The Brain and Muscle Guarding

When the brain senses bony instability or tissue damage in and around the spine, decisions are made that help determine the extent of threat to the individual and what actions need to be taken. One decision is layering the area with protective muscle guarding. By splinting the area with spasms, the hypercontracted muscle effectively reduces painful joints movements.  In the presence of joint dysfunction, the brain senses weakness through mechanoreceptors. The deep spinal muscles like multifidus are the first tissues affected by the motion restricted joint. Micro and Macro trauma can neurologically inhibit these deep muscles causing the brain to compensate and ask for recruitment from QL’s, psoas, and transverse abdominis.  

Remember too neurologically facilitate the release the articulating counterpart must be stabilized and the muscle contraction should be isometric with the intensity of the contraction controlled the clinician. The contraction therefore occurs in a precisely controlled direction with a precisely controlled joint position in all three planes and requires a distinctly executed counterforce. This is similar to what we call Muscle Energy Techniques.

The middle layer core support system is designed for stabilization to allow for extrinsic muscles and fascia to carry out movement in our daily life.  When they’re called in to substitute for the weak spinal group muscles and ligaments it can alter firing and alter activation patterns.  Prolonged joint fixation leads to aberrant movement and posture patterns which in time can be relearned as normal we call this neuroplasticity.

Remember that when a joint is moved beyond its acceptable range of motion or it’s barrier it can cause the facets to become locked open on one side or closed on the other. Dr. Stuart McGill found that when lumbar facet joint became displaced and fixated during a lifting incident the multifidus on the side of the fixated facets began to atrophy within 24 hours. 

The final stage of dysfunction occurs when the middle layer and deep myofascial support systems collapsed due to a joint dysfunction and the load is shifted to the outer layer dynamic muscles such as erectors, and lats.  Spasms develops as tissues designed for movement are forced to act as both movers and stabilizers.  These fast twitch muscles provide burst of energy and do not respond well to compressional loading and soon give out.

This is why we commonly see thickened ropes of erector spinae spasms on the ipsilateral side of the joint dysfunction. When these glucose burning tissues tire and spasm the lubricating fluid between fascia bags begins to dehydrate and the fascia envelops and adhere to neighboring structures often causing the bulk muscle tissue that we beat on session after session.  To help maintain flexibility joint castles require daily or at least frequent elongation to avoid cross linking of fibers.  Long-term joint fixation is a primary cause of reduced flexibility as calcium deposits enter the capsule and associated structures. One goal to help minimize this accumulation is to normalize afferent messages to the brain which will reduce protective muscle guarding around the dysfunctional joint.