Cumulative Trauma Disorder is the affect that acute injury, repetitive trauma, and constant pressure or tension has on nerves, muscles, and bones. This affect is best understood in the terms of a cycle -- the Cumulative Injury Cycle. This cycle separates cumulative-trauma disorder from other injuries.

Acute Injury

Muscle and fascxial tearing from an acute injury causes immediate inflammation. White-blood-cell proliferation, fibrinogen secretion, and adhesion formation start. (1) If not treated correctly soon, the cumulative-injury cycle begins.

Repetitive Motion Injury

Repetitive-motion injury is a function of specific physical factors that can be measured. (2) To understand how repetitive-motion injuries occur, it's helpful to review the model of repetitive motion. (3) This model isn't linear or exact; it's proportional (see sidebar below).

repetitive motion

Examples: Vibration results in high Number of repetitions with low Amplitude and low Relaxation time, causing high Insult. Someone who is weak will use a high percentage of their maximal strength to accomplish task, causing high Force and high Insult.

Constant Pressure/Tension Injury

These two factors decrease circulation and compromise cell recovery. Three major results are cellular retention of calcium, poor repair, and altered function. (1, 4, 7) This injury type, by definition, does not require motion. An isometric contraction, or the muscle tension of poor posture, are good examples of the mechanism of injury.

"The Cumulative Injury Cycle"

The cyclic nature of injury -- one factor triggering the next in a circular series -- has been described for many years. (5) The components of the cycle are defined as follows:

cumulative injury cycle

Weak and Tight Tissues

Repetitive effort, for example, tends to make muscles tighten. (6) A tight muscle tends to weaken; a weak muscle tends to tighten. And on it goes.

Friction - Pressure - Tension

As a result of weak and tight tissues, internal forces rise. Friction, pressure, or tension can be present at the same time. If one or more of these factors is high, an acute injury and inflammation can result -- even without external forces being applied.

Decreased Circulation - Edema

The affect of increased forces on the tissues is decreased circulation. If pressure is applied over one of the vulnerable, low-pressure lymphatic channels, the result is edema. External forces -- in the form of a constant-pressure or tension injury -- may also decrease circulation or cause edema.

Adhesion - Fibrosis

Cellular hypoxia, from restricted circulation, causes fibrosis and adhesions to occur in an between tissues. (7)

When the friction-pressure-tension factor is severe, or when an acute injury occurs, two additional factors come into play.

Tear or Crush

The physical disruption of the tissues -- microscopic or macroscopic -- can occur with sufficient force. This can be an external force, acute injury, or it can result internally.

Inflammation

This results from the injury and starts the adhesion process. The cycle progresses then to the "weak-and-tense" phase. (1)

There are many extrinsic factors which affect the cycle, but, they do it in predictable ways. Smoking, for example, tends to decrease circulation, helping to perpetuate the cycle. Diabetes has a similar affect. Thyroid deficits tend to increase tension in the musculature and therefore influence the "weak-and-tense" factor of the cumulative-injury cycle. Hormonal changes -- as with hysterectomy, excessive body weight, and pregnancy -- lead to predictable alterations to the involved factors. (2)

The cumulative-injury cycle is defined with two possible routes: the inflammatory cycle and the chronic cycle. Each is independent of the other, however, they both may be present together.

Conditions

The cumulative-injury cycle is self perpetuating. It worsens the symptoms and syndromes of cumulative-trauma disorders with a downward-spiral effect. These include carpal-tunnel and cubital-tunnel syndrome, epicondylitis, tenosynovitis, myofascitis, bursitis, peripheral-nerve entrapment, thoracic-outlet syndrome. De Quervain's disease. None of these conditions are a cumulative-trauma disorder without the affects of the cumulative-injury cycle.

Number: References: Summary of reference material:
1.
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Scarpelli DG, Chiga M. Cell injury and errors of metabolism. In: Anderson WAD, Kissane JM, eds. Pathology, 7th edition. St. Louis: C. V. Mosby, 1977;90-147. Explains the tissue reactions to injury including inflammation, hypoxia of the cell, diminished membrane transportation etc.
2.
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Browne CD, Nolan MN, Faithfull DK, Occupational repetition strain injuries. Occupational Repetition Strain Injuries Advisory Committee, Div of Occupational Helath, New South Wales 1984. Discusses the effects of repetitive motion on the musculature and the factors that come to bear in repetitive strain injury.
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Leahy PM, Improved treatments for carpal tunnel. Chiro Sports Med 1995;9: 6-9. Summarizes several hundred cases treated using a "law of repetitive motion" as a guide. Defines the factors involved.
4.
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del Cacho E, Gallego M, Felices C, Bascuas JA. Myofibroblasts and myoephithelial cells in the chicken harderian gland. Histology and Histopathology, 6(3): 303-8, 1991 Jul. Describes research showing cellular metaplasia due to hypoxia.
5.
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Porterfield JA, DeFosa C. Mechanical neck pain, 6: 176-179, WB Saunders 1995 Outlines two simple cycles of injury.
6.
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Gerr F. Letz R, Landrigan PJ. Upper-extremeity musculoskeletal disorders of occupational origin. Annu Rev Publ Health 1991; 12: 543-566 Describes the clinical picture of repetitive strain injury and tissue reactions.
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Dawes KE, Peacock AJ. Characterization of fibroblast mitogens and chemoattractants produced by endothelial cells exposed to hypoxia. Am Jnl of Respiratory Cell & Molecular Biology 10(5): 552-9, 1994 May. Describes research showing the proliferation of fibroblasts under hypoxic states.
Copyright © 1995 by P. Michael Leahy, DC, CCSP

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