Clinical Biomechanics of Carpal Tunnel Syndrome

Summary of Carpal Tunnel Syndrome[edit | edit source]

Etiology[edit | edit source]

Carpal tunnel syndrome (CTS) is a common entrapment neuropathy of the wrist resulting from compression of the median nerve as it travels through the carpal tunnel[1].

This can be caused by:

  1. An increase in the contents of the carpal tunnel.
  2. Decrease in the size of carpal tunnel.

Acute CTS occurs due to rapid onset (i.e., trauma) leading to sustained increase in carpal tunnel pressure causing occluded blood flow and dysesthesia in the arm due to progressive worsening of median nerve function[2]. Chronic CTS is more commonly observed with the pathogenesis divided into 4 categories:

  • Idiopathic
  • Anatomic
  • Systemic
  • Exertional[3]

Clinical Biomechanical Mechanisms of Carpal Tunnel Syndrome[edit | edit source]

Biomechanical Attributes of Nerves During Movement[edit | edit source]

Figure 1 - Physical stresses experienced by nerves. Nerves can either experience tensile stress longitudinally (along the length of the nerve causing elongation and strain) or transversely.

As an individual assumes a posture or movement, the nerve follows the path of least resistance resulting in exposure to various mechanical stresses. Nerves can experience stress as tensile, compressive, shear or as a combination of stresses, where stress is defined as force divided by the area it is exerted on (Fig 1).[4][5] During joint motion, nerves may elongate and glide in order to prevent nerve resistance due to the longitudinal or transverse tensile stresses acting on them[6]. This deformation or change in nerve length from longitudinal tensile stress is called strain[7]. Whereas the displacement of the nerve from its original position (either longitudinal or transverse) is called excursion[8][9].

Depending on the anatomical relationship between the nerve and axis of rotation in the relevant joints, this can affect the direction and magnitude of nerve excursion[9]. This indicates that when the nerve is elongated, the nerve glides towards the moving joint. Similarly, when the tensile stress in the nerve is decreased, the nerve moves away from the moving joint - this is comparable to that of a pulley system[10]. The magnitude of excursion is greatest at the nerve segments proximal to the moving joint and is least in the nerve segments distal to the moving joint.[9][10]

Figure 2 - This biomechanical theory suggests that loading musculoskeletal tissues at low force levels creates an "elastic" deformation where loaded tissues return to their shape in a linear fashion after the force causing the deformation is removed. As the forces and stress on the tissues increase, the "elastic" capability margin decreases, such that the tissue may be unable to return to its original state - "plastic region". In the load-elongation curve, the slope is a measure of the resistance of the nerve to deformation (stiffness or modulus of elasticity in the stress-strain curve). A steep slope indicates more stiffness, less elasticity and less compliance than a smaller slope.

When examining the median nerve during elbow extension, according to a study by Wright et al., the median nerve obtained the highest excursion measurements during elbow flexion[10]. This movement involved the median nerve segment gliding distally toward the elbow, creating nerve excursion. The movement ultimately produced nerve elongation, resulting in an increase in nerve strain.

The mechanical behavior of nerves can be depicted using a load-elongation curve[11] or by a stress-strain curve (if examining force divided by the cross-sectional area of the nerve and elongation as a percent of change from starting length) (Fig 2). As seen in the “toe region”, when a load is initially applied, the tissue lengthens in relation to the applied load, which in this case, is the tensile stress. As the tensile load is increased, the nerve lengthens at a steady rate, as seen in the linear region of the load-elongation curve. The slope of the load-elongation curve is defined as stiffness and refers to the resistance of the nerve to deformation. Similarly, in the stress-strain curve, the slope is called modulus of elasticity. A steep slope indicates the tissue is greater in stiffness, less elasticity and is less compliant than a tissue with a small slope. As the load continues to be applied, at a certain point the nerve will permanently deform, as represented by the ultimate elongation/strain. The nerve eventually reaches ultimate elongation and undergoes mechanical failure in the plastic region - causing damage and failure in the infrastructure of the nerve[12].

Physical Stresses Affecting Nerve Function[edit | edit source]

Figure 3 - The Physical Stress Theory holds that there are several stress mechanisms that affect how tissues react and change the functionality when exposed to disuse, overuse, or injury.

As posited by Mueller and Maluf[13] (Fig 3), the Physical Stress Theory holds that there are several stress mechanisms that affect how tissues react and change the functionality when exposed to disuse, overuse, or injury.

