Biomechanical and morphological background of the pathogenesis of cubital tunnel syndrome

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Abstract

In the structure of peripheral nervous system disorders, tunnel neuropathies account for about a quarter of all cases, among which cubital tunnel syndrome (CTS) holds one of the leading positions. A high prevalence of CTS is noted among individuals of working age with occupational risk factors (repeated flexion/extension, vibration, prolonged pressure on the elbows). This review summarizes epidemiological data and occupational risk factors, anatomical features of the cubital tunnel and biomechanics of the elbow joint that contribute to ulnar nerve compression and the development of CTS, as well as their role in the formation of the "compression–ischemia–edema" pathophysiological changes leading to subsequent demyelination and axonal damage of the ulnar nerve. Management strategies for patients with CTS are discussed: early severity stratification, timely surgical decompression (the benchmark is the first 4–6 months for moderate/severe cases), correction of risk factors, and rehabilitation to improve treatment outcomes.

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INTRODUCTION

The review covers modern concepts of pathophysiological background of compression of the ulnar nerve in the cubital tunnel taking into account the biomechanical factors impacting the tension, deformation and recovery of the nerve cord [1]. The review comprises an analysis of data from open sources (eLibrary, PubMed, Web of Science) with no limitations as to depth of search.

Tunnel syndromes (TS) account for approx. 25% of all diseases of the peripheric nervous system [2, 3]. Of the 30 varieties of TS [4], six are most important in clinical practice [5].

Following the carpal tunnel syndrome, the cubital tunnel syndrome (CTS) found in 0.6–0.8% of population [6, 7].

The incidence rate varies within 20.9–30.0 per 100,000 population [2, 8–11]. Every year, about 75,000 new cases of CTS are registered in the USA [12], 25 new cases of CTS in men and 19 in women per 100,000 people in Great Britain [13].

At the same time, according to surveys conducted in the USA, the prevalence of CTS symptoms varied from 1.8% to 5.9%, and the authors of the survey do not exclude the possibility of actual levels being higher due to low frequency of patients' seeking medical care and complications in CTS diagnostics [14, 15].

The major burden of the disease is with patients of active age from 40 to 50 years (average age being 46 years old), it is virtually not seen in adolescents and young children [7, 15, 16].

The risk factors of development of compression/ischemic neuropathies include superficial location of peripheric nerves, great length, sharp change of trajectory in the process of movement and passage through narrow spaces.

Mechanical compression of the nerve cord in anatomically narrow places (osseofibrous canals, between tendons or muscles) on the background of chronic overstrain of the muscular-ligamentous apparatus stemming from frequently repeated flexion-extension movements or forced posture of the arm flexed in the elbow joint for extended periods of time are the most frequent causes of development of CTS [17].

Therefore, the professional risk group would include persons whose activity involves repeated movement of the elbow joint (athletes, musicians) [2, 18], exposure to vibration [19] or monotonous manual labor with prolonged forced elbow posture (jewelers, carpenters, packers) [2, 16, 20–24].

Traumatization of the ulnar nerve may occur in the event of a prolonged leaning on the elbow while sitting, which is frequently observed among drivers and office workers working at a computer [25–27]. Concomitant pathologies, e.g. diabetes mellitus [18], hypothyroidism, diseases of the liver, anemia, hypercoagulation, systemic diseases, vitamin deficiency, increase the risk of development of CTS [28, 29].

There are rare cases of bilateral CTS in pizzamakers due to a pronounced biomechanical impact on ulnar nerves while performing repeated intensive movements of the arms and elbows, and cases on the background of long-term intake of Naproxen in patients with psoriatic arthritis, or in high-dosage neuroleptic intake [30–32].

Among risk factors, some authors mention smoking, male sex, elevated body mass index [28, 33–35] and elderly age [20, 22]. At the same time, medical literature provides data to the effect that the sex is not a significant risk factor, and the elevated body mass index does not increase the risk of development of CTS [17, 36–38].

The ulnar nerve may be exposed to compression in various levels, but in 60–70% of the cases the compression zone is the cubital tunnel (CT) [17, 39]. At the same time, the majority of cases of development of the cubital tunnel syndrome (CTS) are of idiopathic nature [2, 40].

