Anatomy of ulnar nerve entrapment

Summary

In this article, we provide a comprehensive overview of the anatomical structures involved in ulnar nerve compression –⁠ from the arcade of Struthers and Osborne’s ligament, through the cubital region, and to the distal areas of Guyon’s canal. Our analysis is based not only on data from the literature and cadaveric studies, but also on our own cadaveric and intraoperative experience. We emphasize the importance of systematic release of all potential compression sites and present key surgical technique our experience increase the likelihood of success, particularly in revision procedures. This approach helps to minimize residual compression and maximize functional recovery for patients. The article thus offers a practical guide optimizing surgical care for patients with ulnar nerve neuropathy.

Keywords:

ulnar nerve – cubital tunnel – Guyon´s ulnar canal – Osborne´s ligament – arcade of Struthers

This is an unauthorised machine translation into English made using the DeepL Translate Pro translator. The editors do not guarantee that the content of the article corresponds fully to the original language version

 

Introduction

 

Ulnar nerve entrapment syndrome represents the second most common compressive neuropathy of the upper limb after carpal tunnel syndrome. Nevertheless, surgical treatment may fail, making revision surgery necessary—an outcome neither the surgeon nor the patient welcomes. One contributing factor is insufficient knowledge of the precise anatomical course of the ulnar nerve.

This article therefore focuses on the ulnar nerve and the complex anatomy of its potential compression sites, with particular emphasis on the identification and clinical relevance of specific anatomical structures. Ulnar nerve compression includes both classical locations, such as the ulnar groove, as well as less frequent anatomical variations that may significantly influence the nerve’s course and predispose to compressive neuropathy.

The text systematically presents the anatomical regions of the upper limb in which ulnar nerve compression may occur. It is supported by both clinical and cadaveric studies, contributing to a deeper understanding of the relationships between anatomical structure, function, and clinical relevance of ulnar nerve entrapment.

The aim of this article is to provide peripheral nerve surgeons with a detailed overview of this topic and to assist in optimizing both diagnosis and surgical management of patients with ulnar neuropathy.

 

Anatomy of Ulnar Nerve Entrapment in the Arm

The Arcade of Struthers and the Internal Brachial Ligament

The main potential site of ulnar nerve compression in the arm is the arcade of Struthers. However, both the clinical significance and even the terminology of this anatomical structure remain somewhat controversial.

The structure is named after the Scottish anatomist Sir John Struthers (1823–1899), although Struthers himself did not describe such an arcade in his publications (in contrast to the so-called Struthers’ ligament). He also did not publish any work specifically addressing ulnar nerve entrapment. [1]

The term “arcade of Struthers” was first introduced by Kane et al. in 1973, who described, based on a cadaveric study, an arcade formed by the internal brachial ligament (ligamentum brachiale internum). In their series, the ulnar nerve passed beneath this structure approximately 8 cm proximal to the medial epicondyle in 14 of 20 dissected limbs (70%). The authors, however, incorrectly attributed the first description of this structure to Struthers. [2]

Opinions regarding the existence of this arcade vary widely in the literature. Some studies question its presence [3, 4], whereas other cadaveric and clinical reports confirm it. [5-14]

A detailed anatomical description of the arcade was provided by Spinner and Kaplan in 1976. They defined the fibro-muscular arcade as being located on the medial side of the arm, formed by a thickening of the brachial fascia, superficial fibers of the triceps brachii muscle, and the internal brachial ligament. Laterally, the region is bordered by the humerus covered by deep fibers of the triceps brachii, and anteriorly by the medial intermuscular septum of the arm (septum intermusculare brachii mediale, SIBM).

In the same study, the internal brachial ligament was described as a thin fibrous band measuring 8–12 cm, originating near the insertion of the coracobrachialis muscle. Some fibers of the medial head of the triceps brachii arise from this ligament, contributing to the formation of the arcade. [15]

