cortisol and stress and impact on back pain

A July 2019 study 1 examining the pathological effects of cortisol on the intervertebral disc (IVD) cells and human mesenchymal stem cells (hMSCs) of lower back pain (LBP) patients found evidence that stress-and-pain-induced cortisol—especially when chronic—may contribute to IVD degeneration and inhibit the regenerative process of IVD cells.

What’s at Stake?

Chronic LBP is experienced at some point by over 80 percent of the Western population. When caused by disc degeneration, it is often linked to chronic inflammation in the disc and endplates. The pain associated with disc degeneration induces a biochemical stress response that releases the hormone cortisol into the body. This study explored the in vitro effects of stress—and the subsequent release of cortisol—on IVD and stem cells. Specifically, it examined how cortisol might be involved in the degenerative process and in inhibiting cell regeneration in LBP patients.

The Study

IVD tissue and bone marrow aspirates (BMA) were collected from six male and female spinal fusion surgery patient donors between the ages of 32 and 54 years old. The cell samples were isolated and cultured before utilizing a 3D microenvironment model consisting of DNA-analyzed, histological pellet sections, light microscopy, and colorizing stain to evaluate the effects of cortisol on their density. Glycosaminoglycan (GAG) analyses quantified how much proteoglycan each sample contained, and paraffin-embedded samples were deparaffinized to find the presence of apoptotic cells. The data retrieved was then analyzed using SPSS 25.0 software.

Results

The results of the data collected in this study indicate that cortisol—especially high amounts—is damaging to cell viability, proliferation, and regeneration. Though hMSC cell viability remained stable seven days after cortisol stimulation, the number of viable cells increased over time, and there was a decrease in hMSC cells treated with cortisol after 14 days when compared to the control group. The cell viability in DC pellets was much lower than the control group 28 days after being treated with cortisol.

A higher number of apoptotic cells also occurred when these glucocorticoid levels were stimulated—a result that agreed with those of previous studies where apoptosis appeared to play a significant role in the loss of viable cells during the progression of IVD degeneration. Previously, very high levels of corticosteroids (including cortisol) were shown to induce apoptosis in certain types of cells, including chondrocytes. The results of the current study suggest stress-induced cortisol imbalance increases IVD degeneration by increasing apoptosis.

DNA content in DC pellets were increased seven days after cortisol treatment but decreased on the 28th day, when treated for both concentrations. The DNA content in hMSC pellets treated with cortisol was lower on day seven and 14 after treatment and dropped even further on day 28.

GAG content in the DC pellets decreased for all groups from day seven, to day 28 after treatment, and the DC pellets had much less GAG on day seven than the control groups. There was a significant reduction in GAG production in the hMSC pellets on day 14 after cortisol treatment, as compared to the control group.

The proteoglycan levels in the hMSC pellets all but disappeared by day 28, though levels had been evident in the DC and hMSC groups on day 14 of the study. The pellet sizes on day 28 were also smaller than the controls of both types of cells, suggesting cell proliferation was inhibited by cortisol. On days seven and 28, more fragmented or apoptotic cells in both the DC and hMSC pellets were detected after being treated with cortisol. Another test found less chondrogenesis than the controls in both pellet groups by days seven and 28.

IVDs receive important nutrients through endplate capillary diffusion. Estrogen receptors have been found in the nucleus propolis of the IVD, which points to the possibility that small hormone proteins like cortisol may reach the IVD through this process. In any event, the stress of chronic LBP could create excessive levels of cortisol in patients, compromising chondrogenic differentiation and the hMSCs’ multipotency.

In this study, chronic cortisol exposure compromised cell proliferation and chondrogenesis in DCs and hMSCs, and excessive levels of stress hormones further jeopardized the ability of the cells to regenerate.  The differentiation and immunomodulatory abilities of the in vitro hMSC cells were suppressed by cortisol exposure. The results of this study support the theory that IVD degeneration and regeneration may be negatively affected by pain-induced stress.

