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.

lumbar creep

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

What’s at Stake?

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

flexion and pain

The Study

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

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

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

Results

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

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

Conclusion

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

 

 

biomedical cause, LBP

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

What’s at Stake?

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

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

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

 

Professional LxH Dynamic Disc Model

Professional LxH Dynamic Disc Model

The Study

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

Overarching Theme: Biomedical Triggers

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

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

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

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

Overarching Theme 2: Non-biomedical Triggers

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

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

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

Conclusion

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

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

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

Stuart McGill, ddd spinal models

In an online interview with Bill Morgan, President of Parker University, world-renowned spine researcher and scientist, Stuart McGill, uses dynamic disc models from Dynamic Disc Designs to explain lumbar disc herniations, extrusions, and the mechanisms for lumbar disc injuries and treatments.

When treating spinal injuries, McGill stresses the importance of recognizing that the cause of most disc extrusions and herniations is a combination of factors, occurring over time. The cumulative array of factors may present as an acute condition causing pain, but in most cases, the disruption has not been created by a single loading event.

McGill uses the analogy of cloth to explain how repetitive loading and movement fray the collagen fibers that cover the socket joints, eventually working a hole into the fibers by repetitive stress strains occurring in a back and forth motion.

“The disc is layer upon layer of collagen fibers held together with [a tightly woven lamination matrix]. If you keep moving the disc under load, the hydraulic pressure of the pressurized nucleus slowly starts to work its way through the delamination that forms because of the movement,” he says.

He explains that when the collagen is intact and supple, a person has full range-of-motion without danger of creating tears, but when the spine is stiff and has become adapted to bearing heavy loads, it is in danger of injury.

“The problem comes when you combine the two worlds and confuse the adaptation process,” he says.

“In a modern lifestyle, you might have a person who sits at a computer for eight or more hours in a flexion stressed position which—on its own—may not be that bad. But then they go to the gym for an hour every night and start lifting loads. They’re taking their spine through the range of motion, so cumulatively, the collagen is asked to move, but it’s also pressurized. The nucleus behind gets pressurized and slowly works its way through the delaminated collagen.”

Stuart McGill, Models

Stuart McGill and the many ddd models he uses.

McGill, Dynamic Disc Designs

Professor Stuart McGill and Dynamic Disc Designs endorsement.

Recreating Compression Loading, Disc Bulge, and Proper Thrust Line with our Dynamic Model

Using the disc model, McGill demonstrates how the gel inside the disc remains pressurized under compression, but in cases where the collagen has become delaminated, bending the spine under a load creates a disc bulge.

“This is exactly what we see on dynamic MRI,” he says, manipulating the disc model to demonstrate. “In the laboratory we would inject the nucleus with various radio-opaque markers. We would watch the migration as the bulge would come through. Touch a nerve root and now you would match where the disc bulges with the precise anatomic pathway. If you sit for 20 minutes slouched and your right toe goes on fire, we know it’s the right ring and that’s exactly where the disk bulge is.”

McGill stacks the disc model into a thrust line and squeezes the spine segment to show how proper alignment adapts the movement experience.

“The whole disc is experiencing movement, but there’s no pressure, and nothing comes out to touch the nerve root,” he says.

Empowering the Patient with Simple Posture and Stress Exercise

McGill says his insight is based upon years of experiments studying the exact mechanisms of spinal injury and pain. He recommends using improved posture and stress—lying on the stomach for five minutes with two fists under their chin—to help,” mitigate the dynamics of that very dynamic disc bulge.”

He says the immediate relief provided by this simple exercise can empower a patient with discogenic pain and help alleviate the potential psychological trauma of feeling hopeless at not understanding the source of, or how to mitigate, pain.

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.