In 2011, von Schroeder et al. attempted to redefine this structure. According to their findings, the arcade represents a canal formed by the SIBM, the internal brachial ligament, and the fascia and epimysium of the medial head of the triceps brachii. The canal entrance has a “V-shaped” configuration, created by separation of the septum from the ligament, allowing the ulnar nerve to pass from the anterior to the posterior compartment of the arm. After entering the posterior compartment, the nerve is covered more distally by superficial fibers of the medial head of the triceps brachii connected to the internal brachial ligament; further distally, these fibers merge again with the SIBM. The internal brachial ligament can therefore be understood as a component of the SIBM, which becomes partially separated as the ulnar nerve traverses the septum. In this study, this configuration of the arcade was present in all 11 limb specimens (Figs. 1 and 2). The entrance to the canal was located at a mean distance of 9.6 cm from the medial epicondyle of the humerus, the mean canal length was 5.7 cm, and the nerve exited the canal at a mean distance of 3.9 cm from the medial epicondyle. [13]

This arrangement, however, presupposes that the ulnar nerve travels from the anterior to the posterior compartment of the arm by passing through the SIBM. Other authors have shown that in a considerable proportion of cases (27–43%) the ulnar nerve is located within the posterior compartment throughout its proximal course. [14, 16] These anatomical differences were summarized by Won et al., who classified the relationship between the ulnar nerve and the SIBM into three types: (1) type I, in which the nerve runs solely within the posterior compartment and does not traverse the septum; (2) type II, in which the nerve simply pierces the septum dorsally; and (3) type III, in which the nerve runs within the septum for a short segment (5–55 mm) and then continues dorsally.

A similar perspective is provided by Elmaraghi et al. Based on their clinical experience in 197 patients, the arcade of Struthers was formed by three structures (the SIBM, the internal brachial ligament, and the fascia of the medial head of the triceps brachii) and was present in 34% of cases. In their view, this region becomes potentially symptomatic only when a ligamentous band is present dorsal to the nerve, which, through its motion in conjunction with the septum and fascia, creates a loop around the nerve. [9]

The clinical significance of the arcade of Struthers is also debated. Spinner and Kaplan emphasized its relevance particularly in the setting of anterior ulnar nerve transposition, in which the nerve—after being relocated ventrally—may become entrapped at this level. [15] This view is supported by other studies as well. [3, 4, 10, 13] However, several clinical case reports have been published in which the mere presence of the arcade, even without prior nerve transposition, resulted in ulnar nerve compression. [5, 8, 11, 17] Ochiai et al. and Nakajima et al. were able to verify this intraoperatively using electromyography (EMG). [5, 18] Sivak et al. and Gao et al. demonstrated compression beneath the arcade not only by EMG but also by ultrasound. [11]

Gabel and Amadio, as well as Elmaraghi et al., reported a higher proportion of ulnar nerve compression by the arcade in revision procedures compared with primary operations, suggesting that failure to decompress the nerve at this level may be a cause of unsuccessful primary surgery. [9, 19]

In our experience, the arcade of Struthers accounts for ulnar nerve compression in only a small minority of cases. Nevertheless, it is our standard practice to surgically inspect the nerve proximally from the medial epicondyle of the humerus up to a distance of 8–10 cm, without the need for an extensive skin incision. We place even greater emphasis on this region in revision procedures.

 

Anatomy of Ulnar Nerve Entrapment in the Elbow Region

Medial Intermuscular Septum of the Arm

In the distal portion of the arm, the ulnar nerve courses posterior to SIBM and descends along it toward the medial epicondyle of the humerus, where the septum inserts. At this level, the nerve enters the ulnar groove (sulcus nervi ulnaris humeri).

Although the nerve lies in close proximity to the SIBM in the distal arm, it runs alongside rather than through the septum; therefore, under normal anatomical conditions, the septum does not represent a compressive structure at this site (Fig. 3).

The situation may change following anterior transposition of the ulnar nerve. In its new, more ventral position, the nerve may become entrapped at the site where it crosses the distal portion of the septum. Consequently, during anterior transposition, division of this distal segment of the septum is essential to prevent iatrogenic compression.

 

Supracondylar Process of the Humerus

Although the supracondylar process of the humerus is most commonly associated with median nerve compression, in exceedingly rare cases its presence, particularly when combined with fibrous bands, may result in ulnar nerve injury. Such involvement may occur either in isolation or concomitantly with median nerve compression. [20, 21]

 

Osborne’s Ligament

At the level where the ulnar nerve leaves the ulnar groove, it enters a fibro-osseous passage known as the cubital tunnel (canalis cubitalis).

The lateral wall of this elliptical canal is formed by the humeral condyle, the proximal ulna, and the humeroulnar joint cleft covered by the ulnar collateral ligament of the elbow. The anterior wall is formed by the medial epicondyle of the humerus, and the posterior wall by the olecranon of the ulna.

