Flexion dominant posture is an immense problem today.
This evokes the sternal costal reflex which, as we are well aware of, is a common cause of hyperventilation type syndromes. The anterior motion of the shoulders also causes a load to be applied to the latissimus dorsi, thereby involving the entire back force transmission system. The back force transmission is made up of two superior slings: the oblique dorsal muscle-fascia-tendon slings; and the ventral muscle tendon slings, including the lower component (a continuation of the dorsal sling that ends or begins with the sling formed by the tibialis anterior and the peroneus longus muscles).
Clearly from an understanding of the proceedings of the 1st and 2nd Interdisciplinary World Congress on Low Back Pain, and the works of Gracovetsky, Farfan, Vleeming and Dorman, we can easily see that the thoracic spine itself is not a common primary cause of subluxation, but rather an area of significant compensation from both above and below, and subject to all the forces applied to it from the ribs and extremities.
If we take any one of the aforementioned muscle groups (e.g., the pectoralis major) and subject it to close scrutiny, we can note what transpires. Short pectoralis majors, as a result of postural changes on a time continuum, or as a result of a load applied from below as in pelvic torsional dysfunction, will cause the shoulders to move anterior and internally rotate, thereby activating the latissimus dorsi. This anterior shift of the shoulders applies an axial compressive load to the clavicle and eventually the sternoclavicular joint. This compressive force causes joint dysfunction and sternal distension and evokes constant specific reflex compensatory spasms in remote muscles: multifidus, gluteus maximus, rectus abdominus, and the external obliques as well. The intercostal muscle spasm will inhibit proper ventilation, and breathing becomes shallow and rapid.
Shallow rapid breathing tends to increase alkalinity and activates the nociceptive pathways which react by causing reflex muscle spasm, sympathetic hyperactivity and vasoconstriction. The thoracic spine and rib cage are the recipients of this viscous cycle. Obviously the cause in this case is the pectoralis major; treatment should be directed at influencing the sternal costal joints, thoracic spine and costotransverse articulations by means of adjustive mobilizations using stretching of the pectoralis major muscle. There is no question that at some point the spinal joints will have to be adjusted, but in this case, they are not the cause and should be dealt with after the original and perpetuating factors are cleared.
A second muscle to be looked at could be the latissimus dorsi, and as was mentioned previously, it is activated from above by the pectoralis major shortness. The latissimus dorsi can also be activated from below by dysfunction of any of the components of the back force transmission system. The gluteus maximus, by virtue of a positive arthrokinetic reflex test, can load the contralateral latissimus dorsi via the thoracolumbar fascia and cause all of the aforementioned signs and symptoms of the pectoralis major shortening. The cause this time is in the transverse axis of the iliosacral joint, and the thoracic spine is the area of complaint. The treatment should be directed to the cause and not the thoracic spine initially.
Another example might be the pronated or hyperpronated transverse tarsal joints, either as a cause or a compensatory adaptation by the body to maintain a line of progression during the gait cycle. Reviewing quickly the gait cycle there is a harmonious relationship between the peroneus longus and the tibialis anterior muscle, and any osseous subluxation or compensatory alteration will disrupt this relationship. The disruption will either inhibit the Windlass effect of Hicks, not engaging the converging axes of the transverse tarsal joint or allowing for some half-hearted attempt at them during the toe-off phase of the gait cycle.
The result of this is the compensatory pronated foot. Pronation of the foot will engage the peroneus longus, which blends in with the distal aspect of the long head of the biceps (activated by the inferior dropping of the fibula during dorsiflexion of the foot). The long head of the biceps blends in and becomes continuous with the sacrotuberous ligament, which also amalgamates and becomes uninterrupted with the fascicular fibers of the multifidus muscle. The incessant load applied by this foot dysfunction has now reached the thoracolumbar junction and renders it hypomobile. The remainder of the thoracic spine and associated ribs now undergo compensatory subluxation and our patients present with thoracic pain. The cause was the pronated foot and the treatment should be directed at treating the cause -- the foot.
In all of the above examples, the thoracic spine was the presenting complaint and in none of them was the thoracic spine the primary subluxation. The chiropractic profession has always talked about treating the cause, and I agree, just as long as you know where it is. Remember the words of one of the great men in chiropractic, Dr. C.S. Gonstead, when he said, "Find it, accept it where you find it, fix it, and leave it alone." The key words are accept it where you find it. Can you find "it?"
Keith Innes, DC
Toronto, Ontario, Canada