Immobilization Stress[edit | edit source]

When immobilized (i.e., casting, splinting, bracing), peripheral nerves are exposed to levels of physical stress lower than the equilibrium level (Fig 3). According to the Physical Stress Theory, as a result, the nerve will undergo physiological and structural modifications to atrophy due to the levels of reduced stress and duration of immobilization[13]. In fact, in a study performed by Pachter and Eberstein, they discovered that with as little as 3 weeks of immobilization in the hind limb of rats, this led to myelin degeneration[14].

Lengthening Stress[edit | edit source]

Nerve tissue response during various levels of longitudinal tensile stress is dependent on the duration and magnitude of the stress. Increasing the nerve length can affect nerve blood flow,[12][15] impact nerve conduction velocity with impaired recovery[15][16] and induce functional changes[12]. Current research indicates that lengthening nerves acutely between 6-8% causes fleeting physiological changes that appear to be on the higher side of the normal stress tolerance of the nerve tissue, whereas acute strains of 11% and greater cause long-term damage and are considered as excessive or extreme stress states based on Mueller and Maluf’s Physical Stress Theory.[13]

Several studies have examined changes in nerve blood flow that are induced by increasing nerve strain. Studies of the sciatic nerves in rats have indicated that blood flow is reduced by as much as 50% with a strain of 11%[17] and as much as 100% with a strain of 15.7%[18]. In fact, at a strain of 15%, the tissues are permanently damaged to the point where the tissues are unable to undergo normal blood pathways, leading to minimal recovery of blood flow occurs at this level[19]. Furthermore, nerve conduction was reduced by more than 50% at a strain of 11%[17]. However, slow elongation of nerves has been shown to cause remodeling adaptations in myelin and axon regeneration and degeneration. In a rat model of femur elongation at a rate of 1.0 mm per day, internode length was increased by 17% over 14 days.[19][20]

Compression Stress[edit | edit source]

Compression stresses of low magnitude and short durations are physiologically reversible and create minor changes. However, applied over a long period of time, low magnitude compressive stresses may cause permanent changes in the nerve impairing blood flow. Conversely, compressive stresses of a high magnitude may result in structural alterations in structure and disrupt axonal flow.[12] The pressure in the carpal tunnel syndrome in healthy people typically measure around 3-5 mmHg with the wrist in neutral position.[21][22] Common positions seen in day-to-day activities result in compression pressures that approach or exceed 20-30 mmHg which is seen to impair blood flow.[23] For example, studies indicate that simply placing the hand on a computer mouse was shown to increase the tunnel pressure from 5 mmHg to 16-21 mmHg, and actively moving the mouse increases the pressure even further to 28-33 mmHg.[24] These findings imply that functional positions, even using a computer keyboard and mouse, increases the chances of carpal tunnel by increasing tunnel pressure leading to impaired nerve blood flow and damaging the median nerve. Similarly, rapid loading or high force compression can sever the axons present in the nerve, which can immediately reduce mechanical strength and stiffness of a nerve.[12]

Repetitive Stress[edit | edit source]

Vibration is a common form of repetitive stress seen in the workplace. Based on previous studies, hand-held vibrating tools create vibration stresses that reduce tactile sensation, other sensory disturbances (i.e., paresthesia, neuropathy) and reduced grip force.[25] [26] Long-term exposure to vibration stresses have also been shown to reduce motor nerve conduction velocity and degeneration of myelin after only 400 hours of vibration.[27]

Moreover, repetitive movements are very common in the workplace and are shown to be a primary factor in work-related musculoskeletal disorders (WMSDs).[28] The movements at work impact the tissues in a variety of ways are dependent on the type, magnitude, posture, frequency, duration, and a combination of these factors that may expose the tissue to extreme levels of physical stress. The wrist is used for most daily activities - thus combining all these factors may irritate the carpal tunnel, causing the body to trigger an inflammatory response to add mechanical stability.[29]

Evidence-Based Non-Surgical Modalities[edit | edit source]

The challenge for professionals is to reduce carpal tunnel pressure by improving blood flow and restoring proper nerve states.[12][29] After damage to the nerves from physical stresses, rehabilitation should include gradual increase in stress levels in order to elicit adaptive physiological responses to restore the ability of the nerve to tolerate stresses. As outlined in the Physical Stress Theory[13], it is important to identify the cause for the stress-induced injury, specifically the magnitude, time, direction and posture.

