Stuart McGill, ddd spinal models

In an online interview with Bill Morgan, President of Parker University, world-renowned spine researcher and scientist, Stuart McGill, uses dynamic disc models from Dynamic Disc Designs to explain lumbar disc herniations, extrusions, and the mechanisms for lumbar disc injuries and treatments.

When treating spinal injuries, McGill stresses the importance of recognizing that the cause of most disc extrusions and herniations is a combination of factors, occurring over time. The cumulative array of factors may present as an acute condition causing pain, but in most cases, the disruption has not been created by a single loading event.

McGill uses the analogy of cloth to explain how repetitive loading and movement fray the collagen fibers that cover the socket joints, eventually working a hole into the fibers by repetitive stress strains occurring in a back and forth motion.

“The disc is layer upon layer of collagen fibers held together with [a tightly woven lamination matrix]. If you keep moving the disc under load, the hydraulic pressure of the pressurized nucleus slowly starts to work its way through the delamination that forms because of the movement,” he says.

He explains that when the collagen is intact and supple, a person has full range-of-motion without danger of creating tears, but when the spine is stiff and has become adapted to bearing heavy loads, it is in danger of injury.

“The problem comes when you combine the two worlds and confuse the adaptation process,” he says.

“In a modern lifestyle, you might have a person who sits at a computer for eight or more hours in a flexion stressed position which—on its own—may not be that bad. But then they go to the gym for an hour every night and start lifting loads. They’re taking their spine through the range of motion, so cumulatively, the collagen is asked to move, but it’s also pressurized. The nucleus behind gets pressurized and slowly works its way through the delaminated collagen.”

Stuart McGill, Models

Stuart McGill and the many ddd models he uses.

McGill, Dynamic Disc Designs

Professor Stuart McGill and Dynamic Disc Designs endorsement.

Recreating Compression Loading, Disc Bulge, and Proper Thrust Line with our Dynamic Model

Using the disc model, McGill demonstrates how the gel inside the disc remains pressurized under compression, but in cases where the collagen has become delaminated, bending the spine under a load creates a disc bulge.

“This is exactly what we see on dynamic MRI,” he says, manipulating the disc model to demonstrate. “In the laboratory we would inject the nucleus with various radio-opaque markers. We would watch the migration as the bulge would come through. Touch a nerve root and now you would match where the disc bulges with the precise anatomic pathway. If you sit for 20 minutes slouched and your right toe goes on fire, we know it’s the right ring and that’s exactly where the disk bulge is.”

McGill stacks the disc model into a thrust line and squeezes the spine segment to show how proper alignment adapts the movement experience.

“The whole disc is experiencing movement, but there’s no pressure, and nothing comes out to touch the nerve root,” he says.

Empowering the Patient with Simple Posture and Stress Exercise

McGill says his insight is based upon years of experiments studying the exact mechanisms of spinal injury and pain. He recommends using improved posture and stress—lying on the stomach for five minutes with two fists under their chin—to help,” mitigate the dynamics of that very dynamic disc bulge.”

He says the immediate relief provided by this simple exercise can empower a patient with discogenic pain and help alleviate the potential psychological trauma of feeling hopeless at not understanding the source of, or how to mitigate, pain.

Disc pressure, spine, patient education, models

A study 1examining cadaveric intervertebral discs (IVD) indicates disc degeneration is more closely related to reduced pressure associated with mechanical loading than levels of endplate porosity or thickness. Though endplate porosity increases as the IVD degenerates, the results of the study demonstrated that IVD degeneration is caused by reduced pressure in the nucleus—not the reduction of nutrient transport caused by endplate thickening and a reduction of porosity—and that mechanical loading from nearby discs contributes to endplate porosity in age-related disc degeneration.

disc pressure, degeneration

Disc pressure reduction with degeneration.

What’s at Stake?

