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Explaining back pain with a spine model – Patient-centered Education

connecting the patient to the anatomy of back pain

Connecting with patients is the future of healthcare.  With low back pain and neck pain as the leading cause of disability and lost work days on this planet, getting to the roots of helping people with these conditions is imperative. These origins are mostly biomechanical in nature. But how a practitioner connects the curious patient with a better understanding of their anatomy can be a challenge.

Much research has talked about how important education is important for better outcomes of low back and neck pain. But how does one execute and teach a patient about their biomechanics? The spine is a complex structure and to help patients understand which movements are good and bad for their condition can be tough.

Patient-centred care is leading the way in healthcare. Engaging with patients in a way they can understand their back condition is helpful. MRI, CT and X-ray findings can be quite intimidating and confusing for the patient, but here at Dynamic Disc Designs Corp., we have made it a lot easier for the professional.

Explaining the intricacies of the annular fibres, for example, and what discogenic back pain means is a lot easier with our dynamic disc model that includes a clear see-through lens. The Professional LxH spine model includes many of the anatomical features that have never been shown in a lumbar model before. Created with the physician in mind who want to communicate effectively the biomechanical origins of back pain, now, with a two-part intervertebral disc that includes an elastomeric annulus fibrosus and nucleus pulposus certain postural changes can be taught to the patient in a dynamic and interactive way.

Below are a few videos that other professionals have created using these detailed spine models.

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Lumbar Disc Herniation and Resorption – What does the literature say?

A professional lumbar spine model with a flexible and totally dynamic herniating (or prolapse) nucleus pulposus.

Lumbar disc herniation is a very common condition which often generates pain and disability. It is a physiological process that starts from the inside out as the nucleus pushes radially into the annulus fibrosus. But not all disc herniations cause pain, and many of them don’t cause long-term disability.

The literature has been quite varied in answering questions surrounding resorption rate. Yes, many disc herniations resorb, and it is believed to be due to the anaerobic and avascular nature of the nucleus pulposus. Once the material extends beyond the annular outskirts, the immune system identifies it as foreign and macrophages begin to chew it up.

But not all lumbar disc herniations are equal while some respond to manual therapy and some do not. Some cases require surgery to remove the offending material.

In a recent meta-analysis titled: ‘Incidence of spontaneous resorption of lumbar disc herniation’ 1 a group of authors looked at 11 cohort studies but found only a very limited number of high-quality papers on the subject. What they found was the phenomenon of lumbar disc herniation resorption to be 66.66% and suggested that conservative treatment may be a first line approach to reduce costs associated with unnecessary surgical bills.


Disc herniations are quite varied in nature, and this is likely why there is such variability in the outcomes reported regarding resorption and pain. As a spine modeling company which continuously invests in the property characteristics of materials, we have found that subtle changes to the nucleus pulposus make-up and annulus fibrosus tensile properties have a significant impact on the biomechanical behaviour of our lumbar disc herniation model.

Many mechanically anatomical variations exist which can cause a wide spread of varying symptoms. These symptoms are likely related to the type of herniations with some more central within the spinal canal and others are more lateral. Further to that, Depending on the severity, an astute clinician can be relatively accurate in the anatomical location to help in the mechanical management of lumbar disc herniation.

flexion, lumbar, model, pain, relief

Flexion lumbar loading

 

 

To see how a spine surgeon uses the model to explain a lumbar disc herniation while referencing an MRI, we present Iona Collins of fixmyspine below.

 

 

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Degenerative disc and impact on flexibility

Degenerative disc, flexibility, model

Aging and Degenerative Disc Changes of the IVD’s Impact on Spinal Flexibility

A publication reviewed several studies involving the biomechanics of the intervertebral discs (IVD) with macroscopic changes associated with degenerative disc disease with the aim of finding out how spinal flexibility was affected by dehydration, tears, fissures, osteophytes, and the inevitable collapse of the intervertebral space. The studies under review used cadavers and did not contribute to information about how degenerative disc disease may cause symptomatic back pain. However, the review can contribute to the understanding of disc degeneration disease and its progression, as well as offer insight into what surgical treatments could be beneficial in improving flexibility and spinal functionality in patients.

