various blood vessels, and the median nerve. The carpal tunnel is bounded superficially by the flexor retinaculum, has a deep border formed by palmar aspects of several carpal bones, is bounded laterally by the medial surface of the trapezium, and is bounded medially by the lateral surface of the hamate bone.
Various studies have provided findings which suggest that damage development to neural and tendinous tissues may be associated with symptom development (Barbe et al., 2020; Bove et al., 2019; Chikenji, Gingery, Zhao, Passe et al., 2014; Clark, Al‐Shatti, Barr, Amin, & Barbe, 2004; Clark et al., 2003; Elliott et al., 2009; Elliott, Barr, Clark, Wade, & Barbe, 2010; Ettema, Zhao, An, & Amadio, 2006; Jain et al., 2014). Studies that have biopsied tissues in CTS cases have suggested that the development of median nerve compression may be the consequence of connective tissues experiencing degeneration due to repeated mechanical stress (Festen‐Schrier & Amadio, 2018; Schrier, Vrieze, & Amadio, 2020; Schuind, Ventura, & Pasteels, 1990). Structures affected by repeated stress can include flexor tendons and their synovial sheath (Kerr, Sybert, & Albarracin, 1992). Degenerative noninflammatory fibrosis and thickening of the synovium have been implicated as a factor in median nerve pathology (Chikenji, Gingery, Zhao, Passe et al., 2014; Ettema et al., 2006; Sternbach, 1999). Tendon fibrosis changes may impact the gliding mechanism of the subsynovial connective tissue (SSCT), which moves en bloc with the tendons and median nerve (Ghasemi‐Rad et al., 2014). Increases in vascularity, fibroblast density, and collagen fiber size have been reported in resected synovial specimens and are also indicative of synovial degeneration (Jinrok et al., 2004). If a decrease in SSCT motion were to result from fibrosis, the movement of the tendons would likely increase shear strain in the SSCT (Ghasemi‐Rad et al., 2014). The degree of shear strain would be expected to vary with wrist posture, with the maximum shear predicted at 60 degrees of wrist flexion (Yoshii et al., 2008). High velocity tendon motion has been suggested to place the SSCT at a particularly high risk of shear injury (Yoshii et al., 2011). Hand and finger motions may also result in friction between the flexor digitorum muscles and the median nerve, also potentially leading to cumulative trauma development (Yoshii et al., 2008).
Noninflammatory tendon damage (tendinosis) has also been noted in CTS cases (Kerr et al., 1992). Tendinosis is characterized by microtears in the substance of the tendon and connective tissue, collagen degeneration, and fiber disorientation (Sharma & Maffulli, 2005). These characteristics are also observed during in vitro fatigue failure studies of tendons and studies of fatigue failure in animal studies (Barbe et al., 2013b; Schechtman & Bader, 1997; Shepherd & Screen, 2013; Sun et al., 2010). Patients with this syndrome also demonstrate decreased areal bone mineral density (BMD) in distal forearm bones (i.e., radius and ulna) and reduced bone in hand phalanges, as observed using quantitative ultrasound measurements (Erselcan, Topalkara, Nacitarhan, Akyuz, & Dogan, 2001; Kisala, Pluskiewicz, & Adamczyk, 2019).
Risk factors/activities associated with CTS
A review undertaken by the NIOSH included over 600 epidemiological studies concerning workplace factors associated with numerous MSDs (including CTS) (NIOSH, 1997). The summary of their review on CTS indicated strong evidence for a relationship between exposure to combinations of force and repetition, or force and posture, and development of CTS. CTS frequently presents in working‐aged adults, especially those experiencing prolonged and repetitive flexion and extension of the wrist, especially when combined with forceful gripping (Palmer, 2011). Other potential occupational risk factors may include exposure to HAV and/or exposure to cold conditions. There are several personal risk factors for CTS as well. Of these, being female is one of the strongest (Lee et al., 2019). Females have 2‐3 times the risk compared to males (Lee et al., 2019). Other common personal risk factors include increasing age, having a narrow carpal tunnel, previous wrist trauma or injury, diabetes, rheumatoid arthritis, hypothyroidism, and presence of other neurological disorders (Geoghegan, Clark, Bainbridge, Smith, & Hubbard, 2004).
