Our patient education dynamic spine models help low back pain sufferers better understanding of their pain sources.

A dynamic spine model can empower a patient to help him or her get to know the motions postures and loads related to pain. Once the specific movements are identified, a patient can learn what exercises and movement strategies that will reduce their symptoms. A disc bulge is often an MRI finding but it can also tells a story about hypermobility. For lumbar spinal stenosis, it is also common for a person to have symptoms while their spine is in relative extension. The Lumbar Spinal Stenosis Model helps a practitioner deliver this important message to engage with accurate patient education.

disc height

In this Spine Education video, Dynamic Disc Designs’ Dr. Jerome Fryer demonstrates the benefits of helping lower back pain patients better understand their condition by using dynamic models and visual aids.

“How often do you encounter a patient that explains that their symptoms are worse as the day progresses?” he asks.

Though clinicians understand the key to a graduating pain syndrome involves a complex biomechanical and biochemical matrix in the spine, back pain patients don’t need extensive medical knowledge to appreciate the dynamics of what is happening in their bodies. A simple visual aid can help clarify and simplify their predicament and potential solutions.

 

Hands-On Demo of Diurnal Expression of Fluid from the Disc

Using a dynamic disc model, Fryer demonstrates the diurnal expression of fluid from the disc as the disc height changes over the course of the day.

“We know that the disc height is tallest in the morning,” he says, holding a fully expanded disc model to the camera and then slowly squeezing the dynamic model to demonstrate the loss of height that occurs throughout the day.

“As the day progresses, the disc height will slowly lose its height [causing the facets] to imbricate or shingle. If a patient [complains] their symptoms are more present as the day progresses, you [use] this graph 1 to demonstrate what’s happening in their spine.

“As the person gets up in the morning, there is a quick change in the disc height in the first 10 minutes,” he says, pointing out a steep curve on the graph.

“As the day progresses, the disc height is lost.”

Annular Disruption in Degenerated Discs Reduce Capacity to Maintain Height

Fryer says the situation can be even more extreme when a patient is suffering from degeneration in the disc because the disc can no longer hold its full height, due to disruption in the annulus.

“Helping patients understand symptoms as the day progresses will help them understand why it hurts,” he says. “That gives you more empowered strategies to help patients get motivated, if its posture, or even recumbency, or exercise, or getting out of a chair to help with the disc height changes. These dynamic disc models are very powerful in helping patients with self-awareness.”

For more information on dynamic disc models and patient teaching aids, visit Dynamic Disc Designs.

lumbar creep

A study of male and female humans  1 subjected to three bouts of lumbar flexion-extension prior to, and after 10 minutes of static lumbar flexion confirmed prior animal studies that concluded static flexion caused lumbar creep in nearby viscoelastic tissues and alterations and spasms of the associated muscle functions. Researchers proposed micro-damage in the viscoelastic tissues occurred as the muscles attempted to compensate the relative loss of tension, creating spasms in more than half of the subjects while maintaining static flexion poses.

What’s at Stake?

Workers who must endure long periods of static lumbar flexion suffer high rates of lower back pain and degeneration, making static lumbar flexion a common risk factor for developing lower back pain and degeneration. How this occurs is not well understood. Recent studies have used feline models to better understand the processes involved in how static lumbar flexion creates creep and electromyographic spasms of the multifidi in the lumbar viscoelastic tissues under loads. In these studies, the multifidus muscles developed hyperexcitability during the post-static lumbar flexion resting period, particularly between the 6th and 7th hours of rest, and a full muscular hyperexcitability and creep recovery could take as long as 48 hours, which suggests that a transient neuromuscular disorder occurs after 20 minutes of static lumbar flexion. This new study was conducted to determine if healthy humans would experience the same transient disorder after static lumbar flexion.

flexion and pain

The Study

Study subjects included 24 males and 25 females with an average age of 23.7 years and no history of spinal function disorders. An additional six subjects were included in a control group. Electrodes were applied at the L3-4 level of the erector spinae musculature. Two-dimensional video motion analysis was performed to determine joint angles, and the data was collected prior to calculating lumbar flexion and overall flexion levels.

