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.

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.


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.


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



Stability Hypermobility Model

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

What’s at Stake

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

The Evolution of the Concept of Spinal Stability

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

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

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

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

Stability and Instability

Stability | Instability Model

The Role of Spinal Stability in Back Pain

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

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

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

Advancements Lead to Improved Spinal Assessments

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


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

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







Zygapophyseal Joint Pain in Chronic Whiplash Patients

A study 1 of sensory hypersensitivity in patients suffering from chronic whiplash associated disorder 6 months or more after being involved in a motor vehicle collision (MVC) found that the hypersensitivity was reduced, and pain thresholds were increased after receiving a medial branch block (MBB) procedure of the cervical spine.  The results of the study indicate the cervical zygapophyseal joints most likely contribute to sensory hypersensitivity caused by peripheral and centrally mediated pain.


What’s at Stake?

A common problem of people who have been involved in MVC’s is chronic whiplash associated disorder (WAD). According to research, between 32-56 percent of those involved in MVC’s may continue to suffer from related disability or pain 6 months or longer after their accident. Research has implicated the cervical zygapophyseal joint as a possible source of chronic hypersensitivity in 54-60 percent of subjects with WAD—evidence that is supported across multiple biomechanical and neurophysiological studies. It is thought that tissues that had been seemingly unaffected by the MVC experience sensory hypersensitivity when the body’s pain processing mechanisms are altered in the spinal cord. This sensory hypersensitivity and central nervous system hyperexcitability decrease the pain thresholds in the body, creating an exaggerated response for thermal, electrical, or mechanical stimuli for WAD patients. The prognosis for WAD patients suffering from sensory hypersensitivity is poor, and better understanding of the phenomenon could improve long-term treatment outcomes.

The Study


The pretest-posttest exploratory study involved 18 volunteers (15 females, 3 males) with an average age of 45 years and who had experienced WAD for 6 months or longer, with numerous neck complaints, body tenderness, and decreased range of motion. A control group of 18 healthy patients (15 females, 3 males) with an average age of 45 years also participated in the study. A group of chronic WAD patients with pain reported for 6 months or longer and who had a minimum of 80 percent decrease in neck pain intensity following an intra-articular zygapophyseal joint block procedure also took part in this study. Exclusionary criteria included pregnancy, previous history of headaches or neck pain requiring treatment, central or peripheral neurological problems, coronary artery or peripheral vascular disease.

Researchers rated the subjects’ pain intensity levels on a scale of 1-10 before and after receiving MBB procedures. Quantitative sensory testing (QST) based upon pressure pain thresholds (PPT’s) and cold pain thresholds (CPT’s) were conducted on the control and WAD groups. All measures were recorded, including patient demographic variables and their current MVC litigation status.

Cold Pain Threshold Testing

A 30mm x 30mm thermode set to 32 degrees Celsius placed over the anaesthetized articular pillars of the cervical zygapophyseal joints measured cold pain thresholds in the test subjects as the temperature was decreased at the rate of 1 degree Celsius per second. Patients used a self-controlled switch to indicate when the sensation of cold turned to pain as each bilateral site was tested. (The minimum temperature was 1 degree Celsius.) The average values were gathered for analysis.

Pressure Pain Threshold Testing

The articular pillars of the cervical zygapophyseal joints, peripheral nerve trunk of the median nerve, and the tibialis anterior were measured in the PPT tests, with the subjects using a self-controlled switch to indicate when the sensation of pressure turned to one of pain. The tests were performed three times bilaterally on each site, with a pause of 10 seconds between each test. The average values were recorded and later statistically analyzed.