Understanding the role of IVD endplate thickness and porosity and the role of mechanical loading, age, and sex on determining the efficacy of endplate function is important in the future diagnosis and treatment of disc degeneration. The enervated endplates, when damaged or degenerated, can cause back pain. When properly functioning, they are responsible for the transport of nutrients to the IVD, regulate fluid pressure and metabolite transport between the body of the vertebrae and its nucleus. Disruption in this process can contribute to disc degeneration, inflammation in the vertebrae, and possible infection to the disc.

The level of porosity inside the bony endplates affects the amount of nutrients delivered to the nucleus and the mechanical stability of the vertebrae. A porous endplate allows more nutrients and pressure-regulating fluid to flow into the nucleus of the IVD. A thickened, less porous endplate reduces the nutrient and fluid flow, but creates more structural stability in the IVD, reducing the potential for injury. The proper balance and porosity of the IVD unit is integral to the overall health of the disc, but understanding the mechanism by which the degenerative process occurs is essential in anticipating how a body’s mechanical functions might contribute to a disruption of disc health.

The Study

Researchers compared the relative thickness and porosity of IVD endplates in 40 cadaveric motion segments from 23 cadavers between the ages 48 to 98 years old. The segments were subjected to compression, and the intradiscal stresses were measured and analyzed. Stress profiles were created to determine the average nucleus pressure, as well as the maximum anterior and posterior annulus pressure. The segments were dissected, and discs with endplates on each side were scanned and analyzed for their thickness and porosity in the midsagittal regions. An average value was calculated for the anterior, central, and posterior regions of each of the endplates. A macroscopic and microscopic examination determined the scope and level of disc degeneration in each segment.

The Results

The results of the data sets indicated that nucleus pressure and posterior and anterior annular stresses decreased as the disc degeneration levels increased. There was a slight increase of intradiscal pressure (IDP) with age, but there was no maximum stress increase of the annulus with age. Lower spinal levels were associated with a decrease in IDP.

The endplates were thinner nearer the nucleus, with a 14 % reduction in thickness in the inferior endplates. An analysis of the averaged data set from the three regions of both endplates showed no association between age or level of degeneration and endplate thickness, but there was an inverse relationship between the disc degeneration and endplate thickness. There was a strong relationship between endplate thickness and IDP in an analysis of adjacent discs.

Endplate porosity was more pronounced in the center of the endplate and became less so opposite the annulus. This porosity was not age-dependent but—with the exception of the anterior endplate region— was positively correlated with disc degeneration levels. The levels of endplate porosity was inversely associated with adjacent disc pressure and stress.

Discussion

Endplate thickness was the major determinant of endplate porosity levels. Disc degeneration and mechanical loading measures were also indicated as predictors. The most apparent predictors of endplate thickness (after porosity) included disc pressure and spinal level. IDP was the dominant predictor of disc degeneration.

The study found that disc degeneration was associated most often by disc stress, rather than porosity of the endplate or its thickness. As the levels of disc degeneration increased, porosity of the endplate increased. The porosity of the adjacent disc was inversely affected in terms of pressure and mechanical stress.

Wolff’s law posits that the body’s bone mass and design will compensate for the pressures of mechanical stresses and subsequent anatomical deformation, strengthening the endplates and vertebrae that are subjected to the most physical activity. Reduced loading can thin endplates that are not subjected to pressure. This eventually leads to them becoming more porous. The results of this study affirm this theory, as the lower central endplate regions were harder, thicker, and stronger than those of the anterior-posterior endplate regions. There is an apparent compromise between the strength of the outer bone and the porosity of the central endplate, which allows for stability and nutrient flow where they are needed the most.

There is an evident drop in nucleus pressure during progressive disc degeneration. The reduction of fluid pressure lessons the endplate’s thickness and makes it more porous, leading to bone degeneration and loss. The bone is more likely to buckle and further degrade as it becomes more porous and less stable, reducing nucleus pressure further. This cycle of abnormal pressure reduction is responsible for the continuation of the degenerative process—not the reduced metabolite transport. There is an increased risk of bone fracture with increased porosity and endplate thinning. A fracture would increase stress on the IVD and contribute to the cycle of degeneration, in spite of the increased availability of nutrients that can reach the nucleus through the endplate’s porosity.