The subjects were instructed to stand quietly for three seconds then perform a full anterior flexion position over 2-3 seconds and hold the position for 3-4 seconds. The subjects then extended into an upright position over the course of 2-3 seconds and stand in a static position until the end of the recording. The recordings were 16 seconds long, with approximately 12 seconds of trial consideration. The subjects performed the deep flexion trials three times, with a 3—50 second break in between each trial.

Following the first trial sets, each subject was placed in a full lumbar flexion position on a physical therapy mat, with a foam bolster placed beneath their hips to ensure their pelvis was posteriorly placed and their knees were able to flex. This positioning reduced hamstring stretching and focused any tension (or creep) towards the posterior of the lumbar spine. They were asked to hold this position for 10 minutes while an EMG recording monitored any spasms or muscle activity. After this deep flexion period, the subjects were asked to stand up and perform three more flexion trials. The variables and data from all the trials were then extracted and analyzed.

Results

The results of the trial study indicated that there were clinically relevant changes in the flexion-relaxation response after 10 minutes of deep static lumbar flexion. The erector spinae muscles remained active longer and became active earlier prior to anterior flexion and during extension. This was due to moderate creep in the viscoelastic structures of the spine. The muscle activity intensity remained the same after static flexion, and there appeared to be variation in the flexion-relaxation response between the male and female subjects. Static flexion stances appeared quite often to cause visible EMG spasms.

When the subjects initiated anterior flexion, the muscles in their erector spinae slowly increased contraction to counter the increasing gravity effect on the upper trunk and head. Eventually, the passive forces of the strained viscoelastic structures were able to offset the upper body and head mass gravity, making the muscular forces unnecessary and causing them to disperse. The increase in flexion required the subjects to contract their abdominal muscles to counter the posterior viscoelastic tissue forces.

Conclusion

In this study, static lumbar flexion developed lumbar creep in the viscoelastic structures of the subjects. However, this effect was countered by the subjects’ musculature, which initiated or maintained the necessary active force during the periods of decreased viscoelastic tissue capacity. The results of the study confirm a synergy between the neurological system and the body’s ligaments and muscles that helps preserve skeletal stability and control movement. Further, microdamage to the collagen structure that may create spasms in the muscles appear to be related to viscoelastic tissue creep.

 

 

Stability Hypermobility Model

The authors of a clinical commentary 1 stress the necessity of a unifying framework in which to explore issues of spinal stability—one that broadens the current definition to include nonmechanical sources of pain and functionality. Seeking to expand the understanding of spine stability as it relates to lumbar back pain (and, by extension, pelvic girdle and sacroiliac joint pain), the authors stressed the relative lack of clinical knowledge as it pertains to the delicate interactions between neurofunctions and biomechanical behaviors of the lumbar spine.

What’s at Stake

The definition of spinal stability (or instability) has traditionally been (and is currently) framed in terms of static mechanical behaviors and observations. But recent advancements in diagnostic technology reveal the complexity of spinal functionality, which includes neural and mechanical interactions between the central nervous system and spine that appear to be designed to regulate segmental stability in response to activity involving spinal motion.

The Evolution of the Concept of Spinal Stability

The historical framework on the issue of spinal stability posits that the body’s weight works as a destabilizing influence on the spinal column, while the relative stiffness of the muscles and tissues surrounding the spine provide a stabilizing influence. The traversing muscles of the upright spine increase their levels of stiffness in response to trunk activity. It is assumed that approximately 2 percent activation is required to support the upright spine.

An observation of degenerative spine changes may be inefficient on its own in the diagnosis of lower back pain and stability because it does not consider the quality of trunk musculature and control, which could counterbalance (or contribute to) spinal deficits. This is also true regarding join laxity or hypermobility, which should be considered in relation to muscle control.

Comprehensive analysis of the spine system is therefore necessary to accurately diagnose spinal deficiencies, which is why diagnosticians expanded the historical spinal conceptual framework to include loading events and how delayed trunk muscle reflexes could contribute to back injuries or pain. In this framework, the timing of muscle activation was an important element in maintaining spinal stability and avoiding back injuries.

