Synergistic Dominance, Arthrokinetic Dysfunction, and Lumbo-pelvic Hip Disorder
excerpted from Dalton (2010) Advanced Myoskeletal Techniques
Synergistic dominance is a self-serving substitution system that allows us to carry on with life even though parts of our structure may be slowly breaking down and decompensating.
A typical synergistic substitution pattern often exists in runners with a unilaterally tight/hypertonic iliopsoas (hip flexor) that is reciprocally inhibiting the ipsilateral (same side) gluteus maximus. The hamstrings and adductor magnus (synergists in hip extension) are overly recruited to aid the weakened gluteus maximus in hip extension efforts. This substitution pattern is one of the primary causes of hamstring pulls and is initiated by the late firing of the weakened gluteals during hip extension, especially during activities that include running.
Synergistic dominance eventually leads to a more serious condition called Arthrokinetic Dysfunction, which is the result of prolonged alterations of length-tension forces at a joint, that result in abnormal joint movement and loss of joint play. Synovial fluid dries and cartilages degrade under these conditions. If gone undiagnosed and/or not correctly treated, surgery is sometimes the only answer.
When overworked hamstrings are recruited to compensate for a weakened gluteus maximus, the constant unilateral tug on one ischial tuberosity slackens the sacrotuberous, sacrospinous, long dorsal, and sometimes the iliolumbar ligaments causing the pelvis to lose alignment and stability. The brain frequently forces the piriformis muscle on the affected side into a state of sustained isometric hypercontraction to help stabilize the SI joint. Since muscles (contractile tissue) are not designed to be restraining tissues, problems are soon reflected in painful conditions such as piriformis syndrome, unilateral extended sacrums, backward sacral torsions, and lumbosacral dysfunction.
A common arthrokinetic dysfunction suffered by many running athletes is termed the Lumbo-pelvic Hip Disorder. Typically, this imbalance presents as a unilateral dysfunction. The following muscles tend to be short/tight on one side only: iliopsoas, piriformis, rectus femoris, adductors, latissimus dorsi, and lumbar erectors. The lengthened/weak muscles which permit the asymmetry are gluteus maximus/medius, biceps femoris, transverse abdominus, internal obliques, mutifidi, and some pelvic floor muscles. The painful hip condition that ensues is a result of a unilateral pelvic tilt, functional short leg, compensatory lumbar scoliosis, and jammed lumbar facets on the side opposite the anteriorly/inferiorly rotated ilium.
The pain that accompanies this torsional postural pattern can irritate the superior and/or inferior gluteal nerves. These branches of the sciatic nerve exit on the sacral plexus located on the anterior side of the sacrum. The superior gluteal nerve supplies the gluteus medius/minimus and tensor fascia latae muscles and is often mis-assessed as greater trochanteric bursitis. If the client has trouble lying on one side, the therapist should suspect trochanteric bursitis. But, if the pain comes and goes in the absence of hip movement, one should suspect superior gluteal nerve problems usually a result of SI joint dysfunction.
Inferior gluteal nerve pain is one of the most common incorrectly assessed disorders seen in pain practices. When agitated, (usually SI problems) the inferior gluteal nerve refers pain into the gluteus maximus. This “pain-in-the-butt” irritation is commonly (but wrongly) treated as piriformis syndrome. Beating on the piriformis, particularly the muscle belly, will cause even greater irritation of the inferior gluteal nerve.
Agitation of either of the gluteal nerve branches may be caused by:
- Repetitive movement at work;
- Athletic movement patterns;
- Prolonged sitting;
- Improper lifting.
Frequently, this type of arthrokinetic dysfunction is so intense that it excites alpha and gamma gain in surrounding muscles causing sympathetic spasm and involuntary tightness in all the hip extensors and abductors. As the spasm digs deep into the SI and lumbar joint capsules, all associated hip and back muscles become inflamed and are subjected to increased accumulations of waste products at the injured site. The brain continues to layer the area with spasmodic tissue to protect sensitive nerve structures. This process only serves to further shorten the lumbopelvic connective tissues often creating tissue micro-tearing and increased inflammation.
As this self-perpetuating pain-spasm-pain cycle splints the area with muscle guarding, vital blood supply is choked off causing disruption of the body’s self-regulating mechanisms. The brain attempts to prevent excessive movement by forming dense collagen adhesions or knots that encase and “cast” the muscle. Because the brain fears the muscle itself may be damaged, it tries to protect it…much like a doctor would when casting a broken arm.