Lesson 1.6: Assumptions of Pain

Tissue changes both structurally and functionally as we age. Position and movement senses decline as well. Advancing age also presents with the deterioration of kinesthetic sense at all joints. This general phenomenon is partly due to the progressive degenerative loss of mechanoreceptors. We see this change of tissue when we look at the decline in balance and the increase in fall risk. The mechanoreceptors in the cervical spine may be of greatest importance in the process of senile loss of balance, because these receptors have widespread influence on muscle tone.

Tissue is a support system. Extra tissue does not allow the mechanical system to move as easily.  People who are overweight are not necessarily more vulnerable to mechanical issues because of their weight, but rather because of the limited motion. One can become mechanically vulnerable with weight loss because a considerable amount of movement is gained quickly in the absence of movement control.

Joint play, tight or loose, is part of the deck of cards we are dealt genetically.  All people, independent of individual joint play, are susceptible to mechanical joint dysfunction because we move. A person with a tighter joint play will, however, feel irritation earlier than a person with looser joint play. Joint play itself does not cause pain.

Each side of the body is slightly different.  When a person develops, one side of the body develops a little sooner than the other which results in asymmetry. Tissue can be tighter on one side just like ears and feet are different sizes. Leg length discrepancy is a common asymmetry. If it has not caused problems throughout life, then it is too easy to assume that a leg length discrepancy caused the current issue. The facet joint plane on one side of a vertebra may be oriented more obliquely than the facet joint plane on the opposite side, leading to asymmetrical side-bending or rotation. The asymmetries do not necessarily cause irritation, but do increase the vulnerability to mechanical joint dysfunction.

Decreased overall conditioning leads to decreased ability to control movement, making a person vulnerable to mechanical joint dysfunction. A movement routine of sport fosters learning of movement control ultimately decreasing mechanical vulnerability. It does not matter what the activity is, it is the routine that is important. When an activity routine is changed, the mechanical vulnerability increases. The new routine requires a change in muscle control and it takes about 10,000 repetitions to learn something new. A person is vulnerable as they increase their control of movement through sport, but they should still strive for a variety of activity to protect their joints and increase overall tissue health.

It is impossible to teach correct posture until the mechanical joint dysfunction is resolved. In extension the spine is loaded and stable. This is a position of good posture. A person becomes stuck in flexion at the joint level simply due to repetition which includes sitting and prolonged standing. This is the beginning of bad posture. When the mobility at the joint level is returned to normal then posture can be addressed.  

Hormonal changes can affect the mechanical properties of dense connective tissues changing the tissue pliability.  Hormone changes do not cause pain. The adrenocorticotropic hormone of the pituitary and cortisone of the adrenal cortex both lower the GAG content of the extracellular matrix of connective tissues. Relaxin softens and increases the extensibility of ligaments.  Estrogen may also play a role in determining ligament strength. Hormone changes cause vulnerability to mechanical joint dysfunction because tissue pliability and the ability to control movement is altered.

Viruses also change tissue pliability.  This change in pliability alters the ability to control movement which increases mechanical vulnerability.

People start getting osteoarthritis at age eighteen, illustrating the breakdown of tissue overtime. Repeated tensile loading lowers the tensile strength of cartilage as it does in many other materials. Osteoarthritis can cause pain if there is an inflammatory process, which means that osteorthritis is not always a painful condition. People have osteoarthritic changes long before symptoms develop and they keep them long after the symptoms are relieved. When pain does occur, altered joint mechanics influenced by the anatomical change caused by the osteoarthritis is a likely candidate.

Studies of the tensile failure of cartilage are primarily concerned with the effects of repeated load, and age. Cervical disc degeneration is common; one study reports finding degeneration in over 80 percent of the cervical discs examined in individuals over 60 years of age.

There is an inflammatory component to osteoarthritis.  However, all forms of osteoarthritis, inflammatory or not, cause changes in muscle function such as weakness and reduced extensibility. These muscle function changes are only partly responsible for the movement restrictions that accompany osteoarthritis.

In a research study written in 1994, Jensen reported that 64 percent of people with an imaged radiographic problem had no symptoms. Lumbar disk herniations are often seen on imaging without symptoms.  Many people without back pain have disk protrusions or bulges.

Abnormalities are prevalent in the lumbar spine on MRI examination of people without back pain. Jensen illustrated that disk bulges or protrusions on MRI of people with low back pain and or radiculopathy may be coincidental. Jensen examined 98 asymptomatic people using a MRI. The scans were read independently by two blinded neurologists in a blind study. Only 36 percent of the 98 asymptomatic people had normal discs at all levels.  Sixty-four percent of the people without back pain had an intervertebral disk abnormality.  Thirty-eight percent had an abnormality at more than one level.17