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. 

biomedical cause, LBP

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

What’s at Stake?

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

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

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

 

Professional LxH Dynamic Disc Model

Professional LxH Dynamic Disc Model

The Study

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

Overarching Theme: Biomedical Triggers

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

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

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

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

Overarching Theme 2: Non-biomedical Triggers

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

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

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

Conclusion

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

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

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

Stuart McGill, ddd spinal models

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

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

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

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

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

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

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

Stuart McGill, Models

Stuart McGill and the many ddd models he uses.

McGill, Dynamic Disc Designs

Professor Stuart McGill and Dynamic Disc Designs endorsement.

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

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

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

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

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

Empowering the Patient with Simple Posture and Stress Exercise

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

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

inflammation, re-absorption

A review  1 of the clinical literature regarding lumbar disc herniation (LDH), particularly as it relates to the phenomenon known as “spontaneous LDH regression,” in which the herniation reduces or resolves without surgical treatment, concludes that the inflammatory response that contributes to nerve pain and damage may also be responsible for the spontaneous re-absorption of the herniation. Therefore, except in extreme cases where a neurological deficit or intolerable pain is experienced by the LBP patient, treatment for LDH should be conservative and custom-tailored to address the specific biochemical mechanisms at play in the patient.

What’s at Stake?

The pain and economic disability caused by LDH affects roughly 9 percent of the world’s population and is strongly associated with the aging process. Recent studies have indicated that the malady is more often caused by a failure in the endplate junction, rather than an annulus fibrosis (AF) failure, with its associated nerve ingrowth. This explains why up to 40 percent of patients diagnosed with LHD after imaging tests are asymptomatic.

Typically, LDH and degenerative disc treatments may be surgical, or conservative (non-surgical), with the decision about which approach is appropriate determined cooperatively by the clinician and patient. Because disc herniations often regress spontaneously, without surgical intervention, the authors of this review emphasize the need for clinicians to better understand the biomechanisms at work in LDH in order to make better-informed decisions about which treatment approach might be best for their patients.

Subtypes of LDH that More Frequently Regress

Magnetic Resonance Imaging (MRI) and CT Scan evidence of LDH regression indicate that particular subsets of herniations are more likely to spontaneously regress than others. Specifically, large-sized and sequestered herniations at the L4-L5 spinal segment level are more apt to partially or completely regress than other types of herniations. It is thought the regression is facilitated by the herniation’s exposure to the epidural vascular supply when the posterior longitudinal ligament ruptures. In fact, MRI studies have shown that the spontaneous regression of herniated disc materials is associated less with the size of the rupture and more with the vessels extending beyond the ligaments and supplying blood and nutrients to the inflamed herniation.

Of 36 analyzed herniations imaged in one study, 25 of them resolved spontaneously—17 percent subligamentous, 48 percent transligamentous, and a whopping 82 percent of sequestered herniations, respectively. This suggests the size of the hernia is less of a factor than the PLL rupture. In another study, all sequestered discs self-resolved within 9 months, while extruded discs took a full 12 months to resolve. Disc protrusions did not resolve, even after a full year.

Conclusion

Clinicians should pay particular attention to the subset type of LDH in their patients when deciding whether to treat their condition surgically or conservatively. Further study into the biochemical mechanisms involved in LDH and its potential for self-resolution would be beneficial in long-term LDH patient outcomes and should be a focus of research for clinicians treating patients with LDH.

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

A cross-sectional study 1of the multifidus muscles (MM) and erector spinae muscles of 68 women and 42 men found significantly higher levels of muscles in subjects without disc herniation than in the disc herniation group, indicating that chronic pressure on the root of the spinal nerve may cause degeneration and atrophy of the MM and erector spinae muscles groups.

 

Single-Level Disc Herniation

Model of Single-Level Disc Herniation.

 

The Study

110 LBP patients with an average age of 40 were analyzed and divided into two groups—those with single-level disc degeneration, and those without disc degeneration. Subjects with multilevel degeneration were excluded, as were those with deformities of the spine or a history of spinal surgeries. Both groups were radiographed via MRI at the lumbar levels, and the imaging results were compared to examine the paravertebral muscles, disc heights, and perpendicular distances between the laminae and MM. Statistical analysis using software compared the variables using the Kolmogorov-Smirnov test to investigate data distribution.

Results

The LBP patients without lumbar disc herniation had clinically-significant greater MM and erector spinae muscles than those with radiographically-confirmed disc degeneration. No significant differences existed, however, in the disc heights, perpendicular distances between the MM and the laminae, or the psoas major cross-sectional areas of the two study groups.

Discussion

The MM stabilizes the lumbar spine and, when negatively impacted, contributes to LBP. The muscle group create more force over a smaller range than the longer spine muscle groups, which helps to stabilize movement. The dorsal rami of the spinal nerves stimulates the MM and erector spinae, but the psoas major is stimulated by ventral rami lumbar spinal branches, prior to their joining the lumbar plexus. The medial paraspinal muscles are stimulated from one nerve root, but the iliocostalis and longissimus muscles receives stimulation from many roots. Indications of muscle degeneration include decreased muscle size and increased fat deposits in the area.

Because the MM and erector spinae are stimulated by the dorsal root stemming from a singular level, the chronic and long-lasting pressure on the root due to disc herniation contributes to the degeneration and atrophy of these muscles. This atrophy is not evident in the psoas muscle because it is stimulated by the nerves of many different levels, rather than a singular source. In order for muscle atrophy to occur, there must be at least six weeks of compression, according to this study’s authors.

Conclusion

Evidence of increased fatty deposits and decreased muscle in a cross-sectional lumbar image indicates the existence of muscle degeneration in LBP patients, assuming there has been at least six weeks of compression on the MM or erector spinae muscle groups, which are stimulated by a single nerve root.

