biomedical cause, LBP

An Australian study 1 into what male and female lower back pain (LBP) patients believe about the cause of their LBP flair-ups found that the subjects were most likely to attribute the source of their recent pain to biomedical causes, including active movements and static postures, rather than psycho-social factors. Though current evidence points to a positive correlation between mental health issues, including stress, anxiety, and depression, and LBP, few of the patients in this study attributed the onset of LBP flair-ups to psycho-social causes.

What’s at Stake?

LBP is the most common global cause of disability, lost income, and productivity decreases in the marketplace. Post-acute LBP flair-ups contribute to chronic job absenteeism and economic disruption at the individual and collective societal levels. While many studies have investigated the various causes of acute LBP episodes, few have focused on the fluctuations and triggers of LBP flair-ups.

Initial episodes of LBP are considered by health professionals to be overwhelmingly biomedical/biomechanical in origin, and most patients when queried agree with that assumption.

This study was conducted to determine what LBP patients believe about the triggers of their LBP flair-ups, in the hope that better understanding patient views will lead to more effective management of intermittent, non-acute episodes of LBP.

 

Professional LxH Dynamic Disc Model

Professional LxH Dynamic Disc Model

The Study

One hundred and thirty male and female volunteer subjects with episodic LBP participated in the online study by answering questions about their beliefs about the triggers for their flair-ups. Their answers were analyzed for common factors and were then clustered into various themes and codes by similarities. These common codes were further categorized into two overarching themes—biomedical, and non-biomedical triggers.

Overarching Theme: Biomedical Triggers

More than eighty-four percent of the subjects identified their LBP flair-up triggers as biomedical. Active movement and static postures were the most commonly identified biomedical causes for this group’s LBP recurrences. Patients reporting active movement as a trigger for their recurring LBP were most likely to cite bending and twisting as the most frequent instigator of their pain. Many of these patients felt that the quality of these movements played a role in initiating their LBP. In these cases, it was not the movement itself, but the way they performed the movement that caused their pain.

Roughly 5 percent of the patients reporting active movement as the cause of their LBP flair-ups believed it was repetition of the movement that was responsible for their pain. They claimed that “overdoing” a task could lead to LBP episodes.

Some of the patients reporting biomedical triggers believed their LBP was caused by biomechanical dysfunction. Roughly two percent reported motor control issues, and another 2.3 percent blamed their pain on spinal damage of some kind. Other biomedical themes included knee pain, endometriosis, and constipation. Some patients felt their LBP flair-ups were caused by lack of exercise, and others blamed work for their pain. Two percent reported their flair-ups were caused by not taking maintenance pain medications as prescribed.

Other biomechanical causes included participation in sex, wearing the wrong shoes, and medical treatments.

Overarching Theme 2: Non-biomedical Triggers

Only 15.2 percent of the subjects questioned reported non-biomedical triggers as the source of their LBP. Two participants—one male, and one female—believed the cause of their flair-ups to be related to stress or the weather. A few reported psychological factors—including anxiety, the lack of creative outlets, family problems, and depression— as potential triggers of pain.

The patients who claimed the weather was a factor in their pain were most likely to blame a drop in barometric pressure or the cold. One patient believed the pain episodes were triggered by rain, temperature changes, or warm weather.

Two percent of patients who attributed their discomfort to non-biomedical conditions blamed irregular or bad sleep qualities for their pain. Roughly 1 percent felt their diet had something to do with their LBP flair-ups, and another 1 percent blamed fatigue.

Conclusion

More than half of the patients with intermittent LBP flair-ups believed their pain was caused by biomedical dysfunctions, and only a few believed the source of their pain was something other than biomedical problems. Active movements and static postures were the most cited triggers for LBP.

The findings in this study are consistent with previous literature about what patients believe to be the cause of their LBP. However, the lack of patient emphasis on psychosocial causes of LBP contrast with current evidence that indicates a positive correlation between psychological or mental states and persistent LBP.

The authors of this study emphasize the importance of further research into the validity of the triggers identified by the LBP patients in order to better understand LBP flair-ups and how those experiencing them conceptualize the event. Evidence indicates the efficacy of patient-centric treatment in LBP clinical outcomes, and better understanding what patients believe about their pain will help clinicians to identify more effective treatment plans to manage recurring LBP in their patients.