In the proximal portion of the tunnel, the medial wall is constituted by a fibrous structure first described by Buzzard in 1922. A detailed anatomical description was subsequently provided in 1957 by the English surgeon Geoffrey Vaughan Osborne (1918–2005), and the structure has since borne his name as Osborne’s ligament. [22, 23]

Over time, numerous alternative designations have appeared in the literature, including Osborne’s fascia [24], Osborne’s arcade [25], cubital tunnel retinaculum [26], retrocondylar retinaculum [27], arcuate ligament [28], and epitrochleoanconeus ligament [29].

In his original description, Osborne characterized this structure as a fibrous band connecting the two heads of the flexor carpi ulnaris muscle (FCU). In contemporary anatomical literature, it is more commonly described as a fibrous band spanning the proximal cubital tunnel and forming its roof. Its proximal margin lies at the beginning of the ulnar groove, while distally it becomes less sharply defined and typically blends with the superficial fascia of the FCU. [4, 26–28, 30, 31]

This variability in terminology raises the question of whether eponymous nomenclature should be abandoned in favor of anatomically descriptive terms that more accurately reflect the structure’s morphology, such as cubital or retrocondylar retinaculum (Figs. 4–6). [32]

O’Driscoll et al. performed a detailed anatomical investigation of this structure in 27 cadaveric limbs and classified the so-called cubital tunnel retinaculum into four morphological types: (1) Type 0 (1/27): complete absence of the ligament, associated with ulnar nerve subluxation over the medial epicondyle during elbow flexion; (2) Type 1a (17/27): a thin ligament that becomes stretched during flexion, resulting in narrowing of the proximal cubital tunnel without nerve compression; (3) Type 1b (6/27): a thickened ligament that produces compression of the ulnar nerve beneath it during elbow flexion between 90° and 120°;  (4) Type 2 (3/27): replacement of the ligament by a variable anconeus epitrochlearis muscle. [26]

The reported prevalence of Osborne’s ligament varies considerably in the literature. Dellon identified the ligament in 77% of cases [4], whereas Karatas et al. observed it in only 8% (1/12) of specimens. [33] In contrast, Gonzalez et al. described the ligament in all 39 cadaveric specimens examined [31], and Husarik et al. identified it by magnetic resonance imaging in all 60 individuals studied, with thickening present in 8%. [34] (Table 1)

According to several authors, Osborne’s ligament is responsible for dynamic compression of the ulnar nerve, in which tensioning of the ligament during advanced elbow flexion (approximately 90°) results in increased pressure on the nerve. [22, 26, 35] Macchi et al. performed histopathological analysis and demonstrated that the ligament possesses a three-layered myofascial structure. [28]

In our intraoperative experience, Osborne’s ligament represents the most frequent cause of constrictive ulnar nerve compression in the elbow region. When identified intraoperatively—which occurs in the majority of cases—we routinely divide the ligament. This is consistently followed by a dynamic assessment of nerve stability within the ulnar groove during elbow flexion. If this test reveals (sub)luxation of the nerve during flexion, anterior transposition of the ulnar nerve is performed.

 

Submuscular Membrane and Intermuscular Aponeurosis

Distally, the roof of the cubital tunnel is formed by the two heads of the flexor carpi ulnaris muscle (FCU), which are covered by the dense antebrachial fascia (fascia antebrachii). The ulnar nerve passes between both heads of the FCU and is here covered by a deeper fascial layer.

The presence and morphology of this fascial structure are highly variable, which is reflected in the inconsistent terminology used throughout the literature. Matsuzaki referred to this structure simply as a submuscular membranebeneath the FCU, without providing further detailed anatomical characterization. This membrane was present in all patients operated on for cubital tunnel syndrome in his series. In 43 patients (48%), the author considered this membrane to be responsible for ulnar nerve compression, most commonly at a distance of approximately 3 cm distal to the point where the nerve enters beneath the FCU (Figs. 7–8). [25]

Along its further course, the ulnar nerve continues beneath this membrane and runs obliquely in a radial direction. Upon reaching the border of the FCU, it passes through an opening in the intermuscular septum between the FCU and the flexor digitorum superficialis muscle (FDS).

