicles can result in increased endoneurial pressure, which could compromise endoneurial capillary flow for hours or days, potentially permanently affecting function of the nerve.
Causes
No reports have specifically addressed the incidence and prevalence of UTS in the widespread population. It is generally accepted that the incidence of UTS is much less than that of either carpal tunnel syndrome (CTS) or cubital tunnel syndrome. Numerous factors may cause UTS, and in fact, a large proportion of the literature on UTS is dedicated to case reports that describe the various causes of the disease. Shea and colleagues reported that the mass effect of ganglion cysts and then occupational neuritis were the 2 leading causes of UTS. During the past several decades, however, reports on isolated ulnar neuropathy secondary to occupational activities have been scarce. Other causes include benign lesions, hook of hamate fractures, ulnar artery pathologic conditions or aberrancy, deviant hypothenar muscles, and crystal deposition disease. Chronic, repetitive trauma or compression over the hypothenar eminence has also been implicated as a cause of UTS and is not uncommon in long-distance cyclists. Idiopathic disease has also been reported. Several studies have reported a strong association between the presentation of CTS and UTS, whereas others have disputed this relationship. The carpal and ulnar tunnels lie adjacent to each other. Although the transverse carpal ligament constitutes the roof of the carpal tunnel, it also constitutes the floor of the ulnar tunnel. Pressure changes within the carpal tunnel are transmitted to the ulnar tunnel, and vice versa. A relevant clinical correlate demonstrates this fact: to completely decompress the motor branch of the ulnar nerve, the transverse carpal ligament needs to be sectioned distally beyond the hook of the hamate, as the motor branch runs on the floor of the carpal tunnel. Silver and colleagues reported a series of 59 hands with CTS and found concurrent ulnar sensory deficiencies in 34% of cases. After carpal tunnel release only, they found that 94% of their patients had improvements in ulnar nerve sensation according to the Semmes-Weinstein test. Ablove and colleagues measured the pressure changes in the carpal tunnel and the ulnar tunnel before and after endoscopic and open carpal tunnel release. Following the release, they found that pressure dropped significantly in both anatomic tunnels. They also suggested that carpal tunnel release alone could be used to successfully treat patients with concurrent disease. The association between CTS and UTS has been debated, but the trends in evidence seem to favor a true association between the two syndromes.
In sum, with regard to the cause of UTS, it seems that most cases are secondary to impingement of an organic lesion on a segment of the ulnar nerve. This contrasts with ulnar neuropathy at the elbow (cubital tunnel syndrome) or CTS, in which the most common causes are believed to be idiopathic.
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