Inflammation -- Its Determination and Treatment

By Joseph D. Kurnik, DC

The most common physical affliction shared by all mammals is inflammation of the musculoskeletal tissues. It may afflict the skin, fascial layers, ligaments, tendons, muscles, vessels and nerves. 
The purpose of this article is to discuss inflammatory conditions that may affect musculoskeletal fascial layers, tendons, ligaments, and muscles. This is not intended to be a substitute for chiropractic adjusting procedures. It is intended to discuss and provide a protocol for inflammatory disorders which persist in spite of standard chiropractic procedures. An understanding of inflammation and its determination (locating its presence) can help the discriminating doctor to distinguish spinal radicular symptoms from nonspinal derived radicular signs.

Inflammation is a basic physiological process which applies also to injured soft tissues and improperly used soft tissues. External forces are what most think of when considering injury. Injury to tissues can also arise as a result of improper joint function, incoordination of muscles, and nonuse of muscles. In my article on groin and hip pain (Dynamic Chiropractic, November 18, 1996), I explain how sacroiliac dysfunction leads to buttock and hip flexor strain. The astute chiropractor will also recall the research work of Dr. Irvin Korr, who showed that "subluxation" or "dysfunction" leads to a lower level of threshold irritability of muscles related to dysfunctional spinal joints.

The levator scapula is a great example of a commonly strained and inflamed muscle, secondary to cervical dysfunction. A muscle which contracts too often and too intensely is subject to inflammatory reactions, as well as its origins and insertions. Internally disruptive chemical or biological agents may also injure soft tissues. The end result of external or internal disruptive forces is that blood vessels and other soft tissues in or near the injured area will enlist a dynamic complex of cytologic and histologic reactions.

These reactions are local in nature and are designed to cause the destruction or removal of injurious materials (bacteria, foreign matter or chemicals), and to promote responses that lead to repair and healing. The basic signs of soft tissue inflammation are: rubor, color, swelling, pain, and relatively high skin resistance overlying the inflamed tissue. Often, impairment of structural function is also observed.

In a sense, inflammation is a defensive reaction to all sorts of tissue injury. The names of so very many inflammatory processes are designated by the suffix -itis.

Enzymes in a local area of injury are activated to free bradykinin from large precursor molecules present in the blood and various other soft tissues. The main function of bradykinin is to increase the sensation of pain. Bradykinin also sensitizes free nerve endings, making them hypersensitive to heat and light touch and creating an overall sensation of soreness. A secondary function of bradykinin is to promote the production of histamine. It does this by binding to most cells in the affected area and induces them to release histamine. It also does this indirectly through the amplification of the pain process mentioned above. There are nerve centers in the brain and spinal cord which respond to the amplified pain impulses by sending efferent impulses to the appropriate nerve endings housed in the involved soft tissues. These nerve endings being bombarded by efferent impulses then release substance P, which also binds to most cells and further boosts histamine production.

The function of histamine is that of increasing blood flow into the involved area by dilation of arteries and increasing capillary vessel permeability. The increased permeability allows the escape into interstitial spaces of: 1) fluid; 2) WBCs; 3) kallikrein; and 4) bradykinin precursors. This release into interstitial areas, plus constriction of venules distal to capillaries, creates interstitial space congestion and consequent soft tissue swelling.

Released bradykinin precursors cause additional bradykinin to be formulated. This added bradykinin binds itself to the membranes of nearby cells and ultimately causes the release of polyunsaturated fatty acids (PUFAs) from the membranes. These PUFAs cause the production of prostaglandins. These prostaglandins cause vasodilation in the surrounding tissues and increased capillary permeability. The prostaglandins also bind themselves to receptor sites on involved free pain nerve endings and promote additional pain impulses and bradykinin release. This is important because enzymes in the blood continually work to deactivate bradykinin, and this process keeps bradykinin release going until the source of irritation has been removed.

Summary of Processes

Soft tissue assessment is determined through assessment of the cardinal signs of inflammation: 

1. Pain on palpation.
2. Increased skin temperature.
3. Swelling
4. Redness
5. High skin resistance over the involved site.

The first four signs will vary in appearance, sometimes failing to appear to casual observation and at other times becoming very apparent. A most reliable objective measurement of inflammation is DSR, or differential skin resistance. Skin resistance over an area of deeper tissue inflammation will be relatively high when compared to the surrounding skin area. If treatment is successful, the level of skin resistance will return to levels that match that on surrounding areas. It may also be that in non-symptomatic regions of measurable increased skin resistance metabolic dysfunction preceding overt inflammation may be present. This may be found on areas of metabolic dysfunction being synonymous with an overt pre-inflammatory stage.

Inflammation Based Syndromes

The inflammation process is one of nature's attempts to facilitate healing. If it is allowed to get out of control as a result of improper resolution and continues long enough, various pathological conditions or syndromes will develop. These syndromes will be uncomfortable and painful. They can also lead to dysfunction and impaired performance. These syndromes may be divided into the general pathological groupings that include: 

1. Bursitis
2. Capsulitis (arthritis)
3. Fascitis
4. Ligamentitis
5. Tendinitis
6. Adhesions -- a side effect of 1-5 syndromes above, which can occur with or after the inflammations.

For the sake of brevity, I will skip detailed discussion of the syndromes above and elaborate more on adhesions. One of the consequences of prolonged inflammation is the formation of nonscar tissue adhesions within the spaces that have been inflamed. Adhesions of this sort do not generally evolve on their own and are not usually considered to be part of a syndrome.

Adhesions are defined as tissue components that cause tissue layers, which normally slide freely over one another, to stick or bind together. The adhesion is usually a fibrous tissue constituted from a normal constituent of one of the involved tissues. Involved tissues, especially in chronic cases, will appear thickened and congested and will be resistant to being rolled between the fingers or sliding over deeper tissues.

Adhesions are formed as a result of 1) reparative or 2) reactive processes to soft tissue stress and inflammation. They may result from disease, prolonged restriction of joint motion (joint dysfunction, hypomobility, fixation, subluxation), surgical procedures, bone fracture, external blows to soft tissue, or from injuries causing soft tissue inflammation or effusion/hemorrhage into muscle or other soft tissues. Adhesions may also develop in response to local infection or spontaneous hemorrhage, and are often associated with joint capsulitis and other prolonged inflammatory disorders. The extent of adhesion formation is largely dependent upon the individual system's propensity for producing excessive fibrotic material following trauma.

Adhesions are generally located through palpation. Adhesed tissues will not slide over one another and may be difficult to manually separate. Adhesions have an irritating nature and are often accompanied by inflammation or may be located through a DSR survey.

Treatment for inflamed and adhesed areas generally is as follows: 

1. reduction of any adhesion formations which may be present through a combination of medium frequency, electrical stimulation and soft tissue manipulation;


2. lengthening any tight musculature through the use of low frequency electrical stimulation, followed by specific muscle work;


3. vertebral or joint adjusting;


4. toning or strengthening of involved musculature through isometric or isotonic exercise, provided there is no contraindication such as tendinitis, etc.

I would like to thank the Biofeedback and Advance Therapy Institute of Los Angeles for their assistance in providing vital information for the writing of this article. Additionally, references for given information in this article are available upon request.