Proximally, this septum is thickened into a common aponeurosis of both muscles. Inserra and Spinner referred to this structure as the common intermuscular aponeurosis between the FCU and the FDS of the fourth digit. They emphasized that division of this aponeurosis is required to achieve complete decompression of the ulnar nerve during anterior transposition. [36]

Gonzalez et al. identified a similar structure in 44% of cases (17/39). However, due to the dense muscular arrangement in the region of the ulnar common flexor origin (caput commune ulnare), they were unable to anatomically assign the structure to a specific muscle. [31]

More precise anatomical characterization was provided as early as 1986 by Amadio and Beckenbaugh, who identified the structure as a deep intermuscular flexor–pronator aponeurosis. This aponeurosis lies superficial to the flexor digitorum profundus muscle and deeper than both the FCU and the FDS, extending up to 5 cm distal to the medial epicondyle of the humerus. The authors identified this structure in all 20 cadaveric limbs examined. [37]

Similar findings were reported by Green and Rayan, who observed the same structure in all 19 specimens, at an average distance of 3.7 cm from its distal margin to the medial epicondyle. [30] Mahan et al. measured the average distance of the opening in the intermuscular septum through which the nerve passes to be 3.9 cm distal to the medial epicondyle in a sample of 26 limbs. [27]

A thorough understanding of the complex anatomy of the distal cubital tunnel and the proximal forearm is essential for adequate surgical decompression of the ulnar nerve in cases of clinically significant entrapment. Effective decompression requires division of all structures crossing the nerve, and in cases of nerve transposition, also those structures that did not cause compression in the nerve’s original position but may lead to secondary entrapment in its new course. [27, 31, 36]

Whereas surgical division of the intermuscular aponeurosis is a standard component of ulnar nerve decompression at this level, the submuscular membrane is, in our experience, the most frequently overlooked structure and represents a common cause of residual compression in revision surgery.

 

Snapping Triceps

Instability of the ulnar nerve within the ulnar groove, manifested as subluxation during elbow flexion, is a well-recognized cause of nerve irritation producing symptoms similar to those observed in in situ compression. In this situation, the nerve is repeatedly irritated by friction against the medial epicondyle of the humerus during elbow flexion. This condition is typically associated with absence of Osborne’s ligament and may be present in up to 16% of healthy individuals. [26]

In rare cases, not only the ulnar nerve but also an aberrant portion of the distal insertion of the triceps brachii muscle dislocates over the medial epicondyle. In such instances, a distal extension of the triceps insertion located beyond the medial epicondyle shifts ventrally over the epicondyle during elbow flexion, simultaneously pushing the ulnar nerve anteriorly.

Snapping of the triceps brachii was first described by Rolfsen in 1970, [38] and since then only isolated case reports or small case series have been published. Proposed anatomical explanations include the presence of a fourth head of the triceps brachii, an abnormal distal insertion, or muscular hypertrophy, particularly in bodybuilders. [39–44]

Dellon did not identify a snapping triceps muscle in any of 104 cadaveric limbs examined; however, he reported a statistically significant association between ulnar nerve subluxation and triceps insertion within the cubital tunnel. In the same study, a strong association was observed between the presence of the anconeus epitrochlearis muscle and complete coverage of the ulnar nerve by the medial head of the triceps brachii. [4]

This relationship is further supported by a case report published by O’Hara et al., describing combined ulnar nerve compression in the presence of both muscles. The low-lying distal portion of the triceps insertion is most likely congenital; however, in cases of acquired cubital valgus deformity, a secondary development of this condition has also been suggested. [45]

The presence of a snapping triceps brachii is consistently associated with ulnar nerve dislocation. In such cases, anterior transposition of the ulnar nerve is indicated. In our experience, nerve transposition alone is sufficient, allowing avoidance of resection or transposition of the snapping muscle itself.

 

Anconeus Epitrochlearis Muscle

The anconeus epitrochlearis muscle (also referred to as musculus anconeus sextus) is an accessory muscle extending between the medial epicondyle of the humerus and the olecranon of the ulna (Fig. 9). It is innervated by the ulnar nerve. [46]

This relatively small muscle has no fully established physiological function, although it is presumed to contribute to elbow extension and medial stabilization of the joint. The muscle forms the roof of the cubital tunnel, thereby replacing Osborne’s ligament. By doing so, it may prevent ulnar nerve dislocation during elbow flexion. [47, 48]

The first description of this muscle dates back to 1867 by the Austrian anatomist Václav Leopold Gruber (1814–1890). Since then, numerous cadaveric and clinical studies have been published.