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.

degenerative, MRI, low back pain

A retrospective magnetic resonance imaging (MRI) analysis 1 of lumbar degenerative changes in 283 patients with chronic low back pain (CLBP) found more severe disc degeneration (DD), lower disc height, and more extreme disc displacement at the L4–L5 and L5-S1 of patients with work-related CLBP. The results of the study help to elucidate MRI-visible changes and clinical attributes of work-related CLBP.

What’s at Stake

Lower back pain (LBP) affects up to 84 percent of the world population at some point in life and can contribute to acute or chronic disability in up to 12 percent of those affected. As of 2016, LBP was the leading cause of years lived with a disability, and the U.S. economic burden of LBP is estimated to be somewhere between 84.1 billion to 624.8 billion dollars. Understanding the various stages and degenerative characteristics of LBP can help with appropriate and timely treatment, which may help to reduce cases of CLBP. MRI allows physicians to recognize pathologies, so they can appropriately plan treatment for their LBP patients.

Study Design

The study involved the retrospective review of medical records of adults who had sought treatment for CLBP that had lasted for a period of greater than three months. Inclusion requirements included MRI scans of the entire lumbar spine and clinical lumbar evaluations. Excluded were patients under 18, or those whose LBP was intermittent or had not occurred every day for at least three months. Those experiencing pain that outranked their LBP elsewhere in their body were also excluded from the study, as were patients who could not have an MRI, who had a lumbar infection, spinal trauma, tumor, deformities, or spontaneous septic spondylodiscitis or epidural abscess, previous back surgery, osteoarthritis of the hip, and significant psychological disturbances.

Subject demographics were collected and analyzed, including their occupations, how many hours per week they worked, heavy lifting or lengthy desk sitting involved in their jobs, and the age, sex, body mass index, education level, smoking history, and duration of their LBP. Their LBP scores were recorded using a Visual Analog Scale (VAS) from 0 to 10 (no pain to worst pain). The Oswestry Disability Index (ODI) was used to rank each subject’s functional capacity, where those with a lower percentage were rated healthier.

Imaging Analysis Results

Pre-treatment MRIs of three positions—neutral, flexion, and extension—were performed on each subject by two experienced radiologists and then independently evaluated by an orthopedic surgeon. The subjects were grouped according to their MRI results. The four groups included: normal disc (ND), degenerative disc (DD), bulging disc (BD), and herniated disc (HD). Statistical analysis was performed using special software, and clinically-significant value was assigned. Of the 283 patients with CLBP taking part in the study, 110 were women, and 173 were men, and they ranged in age from 18 to 80, with a mean age of 41.8. The post-MRI groups included 37 subjects in the ND group, 85 in the DD group, 123 in the BD group, and 38 in the HD group. The mean age of the patients in the ND group was significantly lower (31.9) than that of the DD group patients (42.8), HD group (39.3), and the BD group (44.9). The ratio of male to female across all groups was 6:4, but the ratio in the HD group was 84.2 % male to 15.8 % female. The duration of CLBP across all groups was roughly 25 months, but when analyzed group-to-group, it progressively ranged from 15 to 25 months, with the ND group at the lowest range, followed by the DD, BD, and HD groups. The duration of pain was significantly increased from the ND group to the BD group. There were few differences in age, smoking history, or education levels across the groups.

The subjects were further categorized into 10 groups based on their occupations. The three groups that were most prominently represented in the ND, DD, BD, and HD groups were manual workers, desk workers, and technicians. They were similarly represented within their groups. Working hours were also similar across these groups, between 59.7 and 63.2 hours per week. The percentage of subjects who were required to manually handle weighty objects at work was significantly lower than those with no manual handling. The number of working hours spent sitting at a desk was much higher in the DD group, as compared to the other three groups.

When comparing clinical CLBP, the VAS pain scores in the DD, BD, and HD groups were much higher than those of the ND group members. The ODI scores of these three groups were also higher than those of the ND group, and those in the HD group were significantly higher than subjects in the DD and BD groups, indicating less functionality.