With this end in view, it is necessary to analyze the specifics of anatomy of the elbow joint, specifics of composition of the CT and specifics of biomechanics (anatomy of muscular strain and movement), i.e. the functional anatomy of the elbow joint.

SPECIFICS OF TOPOGRAPHY OF THE CUBITAL TUNNEL

Potential sites of ulnar nerve compression at the elbow level include Struthers' arcade, the medial intermuscular septum, the region of the medial epicondyle of the humerus, the cubital tunnel (Mouchet's canal), the retroepicondylar groove, and the area of the flexor-pronator aponeurosis [41–45], with compression possibly occurring at multiple levels simultaneously [2].

Factors that lead to narrowing of the space around the nerve or to its excessive stretching predispose to impairment of its function. Even minor but repetitive injuries over time deplete the physiological reserves of the nerve and lead to the development of neuropathy [6].

A relationship exists between the shape of the cubital tunnel, its cross-sectional area, volume, and the likelihood of developing cubital tunnel syndrome. It has been experimentally demonstrated that the cross-sectional area and volume of the cubital tunnel in the position of maximum elbow flexion are smaller in patients with CTS compared to healthy controls [46].

The main anatomical features predisposing to the development of CTS include the following: the location of the ulnar nerve in rigid osseofibrous and fibromuscular canals, aponeurotic clefts, openings, and ligaments, which render it susceptible to constant friction against bony structures during elbow movements [46]; anatomical variations in the shape of the retroepicondylar groove and the structure of the medial epicondyle of the humerus [47]; the presence of the m. anconeus epitrochlearis instead of Osborne's ligament in 3% to 34% of cases, a muscle characteristic of primates, originating from the medial edge of the olecranon and inserting onto the medial epicondyle [48–52] (although some authors consider it an additional protective mechanism that shields the ulnar nerve from compression [53, 54]); and the vulnerability of the superficially located ulnar nerve, which is protected only by a thin soft-tissue layer, making it particularly susceptible to traumatic injury [2, 4, 47, 55-56]

A study involving 91 patients found anatomic peculiarities of cubital tunnel architecture affecting the development of idiopathic CTS in 60% of the cases [17, 39, 54].

SPECIFICS OF BIOMECHANICS OF N. ULNARIS

In the process of flexion and extension of the elbow joint, the ulnar nerve is subjected to a range of mechanical factors, including compression, longitudinal traction, friction and transverse shear [57].

When the arm is in extension at the elbow, the ulnar nerve lies freely and is not under tension. During flexion, the nerve courses around the medial epicondyle of the humerus posteriorly, passing through the cubital tunnel, where it undergoes significant stretching and tension. This creates mechanically unfavorable conditions and increases the risk of compression.

Surrounded only by a thin soft-tissue structure in the joint area, the nerve lacks sufficient mechanical protection; however, its capacity for transverse displacement allows it to adopt an optimal position, thus reducing excessive traction.

When the elbow is flexed to 90–120°, the maximum medial shear and flattening of the ulnar nerve occur [58]. When the shoulder is abducted in the range of 30–110°, the nerve is displaced by 4.9 mm, while the flexion and extension in the elbow joint (10–90°) causes its excursion (displacement) by an approximate of 5.1 mm [59]. Studies showed that the maximum displacement of the ulnar nerve occurs in the fatty tissue more proximal of the medial condyle. Restriction of nerve mobility (fixation) leads to increased tension, acting as a pathogenetic risk factor for the development of CTS [59, 60].

The most frequent cause of compression of the ulnar nerve is the Osborne's ligament [61, 62] (may be absent in 10–23% cases) [52, 53, 63, 64]. There are reports that when the elbow joint is flexed every 45 degrees, the distance between the medial epicondyle and the olecranon increases by 5, resulting in the tension of the Osborne's ligament and simultaneous relaxation of the medial collateral ligament. In the maximum flexion, the length of the Osborne's ligament increases by 40–50%, which causes the cubital tunnel to narrow this provoking increased pressure on the ulnar nerve [13, 65]. When the elbow joint is being flexed, the shape of the CT is transformed from elliptical to slit-like with reduction of the height, area and sagittal curvature of the tunnel [66].