 

About Disc Degeneration

Degeneration of the IVD causes mechanical and biochemical changes in the disc and its surrounding structures. The space between the discs can collapse, and proteoglycan and water content can be greatly reduced, contributing to the damage of endplates and osteophytosis. The entire motion segment of the IVD is affected macroscopically and biomechanically by the degenerative process, and this can cause a loss of functionality and mobility that contributes to further progression of disc disease in the spine.

 

How the IVD Works

A properly functioning IVD evenly distributes weight-bearing loads across the spinal segments and allows the spine to suffer intense compressive loads without collapsing or losing its range of motion. Inside each IVD is a nucleus pulposus (NP)—a gelatinous substance with proteoglycans, elastin fibers, and Type II collagen. The NP is enclosed by the annulus fibrosis (AP)—a lamellar structure made up of Type I collagen fibers. The angle of the collagen fibers in the AP (30 degrees), alternates with that of the adjacent lamellae, which contain gel rich in proteoglycan and may be surrounded by connective bundles of collagen. Endplates connect the IVD to the surrounding vertebrae. The NP transitions to the AF in a transitional zone that is indicated by diverse types of tissue, rather than a distinct border. Negatively charged proteoglycans are balanced by positive cations within interstitial fluids, contributing to osmotic pressurization in response to its environment. Because of this, the IVD absorbs copious amounts of water, which helps the nucleus to adjust in reaction to high compressive forces.

The NP is bookended by the endplates and the AF, which allows the resulting hydrostatic pressure to balance any swelling pressure during active loading and at rest so that the disc will not bulge or collapse under compression. The structure of the lamellae in the AF is tension-loaded and assists with bending and shear. Vicious fluids flow through the permeable endplates, which help evenly distribute pressure within the nucleus or annular tension. The AF’s collagen bundles create an elasticity that absorbs compressive loads. The exchange of fluids within the IVD creates a balance between tension and flexibility that is integral to the function of the spinal unit.

Degenerative disc, flexibility, model

Degenerative disc model

 

Effects of Degenerative Disease and Aging on the IVD

 

  • Cellular/matrix alterations—Aging and degenerating IVD exhibit early changes in the endplates which in turn cause changes to the nucleus and annulus. A progressive reduction of cells begins in childhood and continues throughout a lifetime, decreasing and fragmenting the proteoglycan content in the nucleus and surrounding areas. In time, this leads to a reduction of the disc’s ability to repair itself. As the cells lose their ability to synthesize, there is further loss of proteoglycan content. Changes at the cellular level create biochemical alterations throughout the entire matrix. In time, the NP loses the ability to attract and retain adequate water and an increase in fibrous tissue takes place. A similar –though lesser—loss of water and collagen in the AF leads to reduced swelling pressure and contributes to the degenerative state.

 

  • Structural changes—Structural failures including tears and clefts follow (or are perhaps caused by) alterations in the NP and AF. Considered a symptom of degenerative disc disease, these changes are related to, but distinct from, the simple aging process. Endplate separations, radial tears, and rim lesions increase in the aging population, and approximately 50 percent of the cadaver specimens in one study showed evidence of IVD degeneration in subjects over 30. Calcification of the cartilaginous endplates cause biomechanical changes that reduce the flexibility of the endplates and make the IVD vulnerable to fracture, reduced water intake, and a lower solute exchange rate between the disc and vertebrae. Collapse of the intervertebral space occurs often in a degenerated IVD, though disc height reduction is not a common result of simple aging. In addition to a reduction in disc height, osteophytes may form around the affected vertebrae. Studies have suggested that these osteophytes may be the body’s attempt at providing supplemental stabilization in the degenerated spine segment.