 

 

LxH Model

In this video, Dr. Jerome Fryer, of Dynamic Disc Designs, shares the newest version of the LxH model, which contains a malleable disc bulge. He explains how using this model—inspired by the nomenclature and definitions of Fardon’s research paper in the Spine Journal1— can help practitioners demonstrate to patients the biomechanics of what is happening in the spine when they are suffering from a disc bulge. 

“[Fardon] defines the disc bulge [as extending] beyond the endplate, [past] its full circumference,” explains Fryer. “This model has a disc bulge extending beyond the… border [at] L4. 

 

Insights into Annular Thinning, Protrusions

Fryer says the new model also contains a protrusion with annular thinning on the left side which is helpful in explaining the nature and definition of protrusion. 

“It’s a contained nucleus with a thinned annular wall,” he says. “So now people can really understand what load looks like and what a disc bulge is.”

He likens the condition to a low pressured car tire—something most adults will be able to relate to when shown a visual model. 

disc bulge, tire bulge

About Dynamic Disc Designs

Fryer creates his Dynamic Disc Design lumbar and cervical spine models in the belief that better understanding the spine will empower patients, encourage stronger clinician-to-patient trust, and lead to more a more positive treatment outcome for spinal patients. For more information on ordering any of the Dynamic Disc Design products, and for up-to-date research on hundreds of spine and pain topics, visit Dynamic Disc Designs

 

lumbar disc herniation

A study investigating kinematic changes in subjects with lumbar disc herniation (LDH) performing five activities of active daily living (ADL) found that LDH patients were more apt than healthy subjects to restrict the lower lumbar (LLx) and upper lumbar (ULx) spinal motions when performing ADLs. The LDH patients used pelvic rotation to compensate for their reduced lumbar flexibility and increased pelvic tilt and lower extremity flexion during problematic ADLs. 

What’s at Stake?

Lower back pain affects up to 85 percent of the worldwide population—especially those over 40—and can contribute to musculoskeletal problems when the lower spine and its surrounding structure is overloaded. Because LBP patients often restrict musculoskeletal motions during ADLs to avoid pain, understanding the kinematic idiosyncrasies of LBP patients during their ADLs is essential when treating spinal issues through physical therapy that involves gait and functional training. 

Past research has indicated LBP patients had less transverse plane movement than healthy subjects during level walking exercises. One study found that LBP subjects were more likely to exhibit spinal or pelvic rotation, while another study came to the opposite conclusion but found that LBP patients had less range of motion (ROM) in the lumbar spine than the control group. Conflicting studies have concluded that LBP patients had significant reductions in the range of hip flexion and spinal movement across all three planes during trunk flexion or better ROM in the lumbar spine, with more restriction in the pelvic or thorax ROM. The divergent conclusions are likely due to the trunk and whole lumbar being considered a single, rigid segment, rather than interconnected segments that operate independently. The prior studies may also have neglected to consider the kinematic differences among LBP patient subgroups. Analyzing the variability of joints and segments is vital when studying LBP patients and their unique kinematics. 

This study focused on how lumbar disc herniation (LDH) specifically contributes to LBP, including the lower trunk, thorax, hip, and pelvis. The goal of the study was to use a computing model to study LBP patients with LDH and understand their pain-related modulation of their lower extremities and multi-segmental trunk kinematics during level walking, stair climbing, trunk flexion, ipsilateral pickup, and contralateral pickup. 

The Study

Twenty-six healthy males with a mean age of approximately 24 years and seven LHD diagnosed male patients who were, on average, approximately 28 years old participated in the study. The disc herniations occurred at L4/5 in three of the LDH patients, L5/S1 in three cases, and at both locations in one patient. 

The motion of thorax, ULx, LLx, pelvis, hip, and knee were tracked via 3D active markers placed in various locations on the subjects’ spines, pelvises, thighs, and shanks. All the markers were placed by a single surgeon, who had previously demonstrated the five ADLs the subjects were to perform. After practicing the motions a few times, the subjects repeated them while data was collected through the active markers. 

The kinematics of the thoracic segment, ULx, LLx, pelvis, hip, and knee were calculated using a modified Gait-full-body computing model that would analyze the motion of each lumbar vertebra using at least three markers. The kinematic spine and hip angles were analyzed with the computing model using a Euler rotation sequence of spinal segments or thigh/pelvis movement, and the thoracic segment as it related to the L1 vertebra. The ROM for all segmental or joint angles during flexion-extension or gait cycles across all three planes in three planes was calculated, and data analysis was performed using a custom program. 

