Frozen Shoulder

CTB in frozen shoulder diagnoses

Sandy Efflandt avatar
Written by Sandy Efflandt
Updated over a week ago

Frozen shoulder comes about, in our experience, because the body has adapted over time to the experience of pain during movement, which feels like an injury to the nervous system. The shoulder is an extremely mobile and vulnerable joint, and is reliant for stability on the concerted effort of many muscles. When some of those become dysfunctional, the delicate balance is disturbed and nociceptive signals flow to the CNS.

Minor stresses and changes in the joint capsule may increase nociceptive load, such as minor fraying of tendons, arthritic development, or compressed joint spacing due to hypertonic muscles that cross the glenohumeral joint.

There are several other ways in which the body’s adaptation mechanisms feed into the frozen shoulder pain syndrome. The typical modern person who sits in front of computers and uses mobile devices a lot is highly vulnerable to what Dr. Vladimir Janda identified as “upper crossed syndrome”, in which the pecs adaptively shorten, protract and overpower the mid and low trapezius. The mid/low trap is one of the muscles that tends to de-facilitate, or go to sleep, when it’s neurologically overpowered by the anterior muscles that tend to pull the scapula into protraction.

Over time, the pecs and serratus anterior begin to bring the scapula into a constant state of protraction, which the trap cannot resist. To maintain some semblance of postural alignment and stability, the trap must be shored up so it can resist the pull. The classic hard inter-scapular area that we see in so many clients is the result of an extensive network of taut fibers in this area. The trapezius exists in a kind of limbo state - hardened at a level of mild stretch, but unable to function as an effective dynamic stabilizer of the scapula.

Taut fibers and trigger points aren’t just a sign of dysfunction. Taut fibers can be recruited by the body as a means of providing rigid support in a muscle without excess energy input. The body needs to provide more support in joints that evidence hypermobility or postural distortion.

The medical system tends to jump to the adhesive capsulitis diagnosis whenever there is reduced range of motion in the shoulder joint. There is no understanding in conventiional medicine of why this happens, or what to do about it. Patients are literally told to wait it out, and after 2 years the body will spontaneously let go of the adhesions.

We see things very differently. First of all, range of motion can be severely compromised by trigger points in muscles, without assuming that dramatic capsular changes have occurred. This is a protective action on the part of the CNS. Over time, fascial adhesions may gradually be introduced, but in any case our treatment is the same. By correcting the postural distortion and nociceptive inputs from both satellite and direct trigger points, the CNS can be retrained through movement to let go of its protective adaptations, including capsular changes. The latter are much slower to change than muscles, but change and normal movement are definitely possible.

Did this answer your question?