The cross-section area of the CT starts to change in the flexion to the angle of 90°, its magnitude being reversely proportional to the degree of flexion. In the maximum flexion posture (135°), the volume of the tunnel may reduce by 55% [13, 14, 65, 67], and its height decrease by 2.5 mm [13, 68].

Flexion, extension, and proximal compression increase tension in the ulnar nerve. The nerve is subjected to traction starting at an elbow flexion angle of 60°, and the magnitude of traction continues to increase linearly (in direct proportion) with increasing amplitude of flexion [14]. The zone of maximum tension is localized 4–6 cm mode distal of the medial epicondyle [69]. It was established in experiments that the complete flexion of the elbow results in the increase of the length of the ulnar nerve by 10% of its base length. The combination of flexion in the elbow joint by 90° with simultaneous abduction of the shoulder by 90° may result in the traction of the nerve by an average of 14% relative to its base length [70, 71], the elongation value being 4.7–8 mm [42, 65, 69]. At the same time, there are reports to the effect that in the process of flexion, there occurs elongation of exactly the proximal part of the nerve with maximum values reaching 18%, while the distal part remains unchanged [69, 72].

In the flexion and extension movements in the elbow joint, the excursion of the ulnar nerve is 9.8–10 mm more proximal and 6 mm more distal of the media epicondyle [22]. The fixation of the nerve trunk may restrict its natural mobility resulting in an overstrain and marked deformation of the distal segment [73].

According to the generally accepted view, traction (stretching) of the ulnar nerve during elbow flexion is the primary mechanism underlying increased intraneural pressure [74].

Elasticity, which allows the nerve to restore its original shape and size after the removal of the load, is provided primarily by the endoneurium and perineurium. The latter acts as a protective barrier, ensuring the mechanical strength of the nerve fibers and modulating external mechanical forces. The perineurium is the most resistant to stretching; its undulating (corrugated) configuration effectively counteracts traction during elbow movements, allowing the nerve fibers to stretch without compromising anatomical integrity or conduction. This adaptive mechanism reduces the compressive force on the nerve during joint movements [75, 76].

However, the elasticity of the nerve has threshold limits. When these limits are exceeded during stretching, structural changes and deformation of the nerve trunk occur, leading to slowing and subsequently to complete conduction block in the event of fiber rupture within the trunk [77]. Experiments established that the traction of the nerve up to 10% of its base length does not bring marked structural changes: conductivity impairments are functional and quickly reversible. Traction of the nerve by more than 20% exceeds the limit of its elasticity resulting in the tear of the finest nerve fibers, and restoration of conductivity may take as mush as 10 to 15 minutes. Traction of 25–30% causes damage not only of the nerve fibers but of vessels with formation of para-neural and intra-stem hematomas. A complete anatomical breakage may occur if the nerve traction exceeds 35–38% of the base length [78, 79].

PATHOPHYSIOLOGICAL NECHANISMS OF THE CUBITAL TUNNEL SYNDROME

The pathogenesis of cubital tunnel syndrome is based on three key phenomena: impaired venous outflow, demyelination and ischemia, where chronic compression of the nerve trunk acts as the triggering mechanism [6, 80]. This compression leads to edema of the surrounding tissues and the nerve itself, followed by the development of vascular disturbances in the compression zone [81].

In the extension posture of the elbow joint, the pressure on the ulnar nerve in the CT area is, on average, 19 mmHg, and in the flexion, it reaches values above 100–200 mmHg, resulting in a direct compression of the ulnar nerve [67, 82].

Chronic compression of the ulnar nerve, combined with a secondary edema, triggers persistent structural reconstruction of the nerve trunk, since the local pressure of 80 mmHg for two hours initiates a pathological cascade: swelling of Schwann cells and disintegration of the endoplasmic reticulum. These degenerative changes persist for up to 28 days after the relief of compression. A single episode of compression, even at a low intracanal pressure of up to 10 mmHg, is sufficient to initiate the processes of demyelination [83].