Newer spinal models included the components of the spine/trunk, as well as neurological or sensorimotor pathways that influence spinal stability and motor behaviors, and a new emphasis was placed on the importance of neural control in avoiding spinal instability.

Stability and Instability

Stability | Instability Model

The Role of Spinal Stability in Back Pain

Research suggests the central nervous system may have an integral role in monitoring spinal stability, but the underlying mechanisms at play in this relationship are unclear. There is an evident relationship between the varying activation levels of the trunk muscles and spinal stability during loading, fatigue, lack of sensory input, a reduction in spinal stiffness post-flexion, exertion, lifting, and managing unstable loads. Conscious or unconscious neuromuscular controls appear to be modulating the rate of muscular activation to avoid spinal instability. The trunk muscles, while capable of activating independently, may be interconnected through thickly layered fascia across multiple spinal segments and extra muscular fascia. This creates biomechanical coupling that helps increase spinal control by dispersing applied spinal forces.

While the neural and mechanical coupling can support and protect a healthy spine, they may contribute to a lack of control in a damaged spine, as the joints could become lax across many levels with degenerative disc disease, injury, or spondylolisthesis. This can create segmental hypermobility that affects muscle control, which could contribute to further instability. In cases of extreme back pain and degenerative lumbar spine problems with fatty infiltration and fibrosis, for example, some deeply segmented muscles, including the multifidus, may atrophy, creating reflex or neural inhibition that can further undermine spinal stability. The timing and ratio of muscle activation across the spectrum of deep-to-superficial levels is integral to spinal stability, meaning a combination of joint hypermobility, reflex inhibition, and muscle wasting could undermine spinal control and stability in lower back patients. Therefore, increasing trunk muscle mechanical stiffness through coactivation is a commonly used strategy to help protect the spine from instability in healthy and lower back pain afflicted individuals.

While many back-pain patients coactivate trunk muscles in an attempt to avoid spinal instability, contractions of 2-5 percent above normal may contribute to muscle pain and spinal fatigue, setting the stage for further instability. In fact, lower back pain patients appear to have more fatigable paraspinal muscle fiber types than healthy individuals, which reduce maximum muscular capacity and contribute to spinal instability. It is possible that these patients might resist fatigue by strengthening their paraspinal muscles.

Advancements Lead to Improved Spinal Assessments

Spinal Imaging advancements are helping diagnosticians in the assessment of spinal kinematics and a systems-based approach to the examination of spinal stability. Other clinical measures include radiographies, ultrasounds, manual testing, and questionnaires, though no single method provides a framework in which to consider spinal stability from a multidimensional perspective. While single-plane digital videoflouroscopy and 2 digital videoflouroscopic systems provide a limited view of spinal kinetics, the authors of this commentary hope for improved clinical diagnosis through better spatial resolution that allows the examination of spinal movement with lateral flexion/extension radiographs.

Conclusion

The issue and understanding of spinal stability continue to evolve. Studies indicate the central nervous system is integral in monitoring and responding to spinal stability. While neural and mechanical coupling help keep healthy spines in check, they can contribute to segmental instability in injured or degenerating spine segments by inducing joint laxity, neural inhibition, muscle weakness, and a reduction in the capacity to generate adequate muscular force. They may also contribute to fatigue, increased tissue loading, and back pain.

Future research should make use of recent scientific and technological diagnostic advancements to expand upon the current understanding and framework of spinal stability. To be effective, this forward-thinking strategy might include reconsidering the very term, “spinal instability” to incorporate the matrix of neuronal, musculature, and biomechanical influences that provide a more complete framework into understanding the issue.

 

 

 

 

 

 

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.

Facet Tropism - Disc Bulge

A study examining the relationship between facet joint angulation, joint tropism, and Degenerative Spondylolisthesis (DS) found a clinically significant link between DS and facet tropism, as well as observing facet tropism in non-DS disc levels of the study subjects. This supports the theory that tropism may pre-exist and contribute to the development of DS, rather than being a by-product of the condition.

 

What’s at Stake?

