Does Spinal Posture Act as a Trigger for an Episodic Headache

A review 1, found in Current Pain and Headache Reports was conducted to see if there was indeed a valid link between spinal posture acting as a trigger for an episodic headache. While the review concluded more research is required, it did present some interesting results.

The Global Issue of Headaches

According to the WHO (World Health Organization), headaches are one of the ten most disabling conditions for human beings. Numerous factors have been studied to contribute to or give rise to the development of a headache. Secondary headaches have been observed to be due to an underlying etiology, for example, trauma, infections, and dysfunctional or abnormal cervical structures. Take note, primary as well as certain secondary headaches arise from complex multi-dimensional interactions between lifestyle, psychosocial, cognitive, biological, and environmental factors. Due to several triggers, identifying underlying mechanisms of headaches continues to be challenging.

Headaches and Spinal Positions

The current world encourages people to remain seated. According to studies, when daily computer use exceeds 3 hours, there’s a higher prevalence of musculoskeletal complaints. Such complaints include experiencing pain in the neck, head, or upper extremity. These complaints are suspected to be linked to slumped sitting postures.

A slumped sitting position involves an increased posterior pelvic rotation, forward head posture, and thoracic flexion. Such postures (if sustained) tend to increase the biomechanical momentum and torque, decrease proprioception, cause creep of spinal tissue, and limit postural variability.



Headaches and posture

Why do such a Review?

While an extensive framework for headache classification is provided by The International Classification of Headache Disorder, outcomes following physiotherapy do vary. Such variability might be explained due to the absence of protocol studies for identifying the role of spinal posture in headaches. That’s why conducting multi-dimensional profiling of patients (suffering from a headache) based on the interactions present between spinal posture, lifestyle, and psychosocial factors may be essential.

The current review had the objective to find support about whether spinal posture could trigger an episodic headache. The review considered a multi-dimensional view on tension-type and cervicogenic headache (this included modern pain neuroscience).

What Did It Find?

The current review described several pathways to support how spinal postures acted as a trigger for an episodic headache. Psychosocial factors could also act as a catalyst for the development of a headache through a maladaptive spinal posture.

However, further research is still required to determine the exact level of contribution of spinal postural dysfunctions and their ability to trigger a headache.

Why is Subchondral Bone Density Higher in People with Low Back Pain

A very recent study from September 2019, 1 published in the journal Skeletal Radiology, brought forward an interesting conclusion related to Low Back Pain or LBP. The results showed that the subchondral bone density was higher in people with LBP.

What was the Context?

According to years of data, LBP happens to be the second most common adult-disability around the world, with the lifetime prevalence being 54-80%. It leads to sociological, economic, and psychological stress. The causes behind LBP include facet joint osteoarthritis (OA), disc degeneration, soft tissue sprain, nerve impingement, instability, infection, and neoplasm. Being more specific, OA of the facet joints (the load-bearing joints of the posterior spine), is considered as the reason of LBP in 15–45% of patients.

Take note; long-term changes in the bone’s mechanical loading alters its microstructure. An increase in the mineral density of the subchondral bone has been observed due to loading on the joint’s subchondral surface. Such a change has been seen in joints of the upper and lower extremities as well as in the joints of the spine.

What Did the Current Study Do?

Apparently, not a lot of research has been conducted for analyzing such changes with a focus on the loading patterns of facet joint and its relation to LBP as well as how the subchondral bone is involved.

The current study had two objectives. It aimed to test the hypothesis that LBP is associated with the density of the lumbar facet subchondral bone. Other than that, it was to use computed tomography osteo absorptiometry to analyze the distribution of the subchondral bone density in the facet joint. The study wanted to better understand the loading pattern of the lumbar spine’s facet joints.

facet joint

The Design

The current research involved 89 volunteers. From them, a total of 33 were recruited as subjects that also had LBP, and a total of 56 were subjects with no LBP. The males were 47, with the females being 42. The mean age came in at 36.5 years.

All of the subjects went through lumber computed tomography (CT) scans. 3D joint surface models were created of each facet joint as well as the subchondral bone density underneath every facet joint surface.