The MRI looked for the degree of DD in the neutral, flexion, and extension positions, as well as the vertebral height (anterior and posterior), slipping distance of spondylolisthesis in all three positions, height of the L1-S1 discs, disc bulge or herniation distance, AP diameter of the spinal canal, and translational motion. The data was analyzed and classified indicating the severity of disfunction or damage. The worst degeneration was at the L-4/L-5 and L-5/S-1 level, followed in severity by L-3/L-4.

The disc bulge distances of L-3/L-4 and L-4/L-5 were higher in the BD and HD subject groups. Also, the distance of L-4/L-5 was much higher in the HD group than in the BD group in the neutral position. The distances of L-4/L-5 were much higher in the BD and HD groups than in the ND and DD groups during flexion position, and that of L-3/L-4 was much higher in the HD group than in the ND and DD groups. The distances of L-4/L-5 and L-5/S-1 were much higher in the BD and HD groups during extension MRIs.

Conclusion

This study used MRI to analyze and compare four types of lumbar disc degeneration in patients with CLBP and found that the ND group represented a significantly younger demographic than that of the other three group members. This suggests that age is a likely contributor to DD in CLBP. The subjects in the BD group had a much longer mean pain duration than those in the ND group, suggesting a less successful clinical future outcome for those patients. There appeared to be little-to-no association between BMI and smoking history and CLBP in any of the subjects involved in this study.

There was a positive correlation between hours worked sitting at a desk—with those in the BD and HD groups working on average more than 60 hours per week and those in the ND and DD groups working fewer hours. Interestingly, the data collected indicated that most CLBP patients did not perform heavy manual labor at work and were highly educated—suggesting a strong connection between office work and CLBP. The MRI scans showed that lower lumbar disc segments (L-4/L-5 and L-5/S-1) were the most significantly degenerated in the CLBP patients, with lower disc height and displacement.

 

 

 

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.

 

 

properties of the annulus, disc model

Researchers examined the effects of endplate fractures  1 on the mechanical properties of the annulus fibrosis (AF) in porcine spinal segments and found that laminate adhesion strength was significantly compromised in the fractured spines. The findings suggest that microdamage may occur beyond the vertebra, into the interlamellar matrix of the AF—information that could be helpful in the diagnosis and treatment of adolescent spinal growth-plate fractures.

The Study

The authors of this study wished to examine the effects of high-intensity pressurization on the intervertebral discs (IVD) to see how it effected the mechanical and physiological properties of the posterior AF. They used 28 fresh, recently-thawed functional porcine spinal units from 14 porcine specimens that were approximately six months old.  Control units were also used as a comparative measure against the units subjected to pressure.

A hydraulic pump and high-pressure inflation needle were used to pump hydraulic fluid into the IVD of specimens. The researchers were careful not to pierce the AF in the samples. Pressure in the needle was measured by a pressure transducer and converted from analogue to digital at 2048 Hz. The needle was subsequently removed, and the vertebral bodies were assessed for damage. Although fractured endplates created an audible ‘pop,’ the condition was only confirmed after dissection of the IVD. The control-group segments were not tested for fractures. Measurements were taken following the dissection, and the end-plate area was quantified. Bilayer AF samples were then dissected and tested for tensile endurance in the circumferential direction. A second multi-layered sample was then dissected and subjected to delamination and a peel test. Mathematical ratios were then plotted to mark the variable results for each sample.

Results

End-plate size measurements remained consistent across the control and fracture group samples. Bilayer stiffness, toe-region stretch ratio and stress, and stress at 30% stretch were consistent in the control and fracture group samples. However, there was a clinically-significant variance in peel strength—but not peel strength variability— between the two groups. In the fracture group, the peel strength was 31 percent lower than in the control group. Dissection and manual delamination were significantly easier in the fracture group of samples, as well.

Discussion

The results of this study indicate that growth-plate fracture damage may not be limited to the vertebra and may cause microdamage in the nearby AF. This was indicated by the reduction of laminate adhesion strength in the posterior AF of the fracture IVD samples subjected to pressure in the tests. This information should be taken into account when practitioners are examining and treating adolescent or childhood vertebral fractures involving the endplates.

