Patient engagement is at the core of a patient-centered approach to spine care. Spine professionals engage with their patients with different tools. We all use language but to enhance it, very often a physical model can support the words chosen to educate.

In the past, models have been static, so it made it very difficult to connect patient’s back and neck pain to the specific movements that cause the pain. At Dynamic Disc Designs, we have developed models to help the practitioner engage in a mechanical way through a better rendering of a motion segment. We have created a dynamic disc with the ability of the models to bulge or herniate. We have integrated a dynamic nucleus pulposus and a stiffer annulus fibrosus as well as added features of the ligamentum flavum to show how the facets are inter-related to one another.

Explore how a dynamic model can enhance the language one uses in a clinical setting of a musculoskeletal practice.

 

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.

A 2018 study 1 of resting state functional magnetic resonance imaging (rs-fMRI) of the cervical spinal cord in fibromyalgia patients and control subjects found there was greater ventral and lesser dorsal Mean ALFF of the cervical spinal cord in patients with fibromyalgia, compared to the control group subjects. The results of the study may indicate that fibromyalgia patients experience enhanced sensitization of nerve responses that could be responsible, in part, for the discomfort and fatigue associated with the disorder.

What’s at Stake

Patients with fibromyalgia report the experience of physical pain throughout the body, as well as cognitive problems, fatigue, anxiety, and depression. The symptoms may be a result of irregularity of the central nervous system (CNS), including central sensitization and possibly a decreased ability to modulate pain responses. Signals to and from pain receptors may be misdirected or skewed in patients with fibromyalgia, creating an altered response to nociceptive and non-nociceptive signals.

Previous imaging studies have demonstrated altered CNS activity or structure and irregular brain activity in response to painful and non-painful stimuli in fibromyalgia patients.  Functional connectivity, networks, and low frequency oscillatory power have been measured through resting state functional magnetic resonance imaging (rs-fMRI), but these studies did little to elucidate the underlying CNS processes that occur in patients with fibromyalgia. Because of the complexity of the CNS signals in the spine, it was necessary to conduct a comparative rs-MRI of healthy controls and fibromyalgia patients to observe alterations of oscillatory frequencies, functional CNS connectivity, and analyze the graph metrics of the fibromyalgia patients.

The Study

The study subjects included 16 fibromyalgia patients whose symptoms met the American College of Rheumatology inclusion criteria for fibromyalgia and 17 healthy participants. Subjects with MRI contraindications, taking opioids for pain or mood-altering medications, and those with depression or anxiety disorder were excluded, as were pregnant or nursing females. All subjects were screened for MRI contraindications and filled out questionnaires regarding their psychological and behavioral state, diagnostic pain, sensory, and fatigue criteria prior to the study.  Further testing assessed the subjects’ sensory, pain, cold pressure response, mechanical hyperalgesia, and mechanical temporal responses.

Each of the subjects was queried regarding their levels of pain prior to, and after their fMRI scans, using a scale of 0 to 10 to grade their pain. Separate amplitude of low frequency fluctuations (ALFF) Measures of Mean were calculated for each study subject across all voxels of the cervical spine data. Normalized images were analyzed for differences, and the significance of the findings was assessed. Gray and white matter Mean ALFF was also analyzed and compared in the study groups. The functional organization and connectivity of spinal cord networks was also observed and compared in both study groups, as other studies have suggested that bilateral motor, sensory, and dorsal horn functional connectivity networks was altered during thermal stimulation in humans and after a spinal cord injury in non-human primates. The researchers in this study wanted to investigate if disrupted spinal cord processing and functional organization may be responsible for some symptoms of fibromyalgia.

 

Results & Conclusions

The fibromyalgia patients had higher measures of fatigue, sensory hypersensitivity, and widespread pain than the control group. Each of the fibromyalgia patients had right shoulder pain, and most experienced arm pain, undermining the research expectation that the patients’ sensitization would be central and found throughout the CNS as a result of their altered cervical spinal cord activity.

The ALFF spinal cord low frequency oscillatory power study indicated a greater Mean ALFF in the ventral hemi-cord of the fibromyalgia patients. The dorsal quadrants of fibromyalgia patients showed lesser Mean ALFF. Mean ALFF was higher in gray matter than in white matter in the patients.