This study used linear interpolation of the HU (Hounsfield units) at four adjacent pixels in each of the CT slice. Furthermore, ANOVA with post hoc Fisher pairwise comparisons was used for testing the association of subchondral bone density with lumbar levels, facet zones, subject gender, and patient age.

What Did the Results Show?

The results presented that subchondral bone density was observed to be the greatest in subjects with LBP as well as female and younger subjects. It was also highest in the superior facets, the center zone of the facets as well as the upper lumbar levels.

Also, it was lowest in subjects that didn’t have LBP, the male subjects, and older subjects. It was also lowest in the caudal zone of the facets, the lower lumbar levels, and the inferior facets.

What Was Concluded?

According to the present study, the data showed the differences present in the subchondral bone density when analyzing subjects with or without LBP. Furthermore, one can see how a higher density in subjects with LBP might be related to an increase in load-bearing because of the degeneration of the lumbar discs or perhaps due to the load’s abnormal distribution in the joint because of the joint’s articular cartilage being degenerated.

The current data hopes it can help others better understand the loading patterns of joints and the associated biomechanical properties.

Do Transient Effects of Sleep Impact Next-Day Pain and Fatigue Experienced by Older Adults with Symptomatic Osteoarthritis

Research has shown that poor quality of sleep is associated with higher rates of pain and fatigue in people dealing with OA (osteoarthritis). The current study 1, in the Journal of Pain, was conducted to determine whether or not sleep impacted the diurnal pattern of next-day pain and fatigue associated with OA. The results showed that good sleep was linked to lower pain and fatigue on awakening. However, the benefit dissipated as the day went by.

The Context

As mentioned, older adults with OA tend to commonly experience pain and fatigue because of poor quality of sleep. More research is still required to examine the influence of nocturnal sleep on pain and fatigue throughout the day.

Understanding such mechanics might prove to be beneficial when dealing with older patients with OA and helping them improve their quality of life.

Pain and Fatigue

The Study

The aim of the current study was to observe the links between self-reported sleep quality and sleep parameters with pain and fatigue experienced through the following day. The study used data covering five consecutive days from older adults with hip and/or knee OA.

The study’s objective was to investigate sleep’s association with diurnal changes in fatigue and pain. The study was conducted to answer whether or not specific times of the day existed during which symptoms are more vulnerable to the effects of poor sleep.

The study included 160 participants (adults aged 65 years and above). People with clinically important levels of fatigue were recruited.

The Western Ontario and McMaster Universities Arthritis Index (WOMAC) five-item pain subscale was used to measure pain intensity. Fatigue was measured, for this study, using the Brief Fatigue Inventory (BFI). Sleep was assessed each morning. Pain intensity and fatigue were assessed five times a day.

Using the Actiwatch-Score, the sleep intervals were established through corroborating self-report of lights off and wake-up times with actigraphy activity counts.

Stata was used for analysis.

Pain and Fatigue disc model

What was Concluded?

The results of the current (sleep quality and OA) study helped conclude that diurnal patterns were demonstrated by pain and fatigue. A good night’s sleep showed significantly lower symptoms in the morning. Good sleep had a significant impact on fatigue compared to pain intensity. A poor night’s sleep was linked to an increase in pain intensity in the morning (though it dissipated as the day progressed). However, more research (with a higher sample size and diversity) was needed to determine any future clinical benefits.


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.

Disc pressure, spine, patient education, models

A study 1examining cadaveric intervertebral discs (IVD) indicates disc degeneration is more closely related to reduced pressure associated with mechanical loading than levels of endplate porosity or thickness. Though endplate porosity increases as the IVD degenerates, the results of the study demonstrated that IVD degeneration is caused by reduced pressure in the nucleus—not the reduction of nutrient transport caused by endplate thickening and a reduction of porosity—and that mechanical loading from nearby discs contributes to endplate porosity in age-related disc degeneration.

disc pressure, degeneration

Disc pressure reduction with degeneration.

What’s at Stake?

