Disc Wedging: Is the Gonstead Model Correct? Some Thoughts

From the June 2008 The “G”Note

What is the cause of the intervertebral disc wedging that we see in vertebral subluxations? Is the original mechanism described in the Gonstead Technique correct? This is an opinion based upon ongoing studies into this issue.

According to the Gonstead Disc Concept that was developed in the 1950-60s and described in Chapter 5: Mechanism of Vertebral Subluxation in the Gonstead Chiropractic Science & Art, disc bulging pushes against the proximal anular fibers. This non-compressible material elevates the disc at the point of bulging. In the model, the bulging tends to go anterior or anterolateral. It is seen on the lateral x-ray wherein the opposing vertebral body endplate lines diverge or “open” to the anterior. On the AP film, if there is a lateral component to the bulging, lateral wedging occurs, that is, the endplates diverge or “open” laterally due to ipsilateral bulging. (Herbst 1970)

Diagram of bulging disc between vertebrae

from Herbst RW. Chapter 5

From what I can discern, the opposite scenario occurs. As we know and as is stated in Chapter 5, disc bulging and herniation tends to occur posteriorly or posterolaterally – early signs of disc degeneration are prevalent in the posterolateral region. (Best et al 1994) If the Gonstead Disc Concept is true, the divergence should occur to the posterior if the bulging is posterior. We rarely see posterior divergence of the endplates in a subluxation. outside of a thoracic spine or sacral base subluxation. Opposing endplate lines divergence is usually to the anterior in subluxation. We usually see comparable but not increased anterior disc height as compared to adjacent segments and approximation of the posterior aspect of the opposing vertebral bodies.

Here are my thoughts on the disc model and why. A considerable amount of disc research has been done since the “Chapters” were published. We can now get a better understanding of what is going on in the disc than what was understood at the time the “Chapters” were published.

Following injury to the disc that causes internal disruption, tears begin to form in the anulus. This may be due to direct injury to the anular fibers and/or acute disc swelling (“disc ingestion”). When there is bulging of the nucleus into the anulus, radial tears form. (Yu et al 1988) Herbst also talks about pressure from the nucleus stretching anular fibers beyond their elastic limits and damaging its fibers. (Herbst 1970) When radial tears broach the innermost anular layers, the containment boundary formed by the inner anulus is disrupted and nuclear material penetrates into the anulus. Fluids go from areas of high pressure to lower pressure due to their non-compressibility.

Both static and dynamic axial compressive forces on the disc has an effect on the biochemistry of the disc. As disc wedging progresses, there is asymmetrical distribution of compressive forces on the disc. It has been found that the highest compressive stress occur in the posterior region of the disc. (Lotz et al 1998) This will undoubtedly have a tremendous effect on this region of the disc where the endplates are approximating (the narrowing wedge side) and probably leads to futher damage and narrowing of the disc space. The results are both biochemical and biomechanical alterations. Fixation and other pathobiomechanical alterations cause further alteration of the dynamic compressive forces on the disc.

Prolonged high compressive forces on the disc (e.g., subluxation?) alters the collagen content. Normally, the anulus has more type I collagen than the nucleus. Type I collagen has limited water content which give the anulus an ability to manage tensile stress. The nucleus has more type II collagen. Long term high compression increases type I collagen and decreases type II in the nucleus. (Hutton et al 1998) Healthy nuclear disc cell population and hydration creates the needed tensile stress on the inner anulus – circumferential hoop stress. This is required for proper function of the healthy anulus. An decrease on water content and cell population adversely affects the tensile stress of the anular collagen fibers. (Lotz et al 1998) If the posterior aspect of the disc is already damaged, this probably aggravates the condition and leads to increased disc wedging and degradation of the disc.

In addition, the vertebral body fails before the anulus under axial compression. (Lotz JC et al 1998) Endplate damage disrupts nutrient transport and results in degradation of the disc. Static compression stress has been shown to cause cell apoptosis/cell death. Lotz et al found that the loss of cell synthesis leads to disorganization of the inner anular lamellae. (Lotz JC et al 1998) This would compromise the ability of the inner anulus to contain the nucleus. The loss of cells and water changes the normal osmotic pressurization in the nucleus which compromises the ability of the disc to resist compressive stresses and further reduces its ability to maintain its biochemical balance.

Haschtmann et al found that endplate fractures sets the stage for disc cell apoptosis or cell death in both the nucleus and anulus. Pro-apoptotic proteins, FasL and TNF-α, were in the nucleus, and matrix metalloproteinase-1 and -13 were found in both the anulus and nucleus after endplate damage. (Haschtmann et al 2008) Disc cell synthesis becomes impaired, and this results in the inability of the disc to maintain hydration and leads to further degradation of the disc and disc space.