 

KEYWORDS: Muscle Degeneration in LBP Patients with Single-Level Disc Herniation, single-level disc degeneration, paravertebral muscles, disc heights, and perpendicular distances between the laminae and MM, pressure on the root due to disc herniation contributes to the degeneration and atrophy of these muscles

  1. Volumetric Muscle Measurements Indicate Significant Muscle Degeneration in Single-Level Disc Herniation Patients
Diurnal Disc Shape

The spine undergoes natural shape and fluid changes over the course of 24 hours. Often, back pain symptoms vary as well over the day and night cycle.  But the small changes and the links to pain have not been researched thoroughly. Here, a group of researchers from Duke University looked at the reliability of measuring intervertebral disc shape with recumbent MRI. This large avascular structure is linked to back pain and has significant diurnal variation in the human body. It would seem wise to further understand its diurnal disc shape changes.

Some people feel pain in the mornings and others feel things more so at the end of the day. Yet others feel pain more so when they lie down.

The intervertebral disc hydraulically keeps vertebrae separated. Water is squeezed out throughout the day as the human frame is vertical, and this water gets resorbed when an individual lays down. During the process, the disc changes shape and height. And when pain is involved, these shape and height changes can bear increased ( or decreased ) physical stress on structures that may be inflammatory. These can include annular fissures, disc bulges, disc herniations, disc protrusions, encroaching nerve or rootlets of nerves and the shingling of facet joints, just to name a few.

The purpose of this study was to determine intra and inter-rater reliability using MRI to measure diurnal changes of the intervertebral discs.

They did find excellent reliability, and interestingly they saw the most significant change in the posterior annulus region of L5-1. The diurnal variations were in line with what others had seen in previous work. Boos at al. in 1996 saw a 1-2mm change over the course of an 8h workday while Hutton et al. in 2003 saw a volume change of 1-2 cm3.

This research is essential if we are to fully understand back pain origins. Often pain syndromes related to the lower back present with symptoms that are diurnal. At Dynamic Disc Designs, we have models to help explain these subtle but significant changes to the discs, assisting patients to understand the onset of their pains and the diurnal disc shape and the natural variations.

 

intradiscal pressure, model

A study of in vivo intradiscal pressure in subjects with and without lower back pain (LBP) sought to find out how disc degeneration affects intradiscal pressure, measure the loading capacity of the L4/L5 IVD segment, and determine any relationship between movement in that disc segment and the spinal loading capacity. The researchers found that there was a significant relationship between spinal loading and the angle of the motion segment in healthy discs in vivo. In degenerated discs, the intradiscal pressure was much lower than that measured in healthy discs. Further study with wider parameters is suggested to fully understand the phenomenon and the problems associated with it.

Study Motivation and Design

The only way to directly measure spinal loading in humans is via the measurement of intradiscal pressure—a complex in vivo task. Most current knowledge about loading capacities were derived from pioneering studies in the 1960’s and 1970’s by Nachemson, but little corroborating evidence has been published on the topic since. These early studies utilized an inefficient means of evaluating intradiscal pressure—the polyethylene coated disc pressure needle until 1965, and after that, another needle designed specifically for intradiscal pressure measurements. This new needle was not without its deficits and required special handling and was prone to destroying structural defects on insertion. The current study’s authors utilized a newly designed silicone-based needle to measure the pressure and spinal load in 28 patients suffering from LBP, sciatica, or both at the L4/L5 segment, and in eight healthy volunteers with an average age of 25 years-old.

Magnetic resonance imaging (MRI) was performed on the healthy subjects prior to the beginning of the study to ensure no disc degeneration in the volunteers. The 28 LBP patients (10 women and 18 men with a mean age 45 years) were also imaged prior to pressure measurements being taken to visualize the amount of water content in their discs. These patients were diagnosed with disc herniation (16 patients) or spondylosis (12 patients).

The subjects were measured while in the prone position, without sedation but with a “local” dose of anesthesia. A guiding needle was used to position the pressure sensor needle into the nucleus pulposus of the L4/L5 IVD discs. Fluoroscopy was used to confirm correct placement of the needle had been achieved. The subjects were measured in eight positions: prone, upright standing, lateral decubitus, flexion and extension standing, and upright, flexion, and extension sitting positions. Radiograms of the lateral view were also taken of each of the subjects during their testing.

Observations

Pressure measurements in this study indicate that respiration creates a fluctuation in intradiscal pressure even when subjects are in the prone position and utilizing no other muscle activities. An IVD that is healthy is also elastic, with an intradiscal pressure that fluctuates in correspondence to muscle activities and respiration. It is possible that the normal pressure changes involved with respiration could be associated with the maintenance of the nutritional content inside the nucleus pulposus. There was a slight difference between horizontal and vertical pressures in healthy and degenerated discs and in the silicon gel, which may indicate that the nucleus pulposus has a similar pressure tropism to silicon gel. Normal discs had high water content, which explains the small difference between the horizontal and vertical pressure measurements. There was, however, a significant difference between the pressures of the total value (horizontal and vertical and whole posture) of healthy and degenerated discs. These values may not have been significant enough to measure in previous studies utilizing the less efficient needle-types. The information obtained in this study through the use of the sensitive silicone pressure needle will help in developing a better understanding of degenerative disc disease.

Professional LxH Model

Our Professional LxH Model

 

KEYWORDS: Link Between Lower Back Pain, Disc Degeneration and Intradiscal Pressure, relationship between spinal loading and the angle of the motion segment in healthy discs, respiration creates a fluctuation in intradiscal pressure, degenerative disc disease