Cervical spine model to demonstrate zygapophyseal joints

Dynamic Cervical Model

Diagnostic Cervical Zygapophyseal Joint Blockade

The patient group with chronic WAD underwent two diagnostic zygapophyseal joint block procedures—one, prior to the study, where a spinal needle was inserted with fluoroscopic guidance into the joint while the patient was in the prone position. An injection containing a local anesthetic and a corticosteroid was made into the affected zygapophyseal joint. If these patients experienced a relief of pain intensity of at least 80 percent but their pain later returned, they received the second MBB injection. In this study, none of the patients were excluded from the second MBB, as each of them had experienced at least an 80 percent reduction of pain from the first procedure, with the return of pain post-procedure.


The WAD patients demonstrated clinically significant changes in their sensory hyperactivity measurements after the blockade of the cervical zygapophyseal joint. These changes included a decrease in CPT’s and increase of PPT’s in the cervical spine and distal sites. This finding is unique in the study of chronic WAD patients and suggests that minimizing the source of pain—in this case, the zygapophyseal joint—may help modulate sensory hypersensitivity in chronic WAD patients, at least in the short-term. The study authors urge larger trials with long-term follow-ups of patients to gather more information and improve the treatment outcomes of patients with WAD.

lumbar vertebra

A study of Modic changes in 228 middle-aged male workers found a strong association between LBP frequency and intensity and Modic changes observed on magnetic resonance imagery (MRI) scans. These Modic chances were most likely to be at the L5-S1 spinal level and were more strongly correlated with LBP symptoms when Type 1 lesions were present.

What’s at Stake?

Bone marrow lesions—also known as vertebral endplate changes— that are visible on MRIs are considered evidence of disc degeneration. There are three types of lesions recognized by Modic: Type 1, where fissuring and an increase in the subchondral marrow vascularity is apparent; Type 2, where there is fatty degeneration of the bone marrow; and Type 3, where subchondral bone sclerosis is suspected.

Previous studies seeking to establish a positive correlation between Modic changes and clinical LBP symptoms have been inconclusive due to flawed designs and/or limited subject pools. This cross-sectional study used middle-aged male workers to investigate how or if Modic changes affected the intensity and frequency of sciatica and LBP in its subjects.

The Study

The subjects involved in this study were all male—128 Finnish train engineers, and 69 Finnish paper mill and chemical factory workers—with a mean age of 47 years. The train engineers had worked at their jobs, which involved long hours of standing and approximately five hours per day of subjection to intense, whole-body vibrations, an average of 21 years. The control group of chemical and paper workers claimed a mostly sedentary experience during their working hours and were not exposed to intense vibrations while on the job.

Both groups were assessed prior to the MRI study about the number of prior LBP and leg pain episodes, particularly those with a duration of 14 days or more. They were asked to comment on the pain’s intensity over the past week and over a three-month period before the study. They were also questioned about any history of LBP and whether they were experiencing LBP on the day of the assessment. MRI scans were taken and analyzed by two radiologists with no knowledge of the names or histories of the scanned subjects. Modic changes were identified and sorted into groups based upon the three types, with mixed types (I and I/II, and II and II/III) combined, representing more active and less active degeneration types. Other disc irregularities were noted independently and blinded to the clinical data analysts when observed. Disc herniation was either normal, bulging, protrusion, or extrusion in the notation. Neural compromise was identified as no compromise, nerve root contact, or compression. Stenosis was defined and noted according to Willen et al criteria.

modic changes, vertebra model

Modic changes with basivertebral nerve vertebra.


Though the engineers reported the highest sciatica and 1 week and 3-month pain scores, Modic changes at one or more levels were like those observed in the control group—roughly 56%. In the combined groups, 15 % of the subjects showed Modic Type I changes only, and 32% had Modic II changes at one or more-disc levels. Ten percent showed Type 1 or II changes at the same, or separate levels. The combined subject groups had 178 Modic changes across various lumbar levels, with 30 % experiencing Type I and 66 % Type II. None of the scans showed Type III Modic changes. Eighty percent of all Modic changes were located at L4-5, or L5/S1 levels, and 61% of these changes were described as “extensive,” while 39% were minimal.