 

  • Pain—A common cause of back pain, degenerative disc disease undermines the spine’s structural integrity and creates tension and spasms in the surrounding muscular structure. In severe cases of disc degeneration, disc prolapse, and collapse, radial tears that cause a leakage of collagen and fluids can increase the frequency and amount of back pain. Another common source of back pain is lesions or uneven loading in the endplates. When there is a reduction in disc height, nerve roots located in between the vertebrae may be squeezed or pinched into the space near the capsule joint, causing radicular pain. This type of pain can intensify with activity or prolonged sitting or standing. Facet join arthritis can cause a decrease in cartilage between the apophyseal or zygapophysial joints and may contribute to back pain.

 

  • Changes in Flexibility—When the IVD are in a degenerative state, the entire motion segment(s) can become more rigid and less flexible. Researchers have theorized that the spine loses its flexibility over time, triggered by an initial dysfunction and followed by instability, which leads to an attempt at stabilization. Thus, disc degeneration is a progressive event which is the result of the spine’s attempt to handle physiological loads. However, there is no evidence that shows a definitive connection between reduced range-of-motion therapies (such as surgical implants that inhibit the range-of-motion) and an improvement of disc degeneration.

 

 

Conclusions

Research into the biomechanics of the IVD systems clarifies some aspects of degenerative disc disease but offers little insight into the specific causes of lower back pain. Degenerative changes of the IVD systems cause changes to the functionality of the spine, with some inconclusive evidence of a loss of flexibility and increasing stiffening over time.  Further studies of the effects of disc degeneration and a possible link to spinal instability are recommended.

 

 

 

 

 

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Study Indicates Pain Signals Can be Transmitted from the Peripheral Sensory Nerves to the CNS

pain, model

A research study of GABAergic communication within rodent peripheral sensory ganglia demonstrated that somatosensory pain signals can be transmitted from the peripheral sensory nerves to the central nervous system (CNS). The study further found that necessary proteins required in GABA synthesis were released by sensory neurons and triggered by depolarization. By infusing the sensory ganglia with GABA or GABA reuptake inhibitors, the researchers could significantly reduce or alleviate acute inflammatory or neuropathic pain and nociception in the rodent subjects. They were also able to cause or exacerbate peripherally-induced nociception by GABA-receptor antagonists to sensory ganglia. The study demonstrated that chronic peripheral-induced nociception could be reduced in vivo by chemogenomic or optogenetic depolarization of the GABAergic root ganglion neurons. This indicates a need for further research into peripheral somatosensory ganglia as a potential site of therapeutic pain remediation.

 

Background

Peripheral nerves create pain to convey information to the brain and central nervous symptoms about damage that may be occurring in the body. Healthy nerves send signals from the origin of the impending damage to the spinal cord. There, peripheral somatosensory signals are analyzed within the synapses. It is believed that, prior to their interaction with the spinal cord, nerve fibers do not receive input from the synapses and that cell bodies are unnecessary to the propagation of action potential (AP) to the spinal cord from its periphery. Some chronic pain conditions could be caused or exacerbated by the somatic sensory neurons stimulating peripheral excitation. The researchers involved in this study examined local GABAergic transmission within the DRG to more fully understand why GABA receptors are present in sensory neuron somata and from where any possible activators of the transmitters may originate.

 

Results

In the in vivo study of rodent peripheral sensory ganglia, the researchers’ data determined that GABA is most likely produced in various sub-types of dorsal root ganglion (DRG) neuron. This observation supports the theory that many different sizes and types of DRG neurons may, upon stimulation, be released. In addition, every type of small-diameter DRG neuron may respond to GABA, which satellite glia will remove from the extra satellite space. This release could also signal and set base GABA levels.

Both GABA and the GABA reuptake inhibitor NO711 produce an antinociceptive effect when administered locally in vivo to DRG. When GABA receptor antagonists are similarly delivered, peripherally-induced pain is exacerbated and a nocifensive behavior occurs—even without applied painful stimuli. The results of this observation indicate a healthy endogenous GABAergic inhibition within DRG, though it is still unknown whether the afferent fiber transmission occurs only within the peripheral segments of the DRG.