In 2021, Suwannakhan et al. supplemented their own cadaveric findings with a meta-analysis of previously published studies. Based on 26 of 40 eligible studies, they determined a prevalence of the anconeus epitrochlearis muscle (MEA) of 14.2% in 14 cadaveric studies (considered asymptomatic individuals) and only 4.5% in 12 studies involving symptomatic patients. This difference was statistically significant (p < 0.001). Based on these findings, the authors supported the hypothesis that the mere presence of the MEA does not necessarily result in ulnar nerve compression and may even exert a protective effect against cubital tunnel syndrome. [47]

The authors of this meta-analysis did not exclude the possibility of ulnar nerve compression caused by the MEA; however, they suggested that this occurs predominantly in cases of muscular hypertrophy.

Kim et al. published a retrospective series of 16 intraoperative findings of MEA in patients with cubital tunnel syndrome, demonstrating considerable variability in the muscle’s morphology and size. The authors emphasized the dynamic changes occurring during elbow movement. In some cases, increasing muscle tension and compression of the ulnar nerve during elbow flexion were clearly observed; in others, the muscle remained relaxed even during advanced flexion and did not exert pressure on the nerve, which was confirmed intraoperatively by inserting a hemostat between the MEA and the ulnar nerve. These cases were considered incidental findings. The influence of muscle size on these dynamic changes, however, was not specifically addressed. [49]

The findings of Suwannakhan et al. are further supported by a combined clinical study by Wilson et al., who identified MEA intraoperatively in only 5% of patients with cubital tunnel syndrome (9 of 168), which was significantly lower than the incidence reported in asymptomatic individuals identified through meta-analysis of cadaveric and radiological studies (15.5%; 98 of 634). The authors therefore argued that the presence of MEA is not a risk factor for cubital tunnel syndrome and may instead confer a protective effect. The muscle becomes symptomatic primarily in cases of hypertrophy of the dominant limb. [48]

In clinical practice, the anconeus epitrochlearis muscle represents the most common anatomical variation in the region of the cubital tunnel. In our opinion, in symptomatic patients, surgical division of the muscle with complete decompression of the underlying ulnar nerve is indicated.

 

Anatomy of Ulnar Nerve Entrapment at the Wrist and in the Hand

After piercing the septum between the FCU and FDS, the ulnar nerve continues distally along the FDS. In the distal forearm, the nerve courses between the FCU and the flexor digitorum profundus muscle, accompanied by the ulnar vessels. It is covered by the antebrachial fascia (fascia antebrachii), which near the wrist is referred to as the palmar carpal ligament (ligamentum carpi palmare).

The proximal margin of this fibrous band is considered the entrance to the ulnar canal. The first description of this anatomical region was provided in 1861 by the French surgeon Jean Casimir Félix Guyon (1831–1920), and the canal is therefore commonly known as Guyon’s canal.

Guyon’s canal represents an approximately 4-cm-long space with frequently ill-defined boundaries. The volar wall (roof) of the canal is formed proximally by the palmar carpal ligament. This is followed by a short segment in which the canal lacks a clearly defined volar boundary and is covered only by fatty connective tissue of the hypothenar subcutaneous layer. Distally, the roof is formed by fibers of the palmaris brevis muscle (PB) (Fig. 10).

The floor (dorsal boundary) is formed proximally by the medial portion of the flexor retinaculum and distally by the pisohamate ligament, followed further distally by the pisometacarpal ligament.

The medial wall is formed proximally by the pisiform bone with the insertion of the FCU tendon, and distally by the connection of the palmaris longus tendon fibers with the fascia of the abductor digiti minimi muscle.

The lateral wall is the most difficult boundary to define. According to various authors, it is largely open or not described at all. [50] Some studies define the lateral wall as the junction of the palmaris longus tendon with the medial portion of the flexor retinaculum, continuing distally with the origin of the flexor digiti minimi muscle. [51]

Other authors include the hook of the hamate (hamulus ossis hamati) as part of the lateral wall. [52] However, it has been demonstrated that the ulnar artery frequently runs directly volar or even radial to this bony structure (Fig. 11). [53]

The distal portion of Guyon’s canal slopes deeper in a dorsal direction. At the level of the hypothenar muscle origins—particularly the flexor digiti minimi, which forms a distally convex fibromuscular arch—the entrance to another space is located: the pisohamate hiatus (hiatus pisohamatus).

