the early 1900s in miners and quarry workers (Laws, 1998). It was only later realized that musculoskeletal and neurologic symptoms were part of the same syndrome. Although the prevalence in the general population is very low, the prevalence in those experiencing prolonged HAV exposure can be as large as 50% and varies with the intensity of the exposure. Risk appears to be increased somewhat in countries with colder climates (Shen & House, 2017). Exposed workers typically exhibit symptoms in middle age, though symptoms can be observed in younger workers with more intensive exposures. The latency period between exposure and symptoms can be quite broad, ranging from less than a year to four decades, depending on the intensity of exposure.
Anatomy/pathology
The tissue damage associated with exposure to HAVS may affect vascular, neurologic, and musculoskeletal structures in the hands, wrist, or forearm. Damage to these various systems may progress at different rates (Pelmear, 2003). The vascular component is also known as VWF and is related to Raynaud’s phenomenon, which is the most recognized manifestation of HAVS. The precise pathological mechanism is not totally clear; however, it is believed that vibration exposure causes endothelial damage through mechanical trauma and oxidative stress, leading to vasoconstriction through activation of the sympathetic nervous system. Nerve fibers (both myelinated and nonmyelinated) are thought to be damaged through vibration exposure. Musculoskeletal symptoms may be due to direct damage to musculoskeletal tissues due to the repetitive forces of vibration and/or may be secondary to nerve damage (Shen & House, 2017).
Risk factors/activities associated with HAVS
Sources of vibration that can cause HAVS are varied and include hand drills, chisels, power chain saws, power jigsaws, sanders, riveters, polishing tools, and many others. There is some indication that high‐frequency vibration is more relevant to the symptoms of HAVS, as such vibration may be absorbed preferentially by the hand and fingers, whereas lower frequency vibration energy may affect the arms and shoulders to a greater extent (Shen & House, 2017). It is a disorder resulting from prolonged exposure to vibration, specifically to the hands and forearms while using vibrating tools. Symptoms include numbness, tingling, and loss of nerve sensitivity. HAVS is a painful and potentially disabling condition of the fingers, hands, and arms due to vibration. There is initially a tingling sensation with numbness in the fingers. The fingers then become white and swollen when cold and then red and painful when warmed up again. Cold or wet weather may aggravate the condition. Picking up objects such as pins or nails becomes difficult as the feeling in the fingers diminishes, and there is loss of strength and grip in the hands. The pain, tingling, and numbness in the arms, wrists, and hands may interfere with sleep.
Commonalities Among MSDs
If one contemplates the summaries of the various MSDs summarized in Table 2.1, certain commonalities become apparent. One is that all appear to be associated with the development of damage to musculoskeletal tissues (and/or other structures). It should not be surprising that these disorders, all of which result can result in significant pain and dysfunction, would be associated with tissue damage. Another consistent refrain is that all of these disorders are associated with exposure to the repetitive application of stress, sometimes expressed in terms of exposure to forceful and repetitive exertions. Adoption of non‐neutral postures is another potential source of repeated stress, as such postures generally serve to increase stress on affected tissues in some form or fashion (and may be adopted frequently). Sometimes, the repeated stress comes in the form of vibration exposure, which has been associated with damaging impacts on musculoskeletal tissues, along with other associated tissues.
Table 2.1 Summary of Common MSDs
| Disorder | Involved structures |
|---|---|
| Low back pain | Degeneration and inflammation in many potential tissue sources, including intervertebral discs, facet and sacroiliac joint, spinal roots, and muscles attached to the vertebrae |
| Hand & wrist tendinopathy | Degenerative changes in extensor pollicis brevis and abductor longus tendons (sheath breakdown, nodularity, tendon fraying) |
| Lateral tendinopathy of the elbow | Degenerative changes in common extensor tendons at the elbow (microtears that lead to partial or complete rupture) |
| Medial tendinopathy of the elbow | Degenerative changes in common flexor tendons at the elbow (increased collagen remodeling and mucoid ground substance) |
| Shoulder tendons (rotator cuff injuries) | Degeneration and inflammation in rotator cuff tendons |
| Muscle fatigue | Many potential contributors, including physiological changes that lead to an energy crisis, dysfunction in calcium homeostasis, neurological changes (altered neuromuscular junctions), and apoptosis |
| Myalgia (muscle pain) | Many potential contributors, including dysfunction in calcium homeostasis and increased inflammation |
| Muscle fibrosis | Increased extracellular matrix production, for example, collagen and fibronectin |
| Carpal tunnel syndrome (median mononeuropathy) | Median nerve entrapment, irritation, inflammation |
| Ulnar tunnel syndrome (ulnar mononeuropathy) | Ulnar nerve entrapment |
| Hand‐arm vibration syndrome | Many potential sources, including damage to vascular, neurological, and/or musculoskeletal structures of the hand, wrist, and forearm |
Whenever one observes damage development in a material exposed to repeated mechanical stress, there is one mechanism that comes to mind that would explain how and why this damage is occurring. This process is, of course, material fatigue failure. Fortunately, the fatigue failure theory has been around since the 1840s, and much is known regarding the response of materials to repeated stress (Stephens, Fatemi, Stephens, & Fuchs, 2001). However, the fact that musculoskeletal tissues are located in a dynamic biological environment, in which exposed materials have a healing capacity, provides an important wrinkle in the development of biological tissue damage. This provides us with competing processes that will control musculoskeletal tissue damage development. Unless some new and unique mechanism of damage development from repeated stress is discovered that applies only to biological materials, we must assume the damage part of the equation is controlled by the mechanism of fatigue failure. We know certain aspects regarding the healing portion of the equation, as well, but much more needs to be learned.
This book examines the development of MSDs as a process of fatigue failure of musculoskeletal tissues, but one modified by complex physiological and biochemical processes (including, but not limited to, tissue healing). To our knowledge, no one has considered such an approach toward understanding the causes of musculoskeletal tissue damage nor for understanding how we might better control MSDs and improve overall musculoskeletal health. We acknowledge at the outset that there is much yet to be learned about this extremely complex process. However, there is much that is known, which may improve our understanding regarding the development and control of MSDs.
Bibliography
1 Abdelmagid, S. M., Barr, A. E., Rico, M., Amin, M., Litvin, J., Popoff, S. N., … Barbe, M. F.