Previous evidence of cross-excitation within the sensory ganglia and the abundance of neurotransmitter receptors expressed within the somatic and perisomatic sensory neuron sites could point to complex integration of peripheral somatosensory information within the DRG. This study adds a possible new theory of pain to the previously proposed “gate-control” idea.

The research study indicates a potential for the use of focally-applied GABA mimetics or GAT1 inhibitors targeting DRG as a means of pain relief. This idea corresponds with recent studies that concluded that direct stimulation of DRGs through implanted stimulation devices provided relief in people who suffered from neuropathic pain. The authors of this study postulate that the DRG neuromodulation effect works due to the peripheral ganglionic gate and that peripherally-acting GABA mimetics could be used to affect long-term pain relief in pain sufferers.

 

 

 

 

 

In Vivo MRI Study Examines the Rate of Disc Fluid Loss Over an 8 Hour Day

Disc Fluid Loss Over an 8 Hour Day

Numerous studies have examined disc volume, height, and disc fluid loss to more clearly understand the effects and rate of cellular diffusion and nutrient and waste transfer on IVD. However, to date, there have been no significant measurements of the rate at which discs lose fluids during normal activity throughout the day. We know that IVD fluids are replenished during overnight rest, but understanding how quickly the fluids dissipate during daily activity could be important in the prevention and treatment of disc degeneration.

The Study

To better understand the rate at which discs lose fluids after an overnight gain, researchers conducted a study 1 of five healthy subjects—four women, and one man— between the ages of 21 and 32 years old. Each of the subjects was screened prior to the beginning of the study to determine that they had no pathologies of the spine. The subjects were instructed to remain moderately active and resist sitting for more than 10 minutes at a time during the 10-hour period preceding the study.

On arrival in the evening, each of the subject was instructed to remain in an upright position for one hour, then they were placed into an MRI scanner for the first (PM) scan. The subjects then slept at the study facility and were instructed not to get out of bed except to use the bathroom. After 8 hours of sleep, they were scanned again at approximately 7am (AM).

All the subjects then began a regimen of 40 minute periods of walking, followed by horizontal MR scans. They repeated this protocol over an 8-hour period, until approximately 3pm.

Results

Analysis of all 19 disc scans indicated an average gain of 10.6 % in disc volume overnight, as measured prior to activity in the morning. There was a clear and substantial decrease in this disc volume after the subjects walked during the day, but even after 8 hours of continuous walking (with breaks only for scans), the amount of volume (of fluid) remained higher than the volume that had been measured the previous night, prior to sleeping. This indicates the discs’ ability to retain fluids over an extended period throughout the day.

Researchers noted a large variance between the disc fluid loss of the study participants—from 11.1 % to -3.5 %. Because the volume is determined by the proteoglycan’s fluid-holding ability and by the seepage through the disc collagen, the enormous range in volume decrease between differing discs could be an indication that diverse types of disc and their fluid-retention (and nutrient and waste-dispensing) abilities could be more, or less susceptible to future degeneration. Future study is needed to determine which disc type is more beneficial and less likely to degenerate. Disc fluid loss and gains are important in understanding optimal metabolism.

Research into IVD Cell Mechanobiology and the Role of Genetics in IVD Degeneration Necessary

Role of Genetics in IVD Degeneration

A review 1  of how biochemical and micromechanical events affect the cellular biology and morphology of intravertebral discs (IVD) during physical motion, loading, and compression determined that important interactions between the nucleus pulposus and annular fibrosis altered cells, micromechanical, mechanobiological, and mechanical features. Because previous studies have indicated a strong genetic link in the propensity for disc degeneration, the authors concluded that more information is needed on how these integral biochemical and micromechanical processes may be triggered by genetic factors and contribute to IVD degeneration, annular tears, and endplate or facet damage that can reduce disc height and flexibility, fluid pressurization, and cause stiffness or dissipation of the disc.