DS is a common condition affecting middle-aged and the elderly population—especially women. Frequently occurring at the L4-L5 spinal level, the condition has been associated with a number of potential causes, including facet joint orientation. Patients with DS may have more sagittal-oriented facet joints, which allows anterior gliding of their superior vertebra. When a patient’s left and right facet joints are asymmetrical by a minimum of 8 degrees, the condition is considered to be tropism. The authors of this study compared patients with DS with a control group of patients who had no DS to determine how facet joint angulation and/or the presence of facet tropism might play a role in the development of DS.

 

The Study

A retrospective radiographic study of 45 patients with single-level DS, presenting with lower back pain (LBP), leg pain with or without neurological effects, and neurogenic claudication compared the images of the subjects in Group A with a control group (B) of 45 non-DS patients surgically treated for disc prolapse or stenosis, matched in sex and age. Patients with previous spinal surgery or trauma, tumors, vertebrae or congenital anomalies, degenerative lumbar scoliosis, and isthmic spondylolisthesis, as well as those with flawed imaging, were excluded from the group.

MRI axial images of various disc levels were processed and analyzed with PACS software in order to calculate the facet joint angles. A difference of 8 degrees of angulation was termed facet tropism. An independent and case-blinded observer assessed the images of both groups, and an analysis was conducted as to the orientation of the facet joints at three levels in both groups.

Results

Group A was comprised of 15 male subjects and 30 female subjects between 38 and 79 years of age, with a mean age of 62.2. Of the 45 Group A patients, 8.8 percent (4/45) presented with DS, two of which (50%) had facet tropism at index level. All four of these subjects also presented with facet tropism at an adjacent distal level. A total of 37 patients (82.2 percent) showed DS in the L4-5 level, and of those patients, 14 (37.8 percent) also had facet tropism at index level. Eleven patients (29.7 percent) presented with tropism at adjacent proximal level, and 29.7 percent (11) showed the condition at adjacent distal level. Four subjects had DS at L5-S1 level, and all of thse patients had facet propism at index level. A single patient also had tropism at adjacent L4-5 level, as well.

Twenty of the 45 Group A patients (44.4 percent) demonstrated facet tropism at the level of DS. IN addition, 12 of the patients (26.6 percent) had it at a proximal  level to DS level, and 15 (33.3 percent) at level distal to the DS level. Nineteen of the subjects (42.2 percent) had it at a single level, 9 showed tropism at two levels, and 4 (8.8 percent) had it at all three of the levels examined. In all, 71.1 percent of the patients in Group A had facet tropism at one or more levels.

The numbers in Group B were considerably lower, with 2 patients showing facet tropism at L3-4, 5 at L4-5, and 2 at L5-S1. Five of the subjects had single-level tropism, and 2 had it at two levels. None of the Group B patients had tropism at all three levels. In all, only 15.5 percent of the Group B subjects had facet tropism.

Conclusion

The study confirms the association between facet joint tropism and DS. More notably, the observation of higher numbers of facet joint tropism at adjacent non-DS levels in the DS group suggests that facet tropism could contribute to the development of DS, rather than being a secondary symptom of the condition. Patients presenting with single level DS should be followed up closely to monitor adjacent spinal segments that could become symptomatic in the future.

 

 

 

 

 

ddd models, dynamic disc models

A systematic clinical literature review 1 found evidence that high intensity zones (HIZ) on MRI scans may indicate a potential risk factor in lower back pain (LBP). The review authors suggest further studies are needed to understand the relevance of lumbar biomarkers in imaging to properly diagnose and classify LBP as it relates to HIZ.

What’s at Stake?

Various lumbar phenotypes have been identified and studied in the past to determine their effects on patients suffering from LBP. MRI is a common LBP diagnostic tool used by practitioners treating patients with LBP, but its effectiveness in identifying the sources of LBP has been questioned by researchers over the years. For three decades, the debate over whether and how imaged biomarkers may relate to LBP has remained inconclusive. This extensive literature review was conducted to seek clarity on how HIZ in MRI may indicate a reliable diagnostic tool for clinicians treating patients with LBP.