There was a positive correlation between the reports of LBP episodes—especially those experienced within the past week and three-month period prior to the study— and observed Modic changes at any level. Modic changes at the L5-S1 levels were positively correlated with previous LBP and/or sciatica, especially where high levels of pain were reported within the past week prior to the study. There was little-to-no correlation between reported pain and Modic changes at higher disc levels or at L4/5.

Type II changes at any level was positively correlated with a higher number of previous LBP, especially episodes occurring during the past week or three-month period prior to the study.

Extensive changes were positively associated with more LBP episodes in the past and higher levels of LBP or sciatica within the past week or three months prior to the study. This was especially true when extensive Modic changes were found at the L5-S1 levels or when minimal changes were noted, but the subject had an extensive history of LBP episodes. The LBP had little correlation with the extent of the Modic changes at upper spinal disc levels or at L4/5.


The results of the study—the first to analyze Modic changes as they relate to specific IVD levels— suggest that there is a positive correlation between Modic changes occurring at the L5-S1 IVD level and that LBP is more likely to be associated with Modic Type 1 lesions at this level than at other levels or with other lesion types. The authors of the study suggest more research—particularly of how Modic changes correlate with pain in a younger subject set—is necessary to verify these findings.



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.


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.

lumbar spinal canal, dural sac volume

A position-dependent MRI study 1 of 32 volunteer subjects found that the increased pressure from cerebrospinal fluid in the spines of the subjects who moved from supine to standing position while being imaged caused a significant expansion in their dural sac cross-sectional area.

The Study

A positional magnetic resonance imaging (MRI) study was conducted to evaluate how postural changes affected the lumbar dural sac. Each of the 32 male subjects was examined while in the supine, standing, and sitting positions. The L3/L4, L4/L5, and L5/S1 discs cross-sectional dural sac area and anteroposterior (AP) dural sac diameters were measured. The AP dural sac diameter and upper-endplate L1 and S1 angles were measured on midsagittal images, as well.

facet, lumbar spinal stenosis model, dural sac

Lumbar Spinal Stenosis Model

The Results

Forty-one percent of the subjects showed evidence of disc degeneration or protrusion, but no evident dural sac compression was found in any of the subjects. There were fluctuations in the mean dural sac cross-sectional area measurements and AP dural sac diameter that was posture-dependent. All subjects showed smaller mean dural sac cross-sectional areas when in a supine position. When changing the position from standing to supine, the dural area decreased more in the L5/S1 level, and the extended sitting position produced the largest increase at L5/S1. This held true for the AP dural sac diameter measurements as viewed on axial and midsagittal images.


Researchers examining the cross-sectional IVDs of asymptomatic subjects noted that there was a clinically-significant difference between the dural sac areas at the L5/S1 level that was posture-dependent, with the smallest area being noted in the images of those who were supine at the time of their MRI. The lumbar cerebrospinal fluid (S-CSF) pressures were higher in those sitting and maintaining upright positions. Gravity caused an increase in the hydrostatic CSF pressure and an expansion of the dural sac in the subjects imaged when standing or sitting, which is why those in the supine position had smaller dural sac cross-sectional area measurements.

No significant dural sac cross-sectional area differences were found at the L3/4 and L4/5 IVD levels between the sitting or standing positions, though the AP dural sac diameter was much shorter in the sitting extended position than in the sitting flexed position.

There was a decrease in the dural sac volume space and craniocaudal diameter when the subjects changed their posture from the sitting flexion to the sitting extended. On bending forward, the AP dural sac diameter increased, and it decreased when the subject bent backwards. However, the dural cross-sectional area had no significant changes at this level.

Different dural sac cross-sectional changes were noted for the L5/S1 level, which showed the highest increase after the subject moved from a supine, to standing, position. The researchers posited that this was caused by expansion of the dural sac creating a gravity related hydrostatic CSF. Subjects in the sitting and extended position showed the largest dural sac cross-sectional area at L5/S1. Researchers believe the shortened dural sac may have expanded into the smaller spinal canal space in this scenario.

