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.

 

 

 

 

 

 

Lower back pain (LBP) patients present with a wide variety of motor control adaptations in response to, and in anticipation of pain. Though these adaptations manifest across a spectrum of functionality, studies have indicated two common phenotypes that represent the trunk posture and movement of most LBP patients. Further study 1 of these two phenotypes can help practitioners target more specific, effective treatments for their patients who have developed motor control adaptations that may undermine and contribute to their long-term spinal health.

 

Variations of Motor Control Adaptations in LBP Patients

People with LBP adapt the way they move to mediate pain or avoid pain. These adaptations may be conscious or unconscious processes, or a combination of the two, but the changes in posture and movement—what we refer to as “motor control”—involve the muscles, joints, nerves, senses, and integrative processes. Studies of how LBP affects posture and motor control have been inconsistent in the conclusions, perhaps because of the built-in redundancy and flexibility of the musculoskeletal system.

There are many ways to adapt posture and movement in response to pain or in anticipation and avoidance of pain. But because each adaptation creates not only short-term solutions, but potential long-term changes in biomechanics, which can become problematic, creating a cycle of disfunction, it is helpful to study the two most prominent phenotypes of motor function adaptions to create targeted treatment and information options for LBP patients presenting these adaptations.

Identified Motor Function Phenotypes

Tight Control: Some LBP patients exhibit increased excitability and accompanying tight control over their trunk movements, which increases reflex gains, attention to how they control movement, tissue loading, and muscle contraction. While having tight control over trunk movements can help the LBP sufferer from short-term injury by constraining movement, it may also contribute to trunk stiffness and increase the amount of force necessary to move. This may manifest in subtle ways or, in extreme cases, lead to a complete bracing of the trunk, making movement difficult and leading to fatigue.

Patients with extreme tight control over their motor control have been shown to experience a reduction in lumbar stiffness and pain after spinal manipulation. This could mean that the adaptation could, itself, be responsible for pain. These patients are also more likely to experience spinal compression due to increased loading. This compression may lead to a reduced fluid flow in the discs, which may contribute to degeneration over time.

Tight control creates low-level muscular activity, even when the spine is at rest. This can create muscle fatigue, pain, and discomfort. The lack of muscle variability and reduced movement associated with tight control of motor function may also compromise tissue health and compromise the load-sharing capabilities, balance, and movement task learning abilities inherent in the body’s structures.

Loose Control: At the opposite end of the spectrum are patients with loose muscle and posture control and less muscular excitability. This creates an increase in spinal movements and subsequent tissue loading. This may help prevent the short-term pain associated with muscle movement, but the spine is unstable and requires musculature to support movement. Less muscle control means potential failure of the mid-range lumbar vertebral alignment segments, which can cause tissue strain and pain. Spinal displacement due to loose control may cause LBP.

 

Clinical Implications for Loose or Tight Muscle and Posture Control in LBP

Understanding whether a LBP patient is exhibiting a loose or tight control muscle and posture adaptation in response to their pain can help practitioners tailor their treatment in a targeted and more beneficial way. Increasing movement and reducing excitability in later stages of LBP adaptive tight control models can help a patient integrate movement variation as their LBP improves. Likewise, exercises and therapies to help loose control patient models develop more control of their musculature and posture may help them avoid the potential long-term consequences of a proper lack of spinal support.

Assessing LBP patients carefully to identify their motor control phenotype prior to the onset of treatment may allow practitioners to more efficiently target and proactively treat potential complications of their particular adaptation due to actual or anticipated pain.

KEYWORD LONG TAIL PHRASES: motor control phenotyping may help target treatment for lower back pain patients, motor control adaptations in response to, and in anticipation of pain, common phenotypes that represent the trunk posture and movement of most LBP patients, two most prominent phenotypes of motor function adaptions, reduction in lumbar stiffness and pain after spinal manipulation.

 

Instability

A study examined the relationship between lumbar disc degeneration and instability in spinal segments of three groups of volunteers and found that factors of spinal instability were closely related to disc height and the age of the study subjects and that disc height was intimately associated with age and spinal instability and was the most consistently affiliated parameter of those examined.

Patients with lower back pain (LBP) and/or sciatica often have evident disc degeneration in MRI their images, especially elderly patients. Because these patients may demonstrate no other neurological symptoms, it is commonly assumed specific evidence of LBP –aside from degeneration and the age of the patient—may not exist. Excessive motion surrounding the affected disc segment can cause LBP and spinal instability, and previous studies on the relationship between instability and LBP have been inconsistent in their findings—in part, because imaging of the subjects was performed while the patients were in the static supine position.

Study Design Utilized Flexion-Extension Standing Postured Imaging Reviews

The authors of the current study were building upon their previous research utilizing images that had been performed on patients during flexion-extension standing postures to examine the relationship between spinal instability and disc degeneration of the L4/L5 motion segment. Because disc degeneration may not be associated with LBP at all stages, the authors of the study devised a method of measurement to examine different types of segmental degeneration and any relationship it may have with spinal instability.

