At Dynamic Disc Designs, we believe research to be the foundation of our spine models so practitioners in musculoskeletal health feel confident in the use of an accurate model while they educate patients about their findings.  Historically, models have been inaccurate and most critically, static, making it very difficult for the doctor to be convincing to the patient in the accuracy of diagnosis.

Research is at the roots of any practice. It fuels practice guidelines and directs both the patient and practitioner down the best path of care. Our models help support that voyage. We have worked hard to bring the best to practitioners of musculoskeletal science by scouring databases of spine science, to arrive at the most accurate model for teaching possible.

With over 1000 papers read in full text, Dr. Jerome Fryer leads the way by making sure our models are keeping up to the standards of best evidence. Weekly literature searches on keywords that surround musculoskeletal health are at the core roots of Dynamic Disc Designs.

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 is a non-scary way and empowering way. We look forward to more research on this topic.

 

 

3d modeling, endplate lesion

An October 2018 study compared MRI’s of 966 lower back pain (LBP) patients to introduce a simplified, reliable method of classification for common endplate lesions. The study also noted associations between endplate lesions and variables, including age, rate of disc degeneration, sex, and Modic changes. The researchers then demonstrated the new system’s reliability by repeated observational rating over a period of days, using outside raters evaluating a percentage of the total sample results. The demographic and physiological findings of the study were largely in agreement with previous IVD endplate lesion studies but also added novel findings that had not previously been published.

basivertebral nerve, bone marrow edema, modic changes

Modic vertebra model- midsagittal cut exposing the basivertebral nerve.

The Study

The subjects in the study were all LBP sufferers under the age of 70, excluding patients with a history of back surgery, spondylodiscitis, or vertebral fractures. Data including age and sex were collected on all patients, and images were scanned and evaluated by an experienced radiologist.

A scoring and classification system for the Lumbar IVD spaces was noted on the images, with the descriptions:

  • Normal—Physiological curvature of both endplates, without the detection of any visual lesions in any of the sagittal MRI IVD space slices.
  • Wavy/Irregular—Curvature in at least one of the endplates, without detectable IVD lesions.
  • Notched—The presence of at least one circular small or V-shaped lesion on an MRI saggital slice.
  • Schmort’s Node—Clearly evident vertebral endplate deep focal defect, where the endplate is rounded, with a smooth margin
  • Fracture—Thickened bone fragment at the edge of an endplate, or any evident fracture of the endplate with similarly-sized fragments

A sampling of the image data was also evaluated multiple times over a period of two days by independent raters to ensure observer reliability. To determine how often each type of endplate lesion appeared associated with disc degeneration and alterations of the MRI signals, subgroups of the study subjects were created, and comparisons were made based on age and sex. A scatter-plot chart was created to track Modic changes, and the relative percentages were calculated and identified against an established threshold.

 

Results

The findings indicated minimal association between patient age at the time of the scan and disc degeneration, as well as minimal Modic changes in older patients, as opposed to entire population studied. The most common types of endplate lesion observed were the “notched” and “Schmorl’s Node” type lesions, and both were more common in male patients than in females. Few of the patients studied had “Wavy/irregular” or “fracture” lesions, which occurred in nearly equal numbers of male and female subjects.

There was a strongly evident correlation between disc degeneration and endplate defects across all LBP subjects in the study. All lesion types increased in all IVD levels where disc degeneration was evident. There was a significant increase in “wavy/irregular” endplate types whenever severe disc degeneration was present. This can be considered a reliable marker for the process of extreme disc degeneration.

Signal alterations were found to be associated with endplate lesions, specifically in “notched,” “wavy/irregular,” and “Schmorl’s Node” endplates. There were nearly twice as many notches in Modic changes of types 1 or 2 corner signal alterations. Schmorl’s nodes showed even more evidence of association.

 

Discussion

Though this study was conducted with the intention of developing a reliable method of endplate defect classification in LBP patients and to find correlations in the distribution of LBP by analyzing a large population of subjects via MRI, previous studies have indicated a correlation between back pain and lesions—something this study did not specifically address.

The results of this study agreed with previous studies that indicated male LBP patients are more likely to have IVD lesions than female patients, though similar lesion-levels were observed in male and female patients who showed evidence of severe disc degeneration, as is found in Schmorl’s nodes and in those with disc fractures.

Most of the patients showed no evidence of endplate lesions on the lumbar MRIs. Of those who who did have lesions, most (18.7 %) experienced them only in a single IVD level, and males were more likely than females (20.7 % to 16.7 %) to show evidence of lesions. Progressively fewer subjects had lesions involving more IVD levels.

There was a very slight correlation between age and lesions in this and some previous studies. That correlation appears to be stronger in the female LBP population than in males—a new observation that has not been discussed in previous studies.

The association between endplate defects and disc degeneration was evident, especially where “wavy/irregular” endplates occurred, indicating severe degeneration of the discs. Signal alterations and endplate lesions also showed a positive correlation, specifically in “wavy/irregular,” “notched,” endplates. This association was significantly evident in Schmorl’s nodes.

 

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.

 

 

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.

 

pain education

In a recent article 1 by G Lorimer Moseley, he explains how pain education is the cornerstone of best practice care for acute and persisting back pain, but does not get the attention it deserves. Though education is universally recommended as a first-line treatment, it does not attract the same amount of attention as when patients are told to remain active and seek psychological therapy. Moseley points out how these are the correct steps to follow for recovery, but without proper pain education, this advice from doctors can feel insulting, illegitimatizing, and infuriating. Once patients are properly educated, however, they can engage in active, psychologically informed strategies, that are potentially far more powerful for treating persistent pain than drugs or anything else doctors can offer.

 

Unfortunately, according to a study 2 by Moseley, most doctors do not know what pain education is or how to practice it. Often they do not even have the content knowledge, and if they do, they do not have time to properly educate their patients. For this reason, Moseley argues that a community approach is necessary so that collective strength can be harnessed to shift the conversation and clinical practice around back pain to focus more on pain education.

Pain education research has identified key concepts that, when patients really understand, it helps them to recover.

 

Examples Moseley gives of these concepts are:

  • The back is strong (ie, it is NOT an inherently unstable structure!) and highly protected by a comprehensive network of danger detectors.
  • Back pain can be brutally painful even when there is no identifiable tissue injury.
  • Tissue healing is an irresistible life force.
  • Pain provides our tissues a protective buffer.
  • The protective buffer offered by pain increases with a huge range of variables including inflammation, cognitive and social cues.
  • Our pain system learns over time to become more protective.
  • The best ways to retrain an overprotective pain system are learning about pain, adopting active management strategies, gradually loading the painful tissue through movement and activity and using psychological therapies.

 

Much still needs to be done to shift the industry’s focus towards pain education, but fortunately, research in this field indicates that pain sufferers who are prepared to retrain their overprotective pain system to be less protective will likely see a gradual recovery.

 

 

KEYWORDS: pain education, acute back pain, persisting back pain

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