Overall, there were greater differences in the dural sac cross-sectional area between supine-to-standing, and supine-to-sitting images than in flexion to extension positions. This indicates the gravity related hydrostatic CSF pressure is greater in these posture changes than in flexion/extension changes.

Though there was no dural sac cross-sectional area influence on the L3/4 and L4/5 segments when the subjects were seated in flexion or extension, their lumbar spinal canal space at all levels decreased when they changed their posture from sitting in flexion to sitting in extension. The researchers postulate dynamic variations of the cross-sectional dural area during flexion and extension are created not only by the degree of IVD bulging or buckling and thickness of the ligamentum flavum, but by a variance in total lumbar spinal canal space. The difference could be more pronounced in lumbar spinal stenosis patients with no additional epidural space to moderate the dural tube.


The study showed that posture affected the size of the dural sac cross-sectional area in a group of asymptomatic volunteer subjects. Specifically, when the subjects changed from the supine to standing position, increased pressure of the CSF expanded their lumbar Dura sac volume. The smallest changes were noted when the subjects were in the supine position.

Total lumbar spinal canal space plays a factor in the dural sac cross-sectional area in flexion and extension. Gravity-related hydrostatic CSF pressure appears to be the most important factor in increasing the dural sac cross-sectional area in otherwise asymptomatic subjects.

no pain, congenital insensitivity

A topical review 1 of the literature on congenital pain insensitivity highlights the complexity of pain perception as it relates to anatomical and physiological defects—congenital, or acquired—and concludes the deficits may preferentially affect carious components of the medial pain system, including the anterior cingulate cortex. Because the studies reviewed failed to locate the origin of the deficits observed, the authors of this review emphasize the need for careful assessment of all pain sensory components in patients to better understand the pathways involved in pain perception. They also propose that gene mapping afflicted patients may help provide understanding about the molecular mechanisms at work in pain perception. This could lead to more effective and selective therapies in the future.

What’s at Stake?

There is overwhelming evidence about the necessity of pain perception to human survival. Studies of patients with congenital disorders that inhibit their abilities to experience or respond to pain show that many people afflicted with pain insensitivity die during childhood due to their inability to notice discomfort from illness or injuries. A recent lack of scholarly interest in the United States about pain insensitivity necessitated an updated review of the clinical literature of the phenomenon to help better understand its mechanisms and origins. The authors of the review stress the importance of a better and more complete assessment of the components of pain perception and insensitivity—possibly through gene mapping of patients—in order to provide more comprehensive and effective therapeutic measures in the future.

About Pain Insensitivity

Medical literature about pain insensitivity has existed since the 1930’s. The condition—in which patients are either unable to experience, have a reduced sensitivity to, or can feel, but have little-to-no-reaction to pain, has been termed “congenital general pure analgesia,” “congenital universal indifference to pain,” and “congenital absence of pain” over the years. More recently, the predominate terms used to describe the affliction have been “congenital insensitivity to pain” or “congenital indifference to pain.” The terms, which have been used interchangeably, have now been distinguished to reference two separate groups of patients, depending upon the specific origins and symptoms of their condition.

Insensitivity to Pain

Patients who are insensitive to pain have a reduced or inability to experience pain sensations. They may be unable to distinguish between different types, intensities, or qualities of painful stimuli.

Indifference to Pain

Patients with a congenital indifference to pain can feel pain but have no affective response to it. They will not react to painful stimuli by withdrawing from the source of pain.

In the past, individuals with pain insensitivity were diagnosed and treated based upon a set of observational criteria that included unaccounted for wounds or lesions and excluded from the diagnosis when their pain impairment that could have been caused by other underlying conditions or injuries. As technological medical diagnostic advancements allowed for better assessment methods of nerve pathologies, patients with irregular sensory nerves who in the past might have been classified as “congenital indifference to pain,” are now classified under a subheading of “congenital pain insensitivity arising from peripheral neuropathies of various types”.