Animal experiments showed that the compression of the nerve induces a sharp increase in the number of Schwann cells both in the direct compression zone and in the distal segments. Proliferative reaction manifests in two weeks and peaks by the 4th week, when the number of cells is six times exceeding the base level [84]. The molecular mechanisms of Schwann cell response, even in the absence of axonal injury or inflammation, remain incompletely understood. The hypothesis is that these cells are capable of responding to mechanical stimuli (mechanosensitivity) [6, 85].

The reason of slow conductivity with no axon loss is incomplete remyelination after demyelination associated with dysfunction of the Schwann cells. The process involved a structural reconstruction of the nerve fiber: thinning of the myelin sheath, change in the axon to fiber ratio, reactive thickening of the epilemma of the nerve (endo-, peri- and epineurium), and increased vascularization of the endoneurium [86–88]. According to the obtained data, a more than six-fold increase was observed in the number of axons with thinned myelin sheaths, along with a proportional decrease in the number of axons with normal myelin sheaths [6].

The degree of injury depends not only on the force and duration of the trauma, but also on the size of the nerve fiber, its position within the nerve trunk, as well as the number and size of the nerve fiber fascicles. It was demonstrated that under traumatic and compressive forces, nerve fibers located at the periphery of the nerve trunk are more severely affected than those located centrally. Thick myelinated fibers show the highest sensitivity to injury. The degree of injury also depends on the architecture of the nerve: nerve trunks containing a small number of large fascicles (oligofascicular) are more severely affected than nerves with a large number of small fascicles (polyfascicular) [81, 89]. Reduced velocity of excitation conduction along the nerve fiber stems from appearance of sections with a thin myelin sheath and shortened inter-nodular spaces, which disrupts the mechanism of saltatory conduction [90].

Proliferation of the Schwann cells is accompanied by a high level of apoptosis [84] characterized by a two-phase process: the first phase aligns with the active proliferation, and the second, with late morphological changes [91]. Proliferation and apoptosis of Schwann cells are triggered even in the absence of morphological signs of axonal damage, structural changes in the neuromuscular junction and despite preserved gross motor potential. If these morphological changes are reversible in the early stages of the disease, at later stages axonal degeneration develops at the level of compression.

Denervation results in a dystrophic process characterized by a marked reduction in the volume of muscle fibers (atrophy) and concurrent proliferation of connective tissue (fibrosis), which ultimately leads to irreversible degeneration of the muscle [92].

The degree of nerve injury depends on the magnitude of pressure, duration of compression and the dynamic character of the pressure. Three degrees of injury are distinguished: neurapraxia, characterized by a rapidly reversible physiological conduction block, preserved anatomical integrity of the axon, and local myelin sheath damage; axonotmesis, involving a focal demyelinating block with disruption of axonal continuity, preserved endoneurial integrity, and Wallerian degeneration distal to the injury site, with possible spontaneous recovery albeit over a prolonged period; and neurotmesis, characterized by severe axonal damage with destruction of the nerve sheaths, pronounced Wallerian degeneration, where spontaneous recovery is impossible or extremely limited, and surgical intervention is required [6, 79, 93].

External pressure on the nerve not only results in its direct injury but also causes disruptions in the blood circulation. While at the pressure below 30 mmHg venous occlusion develops, the pressure above 50 mmHg causes disorders of arterial perfusion [94]. Hypertension above 60–80 mmHg with duration of compression over 2 hours leads to pronounced disorders of microcirculation [77, 95]. Pressure of 200 mmHg leads to endoneurium edema, and the pressure of 400 mmHg for 2 hours causes persistent disorders of blood perfusion [94].

Under conditions of impaired microcirculation, characterized by alternating periods of ischemia and reperfusion, the permeability of cell membranes increases, promoting the transport of proteins from the vascular bed into the endoneurial space. As a result, intraneural edema persists even after blood flow is restored. Experiments established that after the release of compression, endoneurial edema can persist for up to 28 days, whereas microcirculatory disturbances resolve within up to 7 days. Persistent edema and impaired blood flow within the nerve trunk impede adequate gas exchange between capillaries and nerve fibers, leading to the development of sustained hypoxia [83, 96].