The Review

A total of 756 studies were scanned for data relating to search terms that were indicative of their usefulness to the researchers involved in this review. Six studies—five comparison studies, and one cross-sectional population-based study—were ultimately chosen for their relevance, and their data was reviewed in the context of an association between HIZ and LBP. The literature chosen was published between 2000 and 2015 and involved studies of symptomatic subjects and asymptomatic controls between the ages of 21 to 50 years of age.

Results

Three of the comparative studies demonstrated a clinically-significant association between HIZ and LBP. In one study, over 32 percent of the patients with LBP exhibited HIZ in at least one disc. Of these patients, 5.3 percent showed multi-segmental HIZs, with 3.9 percent showing HIZs in the adjacent discs. Furthermore, 57.5 percent of the HIZs subjects had symptoms of LBP, while only .02 percent of the patients without HIZs were symptomatic. There was a correlation between higher LBP incidence and HIZs in the lower lumbar spine or with multiple HIZs, but these statistics were considered clinically-insignificant. In another study, 61 percent of patients with HIZs experienced LBP, compared to only 32 percent of those without HIZs. The median rate of HIZs was lower in subjects without LBP than in those who were symptomatic.

While the data studied in this review indicates a higher prevalence of LBP in patients with identifiable HIZs in imaging studies, other studies have found little-to-no evidence of this correlation, indicating the need for further studies and reviews on the nature of HIZs and LBP in symptomatic and asymptomatic patients.

Conclusion

This systematic literature review suggests an association between HIZs and LBP. However, the authors express the need for further study of the LBP pathology and HIZs morphology/topography as they relate to various spinal phenotypes to determine how variant biomarkers on MRI studies may help determine the existence and source of LBP in patients.

intensive patient education, pathoanatomy

This study 1 published in JAMA (Neurology), randomly selected 202 acute low back pain patients to compare pain education to non-pain education. The results demonstrated not much difference between the groups.

The Methods

Participants engaged with their common physician and in addition to this familiar interaction, each participant was then randomly partitioned into two groups. Each of these groups experienced, in addition to the advice and interaction of their physician, an additional two x hour sessions of either:

Group 1: Normal engagement with doctor PLUS intensive one on one patient education (delivered by clinical psychologist in pain management (M.K.N.) trained) for an additional 2 (1hr) sessions. This patient education was delivered based on Butler’s and Moseley’s work. 2

Group 2: Normal engagement with doctor PLUS placebo patient education (delivered by the same clinical psychologist) for an additional 2 (1hr) sessions. Participants in the placebo patient education group received no information, advice, or education about low back pain from the trial clinician. Participants were encouraged to talk about any topic that they desired.

The Results

Retention rates remained high for both groups at ninety percent. Intensive patient education was not more effective than placebo patient education at reducing pain intensity at the three months. There was a small effect of utilizing intensive at one week and at three months but not at six or twelve months.

 

Discussion

In this study, patient education was used through a psychological framework model rather than a biomechanical model. It is important to understand that this study does not mean that patient education is ineffective or as effective as a placebo. This patient education angle does not attempt to help patients understand the cause of their pain. This approach is more of a top-down psychological strategy of patient education. Methods to subclassify these acute low back pain patients into specific biomechanical categories and then, offer those patients specific education and movement strategies would be helpful to study as groups within the acute low back pain group. These sub-groups could then be compared to placebo.

 


At Dynamic Disc Designs, we believe that empowering patients with a greater sense of self-awareness on the probable mechanical cause of the acute low back pain can be helpful in the management. Initially, pain-reducing strategies through movement awareness of painful structures should be prompt and focus on reducing nociceptive inflammation for the patient. Following the acute phase of low back pain, professionals using our dynamic disc models can further promote the physical awareness of specific postures to help prevent the recurrence and avoid a progression of the condition. Our models allow the practitioner to explain patho-anatomy in a patient-friendly way that does not induce fear avoidance behaviours for the long term.  They also enable the practitioner to provide a realistic forecast of the temporal biological adaptation process within the degenerative cascade framework of natural ageing with a dynamic 3d model. In other words, our dynamic disc models assist the patient engagement process with the opportunity to bring up anatomy in a non-scary and empowering way. We look forward to more research on this topic.