Water is regularly forced out of the disc by compression and returns when compression is reduced, primarily through the endplates. (Best et al 1994, Lotz et al 1998) Endplate damage would compromise this process, particularly in the damaged areas.

The altered structures – e.g., torn anular fibers, infiltration of nuclear material into the anular layers, changed chemical composition of the anulus and nucleus, and lost fluid, collagen, and the matrix – changes the optimal instantaneous axis or center of rotation (IAR), both its location and size. The abnormal IAR may cause progressively abnormal changes to the IAR and may lead to further misalignment of the spinal motion unit and disc damage, and therefore, the probability of greater disc angulation or wedging. In damaged discs, the size of the IAR of each motion may become larger and its location may change and become variable. Some call this “scattered” IAR. Greater “scatter” of the IAR is found in degenerated discs. (Schmidt et al 2008) In a healthy spine, the IAR of each motion unit is finite in size and location for each motion – axial rotation (θY), flexion/extension (θX), lateral bending (θZ), and couple motions. (It’s likely that one of the benefits of the adjustment is to optimize the size and location of the IAR).

Why would the disc remain normal height or increase in height in the anterior? The collagenous matrix – the framework of the nucleus – helps to maintain the disc height along with water. It may be that the matrix and proteoglycan synthesis is still active in this area or more active than that in the damaged regions as damage to the anulus here is minimal or not present. The hydrophilic proteoglycans maintains the water level in the disc. Later, with further degeneration, even the anterior aspect loses the ability to function normally, and the entire disc space is compromised (as seen in D5 or D6 stage of disc degeneration).

Numerous factors are involved in disc wedging and degeneration. It appears that disc wedging is caused initially, in the majority of cases, by damage to the posterior region of the disc. Nuclear material is forcefully pushed into and damages the inner anular layers and the vertebral endplates. There is leakage of nuclear material into the damage anular areas. Nutrient transport is impaired and reduces the synthesis of disc cells and hydration of the disc. Proteins that promote cell death or apoptosis proliferate. The process probably occurs asymmetrically. Hence, disc wedging occurs. In other words, rather than the nuclear material bulging against the anulus and raising the disc height, it lowers the height as nuclear material is disbursed and not replaced. Noxious input to mechanoceptors – proprioceptors and nociceptors – around the disc and peridiscal structures causes reflex responses of muscles and other tissue. Prolonged noxious inputs exacerbate the conditions that lead to worsening the subluxation and disc wedging. Added to this are zygapophyseal joints orientation, alterations to the paraspinal musculature tone, and other spinal and paraspinal factors. If the disc damage is primarily to the anterior, the peridiscal factors may be important contributors to “closing” the wedge to the posterior. Disc damage with contributions from these other factors is probably the cause of disc wedging.

This is an opinion on the topic of the cause of disc wedging in vertebral subluxation. Due to limitations on space, this is only a brief paper. I am further exploring the topic as I update the 1960s era Gonstead disc model. Comments are welcome. Like all chiropractic techniques and all other clinical procedures, nothing is “set in stone” in clinical science, and like Dr. Gonstead, we must continually study and advance the technique to better serve humanity.

References
Best BA, Guilak F, Setton LA, et al. Compressive Mechanical Properties of the Human Anulus Fibrosus and Their Relationship o Biochemical Composition.
Spine 15 January 1994; 19(2):212-221.

Haschtmann D, Stoyanov JV, Gédet P, et al. Vertebral Endplate Trauma Induces Disc Cell Apoptosis and Promotes Organ Degeneration In Vitro. European Spine Journal February 2008; 17(2):289-299.

Herbst RW. Chapter 5: Mechanism of Vertebral Subluxation. In: Herbst RW. Gonstead Chiropractic Science & Art. Mt. Horeb WI: Sci-Chi Publications. pp.49-64. 1970.

Hutton WC, Toribatake Y, Elmer WA, et al. The Effect of Compressive Force Applied to the Intervertebral Disc in Vivo. Spine 1 December 1998; 23(23):2524-2537.

Lotz JC, Colliou OK, Chin JR, et al. Compression-Induced Degeneration of the Intervertebral Disc: A In Vivo Mouse Model and Finite-Element Study. Spine 1 December 1998; 23(23):2493-2506.

Schmidt H, Heurer F, Claes L, et al. The Relation Between the Instantaneous Center of Rotation and Facet Joint Forces – A Finite Element Analysis. Clinical Biomechanics March 2008; 23(3):270-278.

Yu S, Haughton VM, Sether LA, et al. Anulus Fibrosus in Bulging Intervertebral Disks. Radiology December 1988; 169(3):761-763.