While the pressure of 20 mmHg for two hours does not disrupt the axonal transport, the pressure of 30 mmHg for two hours leads to the axonal transport slowing down in the compression zone [97]. Pressure over 50 mmHg for two hours causes a reversible blockage of axonal transport that would recover within 24 hours. With the pressure of 200 and 400 mmHg over two hours, the blockade of fast axonal transport persisted for one and three days, respectively, once the compression was relieved. The time of recovery of normal fast axonal transport correlates with the magnitude of pressure exercised on the nerve [98].

The pathological cascade in chronic nerve compression, involving endoneurial edema, triggers increased production of interleukin-6, which induces fibroblastic proliferation in the synovial sheaths and nerve tissues [99, 100], thereby promoting the development of scar changes within the nerve and the formation of epineurial-adhesive adhesions in the cubital tunnel, further increasing nerve fixation.

The formed cicatricial-adhesive process fixes the ulnar nerve within the osseofibrous canal, sharply limiting its physiological mobility and impeding smooth gliding within the tunnel. This facilitates nerve traction and continuous dynamic trauma to the nerve trunk, further exacerbating venous stasis, ischemia, and scar degeneration of the nerve [79, 92].

Thus, a "vicious circle" typical of compression-ischemic neuropathies is established: nerve compression, venous stasis and lymphostasis, edema (extra- and intraneural), increased intraneural pressure, impaired arterial blood flow and ischemia, structural damage to the nerve trunk (axonal degeneration/demyelination), further increase in intraneural pressure [16, 77, 92].

PATHOPHYSIOLOGICAL CHANGES OF THE NERVE TRUNK UNDER TRACTION

The capacity if the nerve to withstand traction and compression, sliding (excursion) and compression [101, 102], as well as protection against deformation and damage stems from such factors as elasticity, resistance, characteristic undulating motion in the process of relaxation and specifics of sliding (positioning) of the nerve relative to the joint in the process of motion.

In the process of traction, there occurs compression and deformation of the nerve fiber, and the compression force is the highest in the center of the elongated segment of the nerve. One of important biomechanical properties is the elasticity providing for recovery of the initial size and shape once the mechanical load is relieved.

Epineurium and perineurium function as specific dampeners. The elasticity and the strength of nerve trunks during traction mainly depend on the perineurium, while the epineurium provides protection against compression. Due to the corrugated shape of the perineural sheath and the undulating motion of the axons, the nerve fibers may stretch without damage of their anatomic integrity [102].

At the point where the undulating structure of the nerve fiver disappears in the course of its traction, it is the perineurium that protects the nerve from further traction, thus providing protection of fibers within the trunk. As the compression increases, the axons strength along the perineurium, the cross-sectional area of the trunk decreases, and the intra-trunk pressure increases [78, 79]. The elasticity of the nerve trunk has threshold values; and if the ultimate elasticity is not exceeded in the traction, the nerve will recover its base length and elastic properties once the load is relieved. The crossing of the threshold results in irreversible deformation preventing recovery of the nerve structure [78, 92, 102].

The ulnar nerve is a mixed one, and the differences in the structure of the nervous bundles account for their various reactions to compression and ischemia demonstrating a wide spectrum of disorders prevailing in some fiber or other; the functional recovery is in direct dependence from the degree of manifestation of morphological changes and duration of compression. According to experimental data, the initial signs of fibrosis are observed as early as in the end of the third week, and after two months the axons demonstrate a decrease of regenerative capacity, and initial signs of muscle atrophy appear [103, 104]. Within the subsequent 12–18 months, a pronounced fibrosis of denervated muscle develops [103–106], and in 18–24 after the injury, the possibility of productive axonal regeneration is practically reduced to zero due to development of fibrosis and obliteration of Schwann sheaths of the distal section of the nerve [103, 107].

Therefore, it can be concluded that surgical treatment is advisable within the first 4–6 months from disease onset in cases of ineffective conservative management and in moderate-to-severe CTS [103, 105, 108], since the risk of adverse outcomes and possible recurrence significantly increases in severe forms and in long-standing disease, while the recovery period is substantially prolonged [108].

CONCLUSION

It has been shown that nerve compression predominantly causes ischemic damage with chronic fibrosis, whereas stretching leads to structural tears and traction neuropathy. Both processes require timely decompression or minimization of tension to prevent irreversible axonal degeneration. Understanding the pathogenetic mechanisms of ulnar nerve compression is important not only for establishing the causes of cubital tunnel syndrome, but also for selecting the optimal surgical approach in each individual case to achieve the best treatment outcome.