The subjects of the study were LBP or leg pain outpatients who had received radiologic and MRI imaging within a two-month interval during the past three years. Of the 447 patients included in the study, 268 were men, and 179 were women. Their ages ranged from 10 to 86 years, with an average age of roughly 54 years-old.

Instability was measured at the L4/L5 spinal segments during neutral, extension, and flexion postured images and was then analyzed and categorized into three variable types: Anterior slip at L4 onto L5 while in neutral position (SN), sagittal translation (ST), and segmental angulation (SA). Measurements were taken of each slip, and the results were evaluated and noted to determine the degree of apparent instability.

The disc segments were evaluated radiologically for degeneration by looking at and comparing disc height, spur formation of the anterior vertebral edges, endplate sclerosis, and evidence of vacuum phenomenon in the films taken during flexion-extension. Sixty-eight of the subjects had high disc height (HDH), 212 patients were considered to have medium disc height (MDH), and 67 patients were categorized as having low disc height (LDH). Bony spur measurements were taken, and the presence of endplate sclerosis and vacuum phenomenon were noted as either being present or not. The level of disc degeneration was evaluated by MRI and graded from 1 to 5, as “normal,” to “severe” degeneration. The patients were divided into eight groups based upon the severity of their spinal instability, and the relationship between disc height, spur size, endplate sclerosis, vacuum phenomenon, and degeneration in the MRI’s was noted in relation to the types of instability present.

The compared data indicated a link between instability, age, and a reduction in disc height. Though increased age and a loss of disc height have long been suspected to be linked to degeneration and instability of the spine, this study uses MRI to evaluate that relationship more closely, demonstrating that a lower disc height was associated at least a 3mm slippage and a higher disc height was associated with subjects who were younger in age, with larger angulation in the spinal segments. Instability was prevalent in older patients with prominent anterior spur formation and/or vacuum phenomenon.

Age and relative spinal stability were intimately related to disc height, and this instability was progressive in nature and occurred over decades.

 

KEYWORDS: Correlation Between LBP, Age-related Degeneration, and Spinal Instability, relationship between lumbar disc degeneration and instability, comparing disc height, spur formation of the anterior vertebral edges, endplate sclerosis, and evidence of vacuum phenomenon, link between instability, age, and a reduction in disc height, degeneration and instability of the spine

annulus angle and disc height loss

Disc height loss is the common theme in back pain.

And with early disc height loss, hypermobility is related. But how are they associated to one another? Barr in 1948 (1) was the first to describe instability. His description of low back pain related to disc height and the passive stabilizers. A nice review of lumbar instability as an evolving concept was written by Beazell et al. These authors discussed the evolution through Farfan and his model, to Kirkadly-Willis and the three phases of degeneration as well Panjabi’s added concepts of neurological control. To understand the relationship between disc height loss and the development of hypermobility, it may be helpful to highlight the anatomy. In Panjabi’s and Adams “Biomechanics of the Spine”, there is a description of the annulus angles in alternating lemellae at 35 degrees from the horizontal explaining the tensile resistance with movement. What appears to not be described is the relationship of the annulus fibres when a disc loses its height. Below are a series of images, developed by Dr. Jerome Fryer, to help explain the displacement factor.

Annulus Fibrosus

Annulus Orientation

Each disc consists of concentric, alternating in orientation, fibrous sheets that encompass a hydraulic centre core named the nucleus pulposus. Once the disc height is reduced, the annulus angles change. If the length of the annulus fibres do not change, a displacement factor of hypermobility can occur.

annulus angle

Annulus angle change with disc height loss

disc height loss

Disc height loss leads to displacement

As it is often a therapeutic goal to increase spinal stability, increasing disc heights should be at the forefront.

The common theme seen in back or neck pain is intervertebral disc height loss. It is the earliest radiological finding in the degenerative cascade. This height loss leads to many geometrical and morphological changes that results, initially, in hypermobility which often leads to pain. This has been discussed thoroughly in the literature.

The three important changes related to disc height loss include:

  1. increased annular and endplate stress
  2. development of hypermobility
  3. facet approximation with reduced joint space width

These anatomical areas are important because this is where the innervation exists that contributes to pain.

Generally, spinal pain generators can be categorized into three distinct areas…all affected by disc height loss:

  1. discogenic and associated sinuvertebral nerve
  2. vertebral endplate disruption and associated basivertebral nerve
  3. facetogenic with medial branch and subchondrial innervation

A better understanding of the relationship between disc height loss and hypermobility will help us move toward developing models–as this relationship is thought to be the beginning stage of degeneration. A focus on the related biorheology to maintain disc height will be of paramount importance in the decades to come in the prevention of reduced joint space width of the opposing endplates and facet hyaline cartilaginous surfaces.

  1. Barr JS. Low-back and sciatic pain: results of treatment. J Bone Joint Surg Am 1951;33-A: 633–49.