Research

Spinal - Pelvic Syndromes

As with all other joints, the sacroiliac joint is moved by the muscles that attach to the bones that make up the joint. With this realization, we should understand that, because a substantial mass of the muscular system directly attaches to the pelvis, any dysfunction in the sacroiliac joint will directly affect spinal and pelvic balance and coordination. The muscles that attach to the pelvis, both Nutators and Counternutators, extend out to the spine and extremities and directly influence joint angles and range of motion, and initiate, or become complicit in, dysfunctional syndromes throughout the structure; the pelvis torques, the spine twists and the curves alter in both A/P and Lateral aspects. As the core goes, the rest follows.

Pelvic Torsion: AS/PI
Similarities to the above compensation patterns have been described by Gonstead, a pioneer developer of chiropractic methodology. Herbst [1], referencing Gonstead, stated “When the ilium becomes misaligned, it does so in relation to the sacrum, and the actual misalignment occurs in the sacroiliac articulation.” The ilium may travel either in an anterior and superior (AS) or posterior and inferior (PI) direction. Additionally, the ilium will appear to rotate internally (In) or externally (Ex) when viewed on an x-ray film. Gonstead pointed out that the ASIn ilium will show loss of the lumbar curve and the PIEx ilium will show an increased lumbar curve [1]. Gonstead further stated that, on an AS ilium, the posterior aspect of the joint opens and will demonstrate a palpable fluidic, spongy feel, indicating inflammation and nerve irritation. The foot will rotate laterally, and pelvis will rotate to the contralateral side. Misalignments of the ASIn ilium are consistent with the counternutation response to the sacroiliac nutation lesion. The compensatory counternutation pattern relates to the ASIn as the compensatory nutation pattern relates to the PIEx.

Facet Syndrome
Posterior compression of the lumbar vertebral spine occurs with a concurrent posterior shift of the gravitational line, placing more pressure on the facets. Because the facets both transmit load and participate in movement, their surfaces will grind under the added compression, especially during gait, introducing excess shearing forces to the facets, along with the excess axial force. Eventually, the facets will become irritated and possibly inflamed.

Lateral Canal Stenosis with Nerve Root Impingement – e.g. Sciatica
When counternutation goes beyond normal range of motion, the lateral canals from L3-L5 become compressed and narrow (see Lateral View). This overcompensation pattern may place pressure on the nerve root and lead to various nerve entrapment syndromes, including sciatica.

Disc Herniation
The counter-rotation at L3-4 and L5-S1, combined with posterior disc compression, will cause significant stress on the posterior annular fibers of the discs, as they grind with every breath and every step. Over the course of years, the posterior annular fibers will break down and weaken. In erect posture, there is little danger of the nucleus herniating posteriorly because the posterior aspect of the vertebral unit is narrowed by the vertebrae themselves. The anterior fibers will not be markedly damaged, so they will contain the nucleus anteriorly. However, once the person bends forward, the lumbar spine flexes, the posterior aspect opens, and when the degenerated posterior annular fibers are insufficient, the nucleus herniates. Lifting a heavy weight will magnify the chance of herniation but, if the annular fibers are weak enough, it can happen when the person simply bends forward. Preventive treatment options include decompressing the lumbosacral area, by gently flexing the lumbosacral hyperlordosis before the annulus is significantly damaged (see Serolatrac – coming soon).

Spondylolisthesis
With compression of the posterior aspect of the vertebral unit, the anterior aspect widens, and centrifugal force generates anterior movement of the lower lumbar bodies. If this compression occurs before the vertebral growth plates fuse, the parts interarticularis may weaken and fracture, causing anterior movement of the superior vertebral body.

Lumbosacral Hypomobility – Sacroiliac Hypermobility
The posterior compression of the lumbar facets will cause increased shearing forces and reduced motion in the lumbosacral spine. When motion is limited, at any vertebral unit, the vertebrae above and below will compensate with extra motion. In turn, some of the motion that should occur in the lumbosacral spine, particularly during gait, will transfer to the sacroiliac joint, inducing greater hypermobility, in a positive degenerative cycle; i.e., sacroiliac joint hypermobility – lumbosacral hypomobility – sacroiliac joint hypermobility.

Straight Back Syndrome (SBS) aka Anterior Thoracic Vertebrae (ATV)
The initial spinal movement following a nutation lesion will be to rotate and laterally bend towards the side of lesion. Eventually, due to vestibular righting reflexes [2]p34-36, the upper trunk will rotate counter to the lower trunk, causing a twisting of the thoracic spine , as normally expressed through gait. Although this is a normal part of cross-crawl patterning, it becomes problematic if the spine remains in the twisted position, instead of fully reciprocating from side to side. In the compensation to a Nutation Lesion, the twisting will be emphasized and persist relative to the degree of lesion, in accordance with the relative positioning of the AS/PI pelvic torsion, and other structural adaptations. As a result, the upper thoracic curve will flatten, as noted by Lovett [3], who noted that a bent rod will straighten when twisted. In agreement with Lovett, Panjabi [4] stated that “as the spine is laterally bent or axially rotated, it has a tendency to straighten (go into neutral position) from the flexed or extended postures.”