For compression stress, treatment should include mobilization exercise techniques based on the anatomy of the nerve in relation to other structures and focused on restoring the nerve to its original biomechanical states (prior to excessive strain and excursion) that should occur normally during limb movement.[21][22]

Alternatively, ultrasound therapy, ergonomic modifications and, nerve and tendon gliding exercises have been greatly advocated by professionals as other non-surgical treatment measures for CTS[3][30]. In a randomized study by Ebenbichler et. al., they compared ultrasound treatment with “sham ultrasound” treatment. The results concluded that ultrasound therapy led to significantly (P < 0.05) improved symptoms at 2 weeks, 7 weeks, and 6 months. [31]

Typically recommended by ergonomists and medical professionals, ergonomic changes can be made in the workplace and at home to improve discomfort and satisfaction and prevent the occurrence of musculoskeletal disorders prior to even developing an injury. Many recommended measures include fully functional desk chairs, ergonomic computer keyboards and other accessories. However, they have not been scientifically proved to prevent or ameliorate symptoms of CTS.[32][30]

Theoretically, nerve and tendon gliding exercises are proposed to enhance blood flow and decrease tunnel pressure.[30][33] A study by Rozmaryn et al evaluated 240 patients with CTS considering surgery. Prior to surgery they instructed half of these patients to perform nerve and tendon gliding exercises for two years. In those that did not perform these exercises, 71% underwent carpal tunnel release surgery, whereas in the group of patients who did perform these exercises, only 43% underwent surgery.[33]

References[edit | edit source]

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  2. Gillig JD, White S, Rachel JT. Acute Carpal Tunnel Syndrome: A Review of Current Literature. Orthopedic Clinics of North America. 2016. 47(3): 599-607.
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  4. Abrams RA, Butler JM, Bodine-Fowler S, Botte MJ. Tensile properties of the neurorrhaphy site in the rat sciatic nerve. J Hand Surg Am. 1998 May;23(3):465-70. doi: 10.1016/S0363-5023(05)80464-2. PMID: 9620187.
  6. Millesi H, Zöch G, Reihsner R. Mechanical properties of peripheral nerves. Clinical Orthopaedics and Related Research. 1995 May(314):76-83.
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  8. Erel E, Dilley A, Greening J, Morris V, Cohen B, Lynn B. Longitudinal Sliding of the Median Nerve in Patients with Carpal Tunnel Syndrome. Journal of Hand Surgery. 2003;28(5):439-443. doi:10.1016/S0266-7681(03)00107-4
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  21. 21.0 21.1 Gelberman RH, Hergenroeder PT, Hargens AR, Lundborg GN, Akeson WH. The carpal tunnel syndrome. A study of carpal canal pressures. The Journal of Bone and Joint surgery. 1981 Mar;63(3):380-383.Available from:
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  24. Peter J. Keir, Joel M. Bach & David Rempel (1999) Effects of computer mouse design and task on carpal tunnel pressure, Ergonomics, 42:10, 1350-1360, DOI: 10.1080/001401399184992
  25. Akesson I, Lundborg G, Horstmann V, et alNeuropathy in female dental personnel exposed to high frequency vibrations.Occupational and Environmental Medicine 1995;52:116-123.
  26. Lars E. Necking, Jan Fridén & Göran Lundborg (2003) Reduced muscle strength in abduction of the index finger: an important clinical sign in hand‐arm vibration syndrome, Scandinavian Journal of Plastic and Reconstructive Surgery and Hand Surgery, 37:6, 365-370, DOI: 10.1080/02844310310004316
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  30. 30.0 30.1 30.2 Klokkari D, Mamais I. Effectiveness of surgical versus conservative treatment for carpal tunnel syndrome: A systematic review, meta-analysis and qualitative analysis. Hong Kong Physiother J. 2018 Dec;38(2):91-114. doi: 10.1142/S1013702518500087.
  31. Ebenbichler G, Resch K, Nicolakis P, et al.. Ultrasound treatment for treating the carpal tunnel syndrome. BMJ. 1998;316(7133):731-735.
  32. Lincoln AE, Vernick JS, Ogaitis S, Smith GS, Mitchell CS, Agnew J. Interventions for the primary prevention of work-related carpal tunnel syndrome. Am J Prev Med. 2000 May;18(4 Suppl):37-50. doi: 10.1016/s0749-3797(00)00140-9. PMID: 10793280.
  33. 33.0 33.1 Rozmaryn LM, Dovelle S, Rothman ER, Gorman K, Olvey KM, Bartko JJ. Nerve and tendon gliding exercises and the conservative management of carpal tunnel syndrome. J Hand Ther. 1998 Jul-Sep;11(3):171-9. doi: 10.1016/s0894-1130(98)80035-5. PMID: 9730093.