Cubital tunnel syndrome (ulnar nerve entrapment)
Characteristics/description
Cubital tunnel syndrome is the second most common mononeuropathy of the upper extremity (Cutts, 2007; Saito et al., 2018). It involves the entrapment of the ulnar nerve within the cubital tunnel at the elbow, which is of clinical significance since the ulnar nerve is one of the primary nerves supplying motor information to many forearm muscles and most of the hand muscles and sensory information from part of the hand. In addition to compression within the cubital tunnel, the ulnar nerve can also be compressed in the neck at cervical level 8 (C8), in the thoracic outlet (thoracic outlet syndrome), and at the wrist in Guyon’s canal (Fadel, Lancigu, Raimbeau, Roquelaure, & Descatha, 2017). A double crush syndrome is possible and would mean that the ulnar nerve is compressed in two or more of these various sites. Symptoms of cubital tunnel syndrome at any level of entrapment can lead to an intermittent altered sensation in the little and ring fingers, such as sensory loss (typically the first reported symptom), paresthesia (a burning or prickling sensation), or formication (the sensation of having insects crawling on or under the skin) (Fadel et al., 2017). As the condition progresses, there may be development of pain in the medial elbow and hand weakness, and eventually, atrophy of many of the intrinsic muscles of the hand.
Epidemiology
As with all nerve disorders, individuals with diabetes mellitus (diabetes type 2) have increased susceptibility for symptoms of ulnar nerve neuropathy, although these symptoms may occur secondary to a microvascular injury of the nerve, thus causing a local ischemia, or by interfering with local metabolism. Although there have been only a small number of studies examining occupational contributions to cubital tunnel syndrome, its prevalence ranges from 5.9 to 6.9% in workers in the Saint Louis metropolitan area (An, Evanoff, Boyer, & Osei, 2017), Missouri, USA (5.9%), a 6.9% prevalence rate in dock workers in Sao Paulo, Brazil (Saito et al., 2018), and 6.7% in floor cleaners in a systematic review performed in 2009 (van Rijn, Huisstede, Koes, & Burdorf, 2009). It is also reported to be more common in patients whose work involves protracted elbow flexion (e.g., holding a telephone) and flexion of the elbow on hard surfaces, workers who handle vibratory tools, and individuals with past elbow fractures, direct trauma of the ulnar nerve, or marked valgus or varus deformities of the elbow (Cutts, 2007; Saito et al., 2018).
Anatomy/pathology
The ulnar nerve is formed from terminal branches of the medial cord of the brachial plexus and contains nerve processes that originate from spinal cord roots located at cervical 8 and thoracic 1 levels. The ulnar nerve descends distally down the arm toward the elbow just anterior to a medially located intermuscular septum (a connective tissue sheath that both divides and provides attachment for the triceps brachial muscles located posteriorly, and brachialis muscle located anteriorly). The ulnar nerve pierces this septum and passes through a fibro‐osseous space behind the medial epicondyle of the humus that is known as the cubital tunnel. Thereafter, the ulnar nerve passes between the two heads of the flexor carpi ulnaris muscle of the forearm before proceeding distally to the medial wrist and hand. The ulnar nerve innervates several medially located forearm muscles and most of the intrinsic muscles of the hand (such as those acting on the little and ring fingers, the medial two lumbricals, interosseous muscles, and two muscles of the thumb including the adductor pollicis).
This anatomical arrangement places the ulnar nerve posterior to the elbow’s axis of motion, so that during elbow flexion, the nerve is required to stretch up to 5 mm longer than its length at rest as well as slide through the cubital tunnel (Cutts, 2007; Fadel et al., 2017). Alterations in the fibro‐osseous space and increase in intraneural pressure are believed to be key to the pathogenesis of cubital tunnel syndrome. Flexion of the elbow changes the cubital tunnel’s shape from ovoid to ellipse, decreases the cross‐sectional area of the space by 55%, and increases intraneural pressure up to 20 times higher than resting pressure (Apfelberg & Larson, 1973; Novak, Lee, Mackinnon, & Lay, 1994). The floor of the tunnel is made up of the elbow joint capsule and a supporting ligament; bones act as walls on either side (the medial epicondyle of the