 

KEYWORDS: damage during spinal growth-plate fractures, effects of endplate fractures on the mechanical properties of the annulus fibrosis, effects of high-intensity pressurization on the intervertebral discs, mechanical and physiological properties of the posterior AF, delamination and a peel test, Bilayer stiffness, toe-region stretch ratio and stress

 

Dr. Jerome Fryer (CEO of Dynamic Disc Designs Corp):

“Hello everyone. Dr. Jerome Fryer here of Dynamic Disc Designs. I just want to reach out to those customers that have one of my models. There’s been a lot of talk lately on social media regarding how models can be scary. I don’t know how they’re scary. Models are not scary. It really depends on the user and these models are not intended to scare anybody. It’s to teach them their own anatomy, so they can improve their posture and biomechanics to relieve their symptoms. It’s a team player. It’s like a car. You can go out there ram into people or you can drive defensively and respectfully. Anyway, so one thing that’s important when you’re using the model is to relay realistic biomechanics  and use the model in a way that simulates real-time and load.

You want to use it in a way that actually represents the actual tissue. You can talk about all sorts of things, but you can talk about disc height changes as the disc over the course of the day loses a percentage of its height. You can talk about normal loading patterns of the disc as it relates the associated nerves. But, what I would encourage is just to use real-time forces. For example if someone goes to sit down, they change their lumbar angle and they compress their disc. When they sit for a period of time, the disc actually loses further height. You want to show the subtle endplate angle changes as it relates to the facet joint for example, or in the suspected case of disc herniation, you can actually create a disc herniation.

Single-Level Disc Herniation

Model of Single-Level Disc Herniation.

One example is the changing fluid expression over the course of the day. This is an important little graph to help patients understand how first thing in the morning you’ll actually lose their height very quickly in the disc height, so the facets will actually approximate with the changing intradiscal pressure, and then over the course of the day the disc height will slowly reduce. Some people talk about around 4:00 or 5:00 in the evening as the day progresses, my symptoms become pronounced. Then also with first lie down too. You can see there’s a quick change in disc height. Anyways, I just wanted to share with you that it’s how you use the model and you want to use it in ways that are realistic with regards to movement.”

 

 

 

spine pain, models

Ed Cambridge: “Our colleague Jerome Fryer created some models for us, and this is some of the work that has come out of our lab with you and Christian Balkovec about the dynamic changes we see after herniation. Where we have disc height loss at one level, creating hypermobility at the adjacent level. So here you can see, when you move the spine around there is a stiffening effect down in the lower joint and in the upper joint hypermobility. That’s what we see when an injury propagates from one joint to the next. The patient says, “Well, the pain used to be lower but now its starting to creep up my back a little bit.” “

Stuart McGill: “Fabulous. Another little take on that … By the way, these are all cast from real human specimens. So this is the real deal. Once again, Dynamic Disc Designs has been so clever in representing the biofidelity. We start to see how this disc has been damaged, and it’s quite lax as we move it around. So those micro-movements now are triggering pain just at that level. And this joint has normal stiffness, but then look what happens. Over time, the join changes because of the change in mechanics. The lax disc now cases a bit more arthritis in those facet joints, because they are now responsible for much more motion. So then, look what happens to the cascade. As the person now extends, look what happens. The joint that was hypermobile has now bound up, has no mobility because the facets have bound up and all the motion is now left at the previously stiffened joint. The polar opposite. And then you need some kind of mobility to pop those facet joints open again after they’ve been jammed.”

inflammatory mediators

The changing spine and the anatomy. Professional LxH Dynamic Disc Model

Stuart McGill:  “So, when you understand the cascade of change that happens at a joint, it might be kicked off with a little bit of a flattened disc, which puts more load in the facet joints, which causes a little bit of arthritic growth. In two years, the joint has changed and so have the pain patterns and the mechanics. So, it really does lend insight to allow us to understand the cascade of how the patient reports those changes and their pain changes over the years. And it better allows us to show them what to do to wind down the pain sensitivity. “