Overall, the study demonstrated that the cervical spinal cord of the fibromyalgia patients had altered patterns of rs-fMRI low frequency power—greater regional Mean ALFF in the ventral, and lesser in the dorsal spinal cord. The most pronounced difference was noted inside a small cluster in the right dorsal quadrant, at the border between the dorsal horn gray and white matter. There was a strong correlation between levels of patient fatigue reported and the noted differences in Mean ALFF. These observations support the idea of regional differences in nociceptive and non-nociceptive CNS processing pathways in patients with fibromyalgia.

While there is a need for future study of local spinal cord modulatory circuits, these findings suggest that a combination of reduced CNS inhibition, coupled with an increase in dorsal horn excitation could be responsible for the irregular modulation of sensory and pain signals experienced by patients with fibromyalgia. Nociceptive signals might be over-transmitted by spinothalmic projection neurons, and/or a similar process could cause the under-transmission of non-nociceptive signals. Irregular spinal cord signal modulations (decreased, or increased) could increase or lessen signals of any type to any part of the body, which might explain the experience of uncomfortable hot or cold sensations in patients with fibromyalgia. There was also a very strong correlation between the Mean ALFF of the fibromyalgia patients and their fatigue symptom measures.

 

Lower back pain (LBP) patients present with a wide variety of motor control adaptations in response to, and in anticipation of pain. Though these adaptations manifest across a spectrum of functionality, studies have indicated two common phenotypes that represent the trunk posture and movement of most LBP patients. Further study 1 of these two phenotypes can help practitioners target more specific, effective treatments for their patients who have developed motor control adaptations that may undermine and contribute to their long-term spinal health.

 

Variations of Motor Control Adaptations in LBP Patients

People with LBP adapt the way they move to mediate pain or avoid pain. These adaptations may be conscious or unconscious processes, or a combination of the two, but the changes in posture and movement—what we refer to as “motor control”—involve the muscles, joints, nerves, senses, and integrative processes. Studies of how LBP affects posture and motor control have been inconsistent in the conclusions, perhaps because of the built-in redundancy and flexibility of the musculoskeletal system.

There are many ways to adapt posture and movement in response to pain or in anticipation and avoidance of pain. But because each adaptation creates not only short-term solutions, but potential long-term changes in biomechanics, which can become problematic, creating a cycle of disfunction, it is helpful to study the two most prominent phenotypes of motor function adaptions to create targeted treatment and information options for LBP patients presenting these adaptations.

Identified Motor Function Phenotypes

Tight Control: Some LBP patients exhibit increased excitability and accompanying tight control over their trunk movements, which increases reflex gains, attention to how they control movement, tissue loading, and muscle contraction. While having tight control over trunk movements can help the LBP sufferer from short-term injury by constraining movement, it may also contribute to trunk stiffness and increase the amount of force necessary to move. This may manifest in subtle ways or, in extreme cases, lead to a complete bracing of the trunk, making movement difficult and leading to fatigue.

Patients with extreme tight control over their motor control have been shown to experience a reduction in lumbar stiffness and pain after spinal manipulation. This could mean that the adaptation could, itself, be responsible for pain. These patients are also more likely to experience spinal compression due to increased loading. This compression may lead to a reduced fluid flow in the discs, which may contribute to degeneration over time.

Tight control creates low-level muscular activity, even when the spine is at rest. This can create muscle fatigue, pain, and discomfort. The lack of muscle variability and reduced movement associated with tight control of motor function may also compromise tissue health and compromise the load-sharing capabilities, balance, and movement task learning abilities inherent in the body’s structures.

Loose Control: At the opposite end of the spectrum are patients with loose muscle and posture control and less muscular excitability. This creates an increase in spinal movements and subsequent tissue loading. This may help prevent the short-term pain associated with muscle movement, but the spine is unstable and requires musculature to support movement. Less muscle control means potential failure of the mid-range lumbar vertebral alignment segments, which can cause tissue strain and pain. Spinal displacement due to loose control may cause LBP.

 

Clinical Implications for Loose or Tight Muscle and Posture Control in LBP

Understanding whether a LBP patient is exhibiting a loose or tight control muscle and posture adaptation in response to their pain can help practitioners tailor their treatment in a targeted and more beneficial way. Increasing movement and reducing excitability in later stages of LBP adaptive tight control models can help a patient integrate movement variation as their LBP improves. Likewise, exercises and therapies to help loose control patient models develop more control of their musculature and posture may help them avoid the potential long-term consequences of a proper lack of spinal support.

Assessing LBP patients carefully to identify their motor control phenotype prior to the onset of treatment may allow practitioners to more efficiently target and proactively treat potential complications of their particular adaptation due to actual or anticipated pain.