Results

The LDH subjects had much more pelvic rotation and LLx rotation than the healthy subjects during level walking. The LDH group had much less ROM for thoracic flexion, pelvic tilt, and hip abduction during stair climbing, but they showed more ROM for LLx rotation. No clinically significant variance was noted between the two groups for thoracic flexion, trunk flexion or ipsilateral and contralateral pickups. Lumbar flexion ROM was significantly decreased in the LDH group—especially for ULx with nearly no sagittal angular displacement.  

The findings suggest that people with LDH modulate their movement patterns and motor regulation in response to, or avoidance of pain. There were evident kinematic differences between the healthy subjects and LDH patients in this study. LDH patients had more pelvic rotation and increased LLx rotation during level walking, contradicting earlier studies where patients had less than or similar pelvic rotation when compared with healthy subjects. The use of different marker sets, study methods, computer models, and speed of motion might account for the varying test results, but it appears that pelvis and LLx motions in the transverse plane may have a more pronounced effect than that of the other two planes during LDH abnormal motion level walking analysis. 

Conclusion

In regard to the direction or range of motion, there were contrasting kinematic characteristics and different adaptations to LDH between the ULx and LLx in this study. The thoracic motion did not appear to be affected by the LDH when subjects were performing the ADLs, with the exception of stair climbing. During all five ADLs the LDH patients maintained limited lumbar flexion, and their pelvises, knees, and hips compensated for the lost lumbar motion capacity in the sagittal plane during contralateral pickups. In four of the five ADLs (the exception being stair climbing), the LDH patients increased their pelvic rotation significantly. They also had higher rates of antiphase movement between thorax and pelvis in the two pickups and in level walking and stair climbing in the transverse plane between ULx and LLx.

The findings of this study should help provide a more comprehensive understanding of how LDH influences kinematics and lead to more specific treatments and better therapeutic outcomes for LDH patients. 

disc height

In this Spine Education video, Dynamic Disc Designs’ Dr. Jerome Fryer demonstrates the benefits of helping lower back pain patients better understand their condition by using dynamic models and visual aids.

“How often do you encounter a patient that explains that their symptoms are worse as the day progresses?” he asks.

Though clinicians understand the key to a graduating pain syndrome involves a complex biomechanical and biochemical matrix in the spine, back pain patients don’t need extensive medical knowledge to appreciate the dynamics of what is happening in their bodies. A simple visual aid can help clarify and simplify their predicament and potential solutions.

 

Hands-On Demo of Diurnal Expression of Fluid from the Disc

Using a dynamic disc model, Fryer demonstrates the diurnal expression of fluid from the disc as the disc height changes over the course of the day.

“We know that the disc height is tallest in the morning,” he says, holding a fully expanded disc model to the camera and then slowly squeezing the dynamic model to demonstrate the loss of height that occurs throughout the day.

“As the day progresses, the disc height will slowly lose its height [causing the facets] to imbricate or shingle. If a patient [complains] their symptoms are more present as the day progresses, you [use] this graph 1 to demonstrate what’s happening in their spine.

“As the person gets up in the morning, there is a quick change in the disc height in the first 10 minutes,” he says, pointing out a steep curve on the graph.

“As the day progresses, the disc height is lost.”

Annular Disruption in Degenerated Discs Reduce Capacity to Maintain Height

Fryer says the situation can be even more extreme when a patient is suffering from degeneration in the disc because the disc can no longer hold its full height, due to disruption in the annulus.

“Helping patients understand symptoms as the day progresses will help them understand why it hurts,” he says. “That gives you more empowered strategies to help patients get motivated, if its posture, or even recumbency, or exercise, or getting out of a chair to help with the disc height changes. These dynamic disc models are very powerful in helping patients with self-awareness.”

For more information on dynamic disc models and patient teaching aids, visit 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.

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.

 

 

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.

Conclusion

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.

Results

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.