In the normal thoracic spine, the vertebrae and ribs are evenly spaced and move well. However, when the thoracic spine flattens, the space between the each rib and between each thoracic vertebra becomes compressed. Eventually, the space narrows enough to generate sufficient compression to force the vertebrae to shift anteriorly and rotate out of place. Although they may be adjusted back into place, the continued pressure pushes them out again. Like the cervicooccipital and lumbosacral areas, the thoracic area should be decompressed to help the vertebrae move posteriorly and realign, otherwise subluxations in those areas may remain chronic (see Serolatrac – coming soon).

Straight Back Syndrome has been associated with cardiac problems; some information is available in free access articles from chiropractic [5] and medical [6] viewpoints.

Scoliosis
Scoliosis may be seen as an example of a severe reaction to a sacroiliac nutation lesion prior to growth plate fusion. Because it is beyond the scope of this article to provide a detailed explanation, we will look at mainly one muscle group, the erector spinae (see Deep & Superficial Erector Spinae) . With a right sacroiliac lesion, a counternutation effect will occur on the right side, activating the longissimus thoracis pars lumborum and iliocostalis lumborum pars lumborum, which flex and rotate the lumbar spine to the right. At the same time, a nutation pattern occurs on the left side, activating the longissimus thoracis pars thoracis and iliocostalis lumborum pars thoracis, which flex the thoracic spine to the left, with slight left rotation, counter to the right rotation of the trunk. In an uninjured person, the above actions provide a synergistic counter-rotation of the shoulders and pelvis that occurs during gait. However, in a right sacroiliac lesion, the actions of the right counternutation and left nutation muscles are intensified and prolonged, while the opposing muscles are proportionately inhibited, leading to rotational and flexion imbalances. The lumbar spine flexes and rotates to the right, and the thoracic spine flexes and rotates to the left, and an “S” curve begins to develop at a rate of about 23,000 contractions a day (considering respiration and gait). The severity of the mal-alignment is proportional to the degree of ligament sprain and continued re-injury, and may lead to a permanent “S” curve.

Other factors contribute to this complex. When the right sacroiliac joint suffers a nutation lesion, muscle slings such as the left internal and right external obliques combine to protect the right sacroiliac joint by pulling the trunk inferiorly and to the right. The right latissimus dorsi combines with the left gluteus maximus to provide the same motion, but from the posterior aspect (see Muscle Slings). As a result, the pelvis will rotate to the left and, relative to the innominates, the sacrum and spine superior to L4 will rotate to the right. Due to normal coupling mechanisms, the upper lumbar spine will also laterally bend to the right, rotating the vertebral bodies toward the concavity of the curve. The lumbar spine carries the trunk, bringing the left shoulder anteriorly and inferiorly, towards the right hip, while the right shoulder is rotated posteriorly, placing the head to the right of the gravitational line.

The body’s vestibular balancing mechanism (righting reflex) always seeks to maintain, or regain, an erect position. Whether from a quick fall or the gradual effects of chronic muscular pull, the spine compensates by twisting and bending to provide this positioning. The upper thoracics, being more mobile than the lower thoracics, will laterally flex and rotate to the left. Over time, a compound curve will develop, with the apex of the lumbar curve to the left and the apex of the thoracic curve to the right. In both curves, the bodies will rotate into the concavity. This double curve has been demonstrated to be a normal response to a left total scoliosis (where the spine, as a whole, bends and rotates to the right) on both live subjects and cadavers [3].

Since the lumbar bodies of both curves are more in line with the gravitational force, they will carry a larger load than the convex part of the curve. Over time, due to the plasticity of the bones in children, the vertebral bodies may deform and rotate towards the convex side of the curve in order to avoid the increased gravitational pressure [7]. Other neurological factors may also influence the body rotations as part of a total complex. Once the bodies rotate to the convexity of the curve, it is considered pathological.

On an adult, fully formed vertebrae should prevent the development of pathological curves. However, the muscular patterns will create a tendency toward development and maintenance of a compound curve, which may manifest as stress points, e.g. subluxations, along the spine and rib cage. This developmental pattern has been documented by Lovett as early as 1905 [7]. What was unknown, until now, is what initiated this pattern. The Serola Theory proposes that the initiating factor in the compound curve, and potential pathological scoliotic pattern, is the Sacroiliac Nutation Lesion.

In this study, most of the muscles discussed are involved with the pelvic portion of this counter-rotation. More research is needed on the muscles that rotate the cervical and upper thoracic spine and shoulders, based on the biomechanical effects of the Nutation Lesion.

References:
1. Herbst, R.W., The A-P Ilium Misalignment, in Gonstead Chiropractic Science & Art. The Chiropractic Methodology of Clarence S. Gonstead, D.C. 1980, Sci-Chi Publications. p. 1-11.
2. Chusid, J.G., Correlative Neuroanatomy & Functional Neurology. 1979, Los Altos, CA: Lange Medical Publications.
3. Lovett, R., The Mechanism of the Normal Spine and its Relation to Scoliosis. Boston Medical and Surgical Journal, 1905. CLIII(13): p. 349-358.
4. White, A. and M. Panjabi, Clinical Biomechanics of the Spine. 2nd ed. 1990, Philadelphia, PA: J.B. Lippincott Company.
5. Gold, P.M., et al., Straight Back Syndrome: positive response to spinal manipulation and adjunctive therapy - A case report. J Can Chiropr Assoc, 2013. 57(2): p. 143-9.
6. Esser, S.M., M.H. Monroe, and L. Littmann, Straight back syndrome. Eur Heart J, 2009. 30(14): p. 1752.