This hiatus contains the deep branch of the ulnar nerve (ramus profundus nervi ulnaris) and the deep palmar branch of the ulnar artery (ramus palmaris profundus arteriae ulnaris), which curve around the distal portion of the hamate. Meanwhile, the superficial branch of the ulnar nerve (ramus superficialis) and the main trunk of the ulnar artery continue distally within the axis of Guyon’s canal.

The floor of the pisohamate hiatus is formed by part of the pisohamate ligament. The space then continues radially as the pisohamate canal (canalis pisohamatus), running between layers of the opponens digiti minimi muscle and further into the midpalmar space (spatium palmare medium) (Fig. 12). [51]

Based on clinical symptoms resulting from ulnar nerve lesions at different levels of Guyon’s canal, this anatomical region is often divided into several zones. The number of described zones varies in the literature, with some authors subdividing this relatively small area into as many as six compartments. [52, 54]

We prefer a simpler and clinically practical three-zone classification: (1) Zone I includes the proximal portion of the canal, where the nerve trunk has not yet bifurcated. Lesions at this level result in complete sensorimotor deficits in the ulnar nerve distribution distal to the injury. (2) Zone II involves only the deep branch of the ulnar nerve after its separation from the main trunk at the level of the pisohamate hiatus or distal to it. Since this region lies beyond the motor branches to the hypothenar muscles—including the abductor digiti minimi—clinical impairment predominantly affects the interosseous muscles and the adductor pollicis. (3) Zone III involves only the superficial branch of the ulnar nerve. Although this branch remains mixed, with two motor branches supplying the palmaris brevis, sensory fibers clearly predominate. Clinically, lesions produce sensory loss over the fifth digit and the ulnar half of the palmar surface of the fourth digit. Motor impairment of the palmaris brevis is not reliably assessable on clinical examination. [55–58]

The only potential sign is wrinkling of the hypothenar skin during abduction of the little finger. [54]

In cases of suspected ulnar nerve compression at the wrist or in the hand, surgical treatment always requires decompression of the ulnar nerve along the entire length of Guyon’s canal, regardless of the clinical presentation.

We emphasize the importance of preoperative ultrasound evaluation, which may help identify underlying causes of compression such as ganglion cysts, lipomas, ulnar artery thrombosis, or displaced carpal bone fractures.

 

Conclusion

A detailed understanding of the anatomical relationships and variations along the course of the ulnar nerve is essential for successful diagnosis and surgical treatment of ulnar nerve entrapment.

This article highlights that the ulnar nerve may be compressed at multiple anatomical sites, and that the clinical significance of these structures often differs. Systematic identification of all potential compression points is crucial, particularly in revision surgery, where overlooked entrapment sites may account for failure of previous procedures.

Surgeons must also recognize that certain structures may become compressive only after anterior transposition of the ulnar nerve, and operative technique must therefore be adapted accordingly.

 

Table 1. Summary of studies describing the prevalence of Osborn's ligament in asymptomatic individuals.

 

 

	Type of study	Number of limbs	Number of positive findings	%
Dellon (1986) [4]	autopsy	64	49	77
Karatas et al. (2009) [33]	autopsy	12	1	8
Gonzalez et al. (2001) [31]	autopsy	39	39	1
James et al. (2011) [35]	autopsy	11	10	91
O'Driscoll et al. (1991) [26]	autopsy	27	26	96
Husarik et al. (2009) [34]	radiological (MR)	60	60	1

 

Table 2. Overview of structures with the potential to compress the ulnar nerve.

	Site of constriction	Note
Arm	Arcade of Struthers and internal ligament of the arm	rare, nerve compression during transposition
	septum intermusculare brachii mediale	nerve compression during transposition
Elbow region	supracondylar process of the humerus	very rarely
	Osborne's ligament	common cause of compression
	submuscular membrane and intermuscular aponeurosis of FCU	submuscular membrane often overlooked
	snapping triceps	associated with nerve subluxation
	musculus epitrochleoanconeus	most common variety
Wrist and hand (Guyon's canal)	zone I (proximal part)	mixed sensorimotor lesion
	Zone II (pisohamate hiatus)	motor lesion
	Zone III	sensory lesion