 

An Examination of the Intervertebral Disc

The authors of the review emphasized that the three separate anatomic structures of the IVD—namely, the annulus fibrosis, nucleus pulposus, and cartilage endplates, which regulate waste and nutrients and may help pressurize fluids—work together to make the IVD function mechanically.

Negative charges in the gelatinous nucleus pulposus, which is made up of mostly water, glycosomino-glycans, collagens, and other proteins—contribute to pressure and swelling, which helps support spinal loads and distribute forces evenly throughout the annulus fibrosis—a lamellar structure made up of bundles of collagen fibers that help control the tension and stiffness in axial, circumferential, and radial directions during physiologic joint motions.

Pathologic changes in the biochemistry and structure of the extracellular matrix may involve a loss of hydration, decrease in disc height and cell density, disorganization of the lamellar annulus, loss of proteoglycan content, changes in the levels or activity of matrix metalloproteinase, and changes in the proteoglycan structure, leading to degeneration or loss of the negative charge’s fixed density and the swelling pressure that is necessary to assist in spinal loading.

 

Genetic Influence on Degeneration and Cell Morphology

The authors of the review stated that there is much evidence to support the theory that disc degeneration could be genetically-influenced, but emphasized that other factors—including heavy lifting, impact, gait, lifestyle factors, posture, and muscle use— may also be involved in altering the biochemical and mechanical processes within the IVD. Those who are genetically predisposed may be more at risk of disc degeneration triggered by the biochemical and cellular responses to mechanical factors.

 

Intervertebral Cell Morphology

Compressive conditions, tensile stretching, strains, and stresses are all physiologic conditions that contribute to the electro-kinetic, fluid flows, hydrostatic, and osmotic effects of intervertebral disc cell responses.  In adults, the nucleus pulposus is filled with chondrocyte-like cells that may have traversed the endplate or inner annulus fibrosis into the nucleus. Studies have demonstrated that these cells –particularly the innermost cells—contain vimentin filaments that are frequently associated with articular cartilage and other tissues enduring compression. The morphology of examined fibroblast and chondrocyte cells indicate that they are ellipsoidal and contain long axes that are in line with the lamellas’ collagen fibers. Alternatively, the cells normally found in the annulus fibrosis are rounder, with more space in between, and may be surrounded by a type of collagen called chondron.

When IVD degeneration is present, other types of cells are found within the nucleus pulposus, including Schwann cells, nerve fibers, fibroblasts, and endothelial cells. There is also an increase in vasculature –and hydraulic permeability of fluids and proteoglycan contents—associated with the proliferation of array of cells. These factors create electro kinetic effects in the regulation of ion and water movement, as well as the cells’ abilities to send signals to the unit in response to mechanical loading. Similar changes in the annulus fibrosis may be responsible for many of the overt alterations observed in IVD degeneration because of the dependence of the unit upon tissue hydration and negative charge to regulate complex interchanges.

 

Other Changes Noted in IVD Degeneration

High levels of hydrostatic pressure occur with the cells of the IVD during resting and loading. Pressure levels higher or lower than average may inhibit proteoglycan synthesis and create an increase of nitric oxide and MMP-3 production. The cells of the nucleus pulposus and inner annulus fibrosis may be affected by compression, but there is little research to support or disclaim this theory. In addition to fluid movement and mechanically-induced disruptions within the IVD, iron concentrates, Ph, osmolarity, and extracellular hydration also occur.

Many loading conditions may contribute to tensile strains within the IVD. These may include a decrease in the proteoglycan and type 1 and 2 collagen content. High-frequency vibration may increase the release of ATP in the annulus fibrosis cells, and type 3 collagen may be decreased after prolonged exposure to vibration. Studies indicate the release of ATP may help modulate the response to vibration and other mechanical stimuli within the disc cell.