Components of Pain Perception

There are three recognized components to pain perception—sensory-discriminative, affective-motivational, and cognitive-evaluative. Those suffering from pain insensitivity may demonstrate their sensorial deficits across a broad range of responses to stimuli.

Pain Discrimination Loss

When a patient loses the ability to discriminate between types of painful or uncomfortable stimuli, they may not be able to distinguish between sharp and dull sensations or hot and cold temperatures. They may, however, experience a negative emotional reaction to these stimuli, even though they cannot name the source of their discomfort.

Affective-Motivational Response Deficit

Patients with affective-motivational response loss experience painful and uncomfortable stimuli but have no reaction to it. When a patient has this condition, also known as “Pain Indifference,” they do not withdraw from painful stimuli. This makes them vulnerable to burns and other injuries. Some patients with affective-motivational deficits may have a negative reaction to pain but will not withdraw from it and will allow repeated painful stimulus to be applied without objection.

Pathways to Pain

Pain perception is modulated in large part by two ascending pathways—the lateral pain system projecting through lateral thalamic nuclei to the somatosensory cortex, and the medial pain system, which projects to the anterior cingulate cortex and insula through the medial thalamic nuclei. The sensory-discriminative pain component is modulated by the lateral system, and the affective response to pain is modulated through the medial system.

Pain perception impairments may be caused by lesions in specific regions of the brain or loss of peripheral afferents, which may create deficits in sensory and affective pain responses. Depending on the size and location of a lesion, the impairment may be localized and subtle or severe.

Congenital and Hereditary Pain Insensitivity Syndromes

Many children with peripheral neuropathies experience sensory-discriminative and affective-motivational impairments and may be diagnosed with hereditary sensory and autonomic abnormalities (HSAN). There are five sub-categories of HSAN currently recognized, and all of the types are known to exhibit small-diameter C and A-delta fiber involvement. These fibers are responsible for the transmission of pain sensation.

There is a wide spectrum of HSAN features, including an inability to experience the sensation of burns, digit mutilation, and injuries to the joints. Many of the patients are unable to distinguish between the type and intensity of painful stimuli and do not take precautionary measures to prevent the recurrence of pain or remove themselves from painful situations. Genetic causes have been investigated, and specific genes have been identified for many forms of HSAN, but the condition is at present uncurable.


Congenital Pain Indifference

Patients with congenital indifference to pain may have normal sensory reactions when examined but experience painless injuries as early as infancy. On past examination of peripheral nerve samples, clinicians found no abnormalities and thus characterized the disorder as a deficit in pain response. Because no analysis of nerve fiber density was performed on these patients, it is unclear if their disorder might have been caused by a selective loss of nerve fibers.

It has been suggested that these patients might have been experiencing a neurotransmitter disturbance that affected their central sensory processing pathways. Other reports indicate that this type of disorder may have peripheral and central nerve origins.



Deficits in pain perception can also occur as a result of brain lesions in areas that modulate the processing of painful stimuli. This can create congenital pain insensitivity-type disorders. When these lesions occur in the anterior cingulate cortex or insular cortex, they may affect the function of the medial pain system and cause a loss of affective-motivational function. Sensory-discriminative components of pain may be affected by lesions in the primary and secondary somatosensory cortex affecting the lateral pain system.

Patients with affective-motivational deficits who retain a sense of sensory discrimination are suffering from ‘asymbolia for pain.’ They may experience pain but have no—or an unusual—response to it, such as laughter. It is possible an impairment of the sensory-discriminative pain components, without affective-motivational components, could be caused by central lesions.


The variations of pain insensitivity syndromes and the deficits they cause make clear the complexity of pain perception physiological and anatomical processes. Though it remains unclear exactly how the disorder originates, current research suggests the need for a more complete assessment of how the different components of pain perception affect sensory intensity and response in HSAN patients. Genetic mapping may assist clinicians in developing better, more selective therapies for patients in the future.