KEYWORD LONG TAIL PHRASES: motor control phenotyping may help target treatment for lower back pain patients, motor control adaptations in response to, and in anticipation of pain, common phenotypes that represent the trunk posture and movement of most LBP patients, two most prominent phenotypes of motor function adaptions, reduction in lumbar stiffness and pain after spinal manipulation.

 

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.”

 

 

 

A new study 1 sought to create an etiology-based system of classification by identifying and characterizing typical endplate irregularities and found that tidemark avulsions were a predominant pathology in the cadaveric spine sample images. This represents a previously unidentified observation and, along with the histologic classification system developed in the study, should assist practitioners in organizing their patients into categories that will help to diagnose, research, and treat their spine symptoms.

 

The Study

Researchers used magnetic resonance imaging (MRI) to analyze and categorize 15 donated human cadaveric spines from 11 males and four females between the ages of 49 to 67 years old. Each of the spine samples showed evidence of moderate to severe disc degeneration. Motion segments were excluded if they appeared with imaging to have experienced pre-mortem surgery, deformity, or fracture. No medical history about the donors was obtained.

Histological Observation

Spinal segments were extracted using a band saw, and their various features were stained with different colors for observation. Each of the sections were imaged with polarized lights under a microscope, and two raters developed a classification system to identify and record various focal tissue-scale endplate irregularities and their anatomical location.

Researchers noticed a novel histological phenomenon wherein there appeared to be a separation of the annulus from the vertebra at the tidemark (the insertion point of outer annular fibers into the calcified layer of cartilage). They immune-stained the “tidemark avulsions” to search for the 9.5 neuronal marker protein gene using a polymer detection system. Each of the slides was then analyzed to identify the presence or absence of nerves in the bone nearest the endplate irregularity.

endplate irregulariities, models

Models to help explain back pain as it relates to endplate irregularities.

MRI Analysis

Each spine was studied via MRI to identify the presence of absence of tidemark avulsions, and their location was noted. Two orthopedic specialist clinicians were used to assess the findings. These researchers—neither of whom was previously used as a rater— were blinded to the histologic findings.

Findings

The endplate irregularities were grouped into three categories based upon their features and location. They were then subcategorized to further classify their pathologies.

The categories and subcategories identified were:

  • Avulsions: There was a separation of the tissue at the place where the disc joined the vertebra. Two types of avulsions were observed—tidemark (separation occurring at the tidemark location, where outer annulus fibers join the layer of calcified cartilage, and CEP-bone avulsion—occurring where the bone meets the cartilage endplate (CEP).
  • Nodes: Traumatic nodes occurred when there was a herniation of the nuclear materials reaching through the endplate. When abnormal fibrocartilage ingrowth or bony erosions were found, the were classified as Erosive.
  • Rim degeneration: This classification was reserved for samples that showed loss of organization in the annular fiber, bone marrow alterations, or degradation of the bone-marrow interface.

Endplate Irregularity Observations

The most common irregularities noted were rim degeneration (50 %) and avulsions (35%). Nodes were less common (15%) and found mostly in the thoracic spine, where the avulsions and rim degenerations were found in the lumbar spine samples. Eighty-seven percent of the noted avulsions were found in the anterior discs.

Though linear regression showed little association between endplate irregularities and age, the largest number of tidemark avulsions (90%) were found in the oldest spine samples. Interestingly, the annular fibers in the tidemark avulsions appeared to change their direction after crossing the tidemark. Of the 35 discs that showed tidemark avulsions, 14 of them contained multiple avulsions. Marrow changes and increased innervation was noted along vertebral bones beside endplate irregularities. An increase of nerve density was observed even in bones adjacent to very small tidemark avulsions.

Conclusion

The ability to identify tidemark avulsions on MRI may help practitioners identify and treat disc-vertebra injuries in a targeted way. High density images in the study showed that fluid can collect around avulsion irregularities, potentially creating gas in the extra-cellular spaces surrounding thee separation. High-intensity regions in MRI may indicate disc delamination or potentially painful lesions.  It is possible that tidemark avulsions may create anterior widening and create a scenario wherein the disc may detach from the vertebra. Overall, the findings of this study should contribute to a beneficial system of classification, allowing clinicians to more effectively diagnose and treat their lower back pain patients.

KEYWORDS: endplate irregularities, tidemark avulsions, endplate pathologies, histologic classification system, separation of the annulus from the vertebra at the tidemark, CEP-bone avulsion, traumatic nodes, rim degeneration