 

Conclusion

Studies of IVD suggest anabolic and catabolic consequences of mechanical stimuli. These responses vary between the inner annulus fibrosis and nucleus pulposus, with higher catabolic responses being evident under significant loading stress and lower magnitude responses occurring with static compression, hydrostatic or osmotic pressures. The studies also suggest a connection between the physiologic range of stimuli and micromechanical consequences that promote cellular repair. These signaling mechanisms, though not sufficiently understood, may involve intracellular Ca transients, remodeling, and ATP release, which act as second messengers to the IVD cells and help regulate genetic expression and subsequent biosynthesis.

Future studies are necessary to fully understand the biologic and chemical signaling devices that serve to regulate the IVD response to mechanical and micromechanical stimuli, as well as the evidently important interactions between genetics, mechanical stresses, cytokines, and the inflammatory responses that appear to play a part in IVD degeneration.

Study Finds Prolapse Injury Influenced by Flexion Degree and Level of Hydration, not Rate of Loading

flexion, hydration, lumbar disc herniation, model

A study 1 of isolated and adapted bovine spinal segments examined the extent to which flexion, hydration, and loading rates were responsible for the breakdown of the nucleus pulpous structure and found that the rate of loading had little effect on disc damage with full annular division. Instead, the degree of flexion and the hydration level of the disc were the most influential biochemical measures of nucleus polyposis disruption, protrusion, and breakdown. The study concluded that the nucleus is most at-risk of damage when fully hydrated and fully flexed.

 

The Study

To ensure the discs being studied were healthy and in no way degenerated, study samples were obtained from recently slaughtered two-year-old cows and frozen, then thawed and fully-hydrated just prior to use. The intervertebral discs were then isolated and all ligaments and muscles were removed. The vertebral segments were sawn partially through and attached to a stainless-steel plate using an adhesive.

The segments were radiographed shortly after collection and prior to freezing using a rubber band to create the flexion state and inverting the tail so that it straightened under its own weight, creating the non-flexed state. After freezing, the tail segments were thawed and hydrated fully or partially. A computer-controlled hydraulic device was used to compress the disc segments. Time, load, and the amount of displacement were recorded as flexion, hydration levels, and loading rates in separate tests with contrasting (flex or non-flexed) conditions.

Following the sectioning and initial compression testing, the nucleus pulposis of each of the 96 samples was split, examined, and photographed to locate any signs of disruption. The researchers concluded that the height of intervertebral discs increases at a slower rate when the disc is more hydrated. Because each of the discs studied had statistically similar hydration levels, the research suggests that the duration of a static load will influence disc height and hydration levels. This means that hydration levels within a disc can be manipulated by static preloads—a finding in agreement with previous studies. For the purposes of this study, the researchers concluded that disc height was stabilized after approximately 20 hours, and the disc was considered fully hydrated at that time.

Following the disc analysis, the study samples were categorized into five groups based upon the amount and type of damage that had occurred to the disc nucleus. The damage was assigned a weighting (W) value between 0-4 (“O” representing no observable damage and “4” representing complete or partial nuclear displacement), and values of 2 percent and 5 percent were used to distinguish between discs that had been moderately or severely impacted and whether they had sustained any disruption or movement of annular materials. An average damage weighting (ADW) scale was then applied to each biochemically-tested sample group.

Conclusions

 

The disc samples that were fully flexed and fully hydrated had damage that included nuclear sequestration or the formation of a cleft, or both. Discs that had been fully flexed and partially hydrated experienced some, though less severe, damage than those in the fully hydrated/flexed study group. There was little variance between the levels of damage in the non-flexed, fully hydrated and non-flexed, partially hydrated sample groups. The study authors concluded that the degrees of flexion and hydration were significant factors in intervertebral disc damage, but loading rate had little bearing on the severity of nuclear disruption.

While nuclear prolapse is reproducible in healthy disc samples by fully hydrating and flexing them, the compressive loading rate has little or no bearing in nucleus prolapse of discs with annular wall degradation. This study challenges the presumption that disc prolapse is caused by a degenerative process involving repeated mechanical stress. Instead, the healthy disc nucleus is at risk of annular tears or prolapse when fully hydrated and flexed.