 

ADDITIONAL INFORMATION

ДОПОЛНИТЕЛЬНАЯ ИНФОРМАЦИЯ

Study funding. The study was the authors' initiative without external funding.

Источник финансирования. Работа выполнена по инициативе авторов без привлечения финансирования.

Conflict of interest. The authors declare that there are no obvious or potential conflicts of interest associated with the content of this article.

Конфликт интересов. Авторы декларируют отсутствие явных и потенциальных конфликтов интересов, связанных с содержанием настоящей статьи.

Contribution of individual authors. Edilgireeva L.A.: study concept, data collection and statistical analysis, drafting of the manuscript. Nikolenko V.N.: analysis of anatomical data. Bashlachev M.G.: evaluation of results, literature search. Malsagova I.Ya.: analysis, result discussion, writing assistance. Zonov M.G.: data collection and analysis.

All authors gave their final approval of the manuscript for submission, and agreed to be accountable for all aspects of the work, implying proper study and resolution of issues related to the accuracy or integrity of any part of the work.

Участие авторов. Эдильгиреева Л.А.: концепция исследования, сбор, анализ и статистическая обработка данных, написание текста. Николенко В.Н.: анализ анатомических данных. Башлачев М.Г.: оценка результатов, поиск литературы. Мальсагова И.Я.: анализ данных, участие в обсуждении итогов, помощь в написании. Зонов М.Г.: сбор и анализ данных.

Все авторы одобрили финальную версию статьи перед публикацией, выразили согласие нести ответственность за все аспекты работы, подразумевающую надлежащее изучение и решение вопросов, связанных с точностью или добросовестностью любой части работы.

Statement of originality. No previously published material (text, images, or data) was used in this work.

Оригинальность. При создании настоящей работы авторы не использовали ранее опубликованные сведения (текст, иллюстрации, данные).

Data availability statement. The editorial policy regarding data sharing does not apply to this work.

Доступ к данным. Редакционная политика в отношении совместного использования данных к настоящей работе не применима.

Generative AI. No generative artificial intelligence technologies were used to prepare this article.

Генеративный искусственный интеллект. При создании настоящей статьи технологии генеративного искусственного интеллекта не использовали.

Provenance and peer review. This paper was submitted unsolicited and reviewed following the standard procedure. The peer review process involved 2 external reviewers.

Рассмотрение и рецензирование. Настоящая работа подана в журнал в инициативном порядке и рассмотрена по обычной процедуре. В рецензировании участвовали 2 внешних рецензента.

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About the authors

L. A. Edilgireeva

Sechenov First Moscow State Medical University (Sechenov University)

Author for correspondence.
Email: edilgireeva.leila@mail.ru
ORCID iD: 0000-0001-6067-8962

MD, Postgraduate at the Department of Nervous Diseases and Neurosurgery

Russian Federation, Moscow

V. N. Nikolenko

Sechenov First Moscow State Medical University (Sechenov University)

Email: nikolenko_v_n@staff.sechenov.ru
ORCID iD: 0000-0001-9532-9957

MD, Dr. Sci. (Medicine), Professor, Head of the Department of Human Anatomy

Russian Federation, Moscow

M. G. Bashlachev

Sechenov First Moscow State Medical University (Sechenov University)

Email: bashlachev.m@gmail.com
ORCID iD: 0000-0002-0442-4770

MD, Cand. Sci. (Medicine), Neurosurgeon at University Clinical Hospital No. 3

Russian Federation, Moscow

I. Y. Malsagova

Institute for Advanced Training of Education Workers of the Republic of Ingushetia

Email: innamals888@mail.ru
ORCID iD: 0000-0003-4657-4766

MD, Cand. Sci. (Medicine), Rector

Russian Federation, Nazran

M. G. Zonov

Sechenov First Moscow State Medical University (Sechenov University)

Email: mg.zonov@gmail.com
ORCID iD: 0000-0002-1833-790X

MD, Neurosurgeon at University Clinical Hospital No. 3

Russian Federation, Moscow

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