Understanding the role of IVD endplate thickness and porosity and the role of mechanical loading, age, and sex on determining the efficacy of endplate function is important in the future diagnosis and treatment of disc degeneration. The enervated endplates, when damaged or degenerated, can cause back pain. When properly functioning, they are responsible for the transport of nutrients to the IVD, regulate fluid pressure and metabolite transport between the body of the vertebrae and its nucleus. Disruption in this process can contribute to disc degeneration, inflammation in the vertebrae, and possible infection to the disc.

The level of porosity inside the bony endplates affects the amount of nutrients delivered to the nucleus and the mechanical stability of the vertebrae. A porous endplate allows more nutrients and pressure-regulating fluid to flow into the nucleus of the IVD. A thickened, less porous endplate reduces the nutrient and fluid flow, but creates more structural stability in the IVD, reducing the potential for injury. The proper balance and porosity of the IVD unit is integral to the overall health of the disc, but understanding the mechanism by which the degenerative process occurs is essential in anticipating how a body’s mechanical functions might contribute to a disruption of disc health.

The Study

Researchers compared the relative thickness and porosity of IVD endplates in 40 cadaveric motion segments from 23 cadavers between the ages 48 to 98 years old. The segments were subjected to compression, and the intradiscal stresses were measured and analyzed. Stress profiles were created to determine the average nucleus pressure, as well as the maximum anterior and posterior annulus pressure. The segments were dissected, and discs with endplates on each side were scanned and analyzed for their thickness and porosity in the midsagittal regions. An average value was calculated for the anterior, central, and posterior regions of each of the endplates. A macroscopic and microscopic examination determined the scope and level of disc degeneration in each segment.

The Results

The results of the data sets indicated that nucleus pressure and posterior and anterior annular stresses decreased as the disc degeneration levels increased. There was a slight increase of intradiscal pressure (IDP) with age, but there was no maximum stress increase of the annulus with age. Lower spinal levels were associated with a decrease in IDP.

The endplates were thinner nearer the nucleus, with a 14 % reduction in thickness in the inferior endplates. An analysis of the averaged data set from the three regions of both endplates showed no association between age or level of degeneration and endplate thickness, but there was an inverse relationship between the disc degeneration and endplate thickness. There was a strong relationship between endplate thickness and IDP in an analysis of adjacent discs.

Endplate porosity was more pronounced in the center of the endplate and became less so opposite the annulus. This porosity was not age-dependent but—with the exception of the anterior endplate region— was positively correlated with disc degeneration levels. The levels of endplate porosity was inversely associated with adjacent disc pressure and stress.


Endplate thickness was the major determinant of endplate porosity levels. Disc degeneration and mechanical loading measures were also indicated as predictors. The most apparent predictors of endplate thickness (after porosity) included disc pressure and spinal level. IDP was the dominant predictor of disc degeneration.

The study found that disc degeneration was associated most often by disc stress, rather than porosity of the endplate or its thickness. As the levels of disc degeneration increased, porosity of the endplate increased. The porosity of the adjacent disc was inversely affected in terms of pressure and mechanical stress.

Wolff’s law posits that the body’s bone mass and design will compensate for the pressures of mechanical stresses and subsequent anatomical deformation, strengthening the endplates and vertebrae that are subjected to the most physical activity. Reduced loading can thin endplates that are not subjected to pressure. This eventually leads to them becoming more porous. The results of this study affirm this theory, as the lower central endplate regions were harder, thicker, and stronger than those of the anterior-posterior endplate regions. There is an apparent compromise between the strength of the outer bone and the porosity of the central endplate, which allows for stability and nutrient flow where they are needed the most.

There is an evident drop in nucleus pressure during progressive disc degeneration. The reduction of fluid pressure lessons the endplate’s thickness and makes it more porous, leading to bone degeneration and loss. The bone is more likely to buckle and further degrade as it becomes more porous and less stable, reducing nucleus pressure further. This cycle of abnormal pressure reduction is responsible for the continuation of the degenerative process—not the reduced metabolite transport. There is an increased risk of bone fracture with increased porosity and endplate thinning. A fracture would increase stress on the IVD and contribute to the cycle of degeneration, in spite of the increased availability of nutrients that can reach the nucleus through the endplate’s porosity.