Introduction
The term ‘spinal stability’ is yet to be consensually and accurately defined to be
used interchangeably in biomechanics and clinical medicine.[1 ] The diagnosis of ‘instability’ in the spine becomes all the more significant since
once it is diagnosed clinically, it has to be managed with immediate care and mobilization
of specialized medical resources.[2 ]
[3 ]
[4 ] Investigations over the years have concluded that spine instability, classically
defined as a deviation of the segmental load-displacement relationship from the normal,
may not be clinically correlated with pathological and symptomatic instability resulting
in low back pain[5 ] Accordingly, even if generalized loss or change in stiffness properties may have
relevance in certain biomechanical terms, it does not make this apparent instability
a clinically meaningful entity.[6 ] It is the contradiction between clinical and biomechanical definitions of instability
that raises the questions if all symptomatic and clinically detected spinal instabilities
violate the bio-mechanical definition of stability, or if all biomechanical or mathematical
definitions of instability gives rise to clinical manifestations of back pain.
While the widely accepted Pope and Panjabi's definition, clinical instability of the
spine attempts to objectively encompass both the clinical (tissue damage, pain and
deformity) and biomechanical (inappropriate and abnormal intervertebral displacements
on loading) views of spine instability,[7 ] ([Fig. 1 ]) the absence of a general congruity between these two aspects (clinical and biomechanical)
observed in non-specific low back pain (NSLBP) puts to doubt the accuracy and completeness
of the definition.[8 ] The review presented here discusses (i) different aspects of the biomechanical concept
of stability of the spine specifically centered around the idea of stiffness and the
load-displacement relationship of the spine segments; (ii) the lack of agreement between
the clinical and bio-mechanical ideas of instability, and (iii) it summarizes the
direction of current research trends focusing on investigating the relationship between
the relationship of stiffness of the spine and instability from the clinical perspective.
Since stability is an elusive term that could lead to confusion, a formal idea and
a framework that encompasses both static and dynamics spine systems was attempted
to be presented in this review to facilitate the understanding of spine stability
as a dynamic concept. When considering the spine as a dynamic system, a static concept
of spine stability may be adequate for discussing the involved issues. This review
highlights the dichotomy of a universal definition of stability, discusses the limitation
of the definition of one concept (static) to be unable to completely explain the other
(dynamic), and describes the overlap between the anatomical and physiological definitions
of spine.
Discussion
Direct and indirect costs of back pain amounts to the tune of ∼ $600 billion per year
in the USA alone.[9 ] Surprisingly, only ∼ 15% of low back pain (LBP) patients have a definite pathoanatomic
explanation for their pain.[10 ] The etiology of pain remains unknown in 80 to 90% of patients, who are clustered
together as the NSLBP cohort.[4 ]
[11 ] Of the large group of sufferers associated with a non-specific etiology, 20 to 30%
are diagnosed having ‘lumbar instability’.[8 ]
[12 ] The implications of this diagnosis, as mentioned earlier, are great in terms of
the urgency and level of medical attention and health service utilization it demands.
In this review paper, the following aspects of physical and clinical instability will
be reviewed in terms of concept, conflicts and future directions for validation of
the currently available assessment modalities.
What do We Understand by Biomechanical ‘Spine Instability’?
Fritz et al, while reviewing segmental instability of the lumbar spine, have expressed
that the current definitions available for spinal instability are controversial and
have advocated for efforts to define and formulate the accurate diagnostic methods
and efficacious treatment approaches.[13 ]
[14 ]
[15 ] Anders Bergmark, from Sweden, pioneered biomechanical research that formalized the
concept of spine stability in a muscular system.[16 ]
[17 ]
[18 ] A mathematical spine model was proposed that possessed stiffness characteristics
and represented 40 muscle attachments that could create virtual moments around individual
spine joint segments. He formulated the concepts of energy wells, stiffness, stability
and instability in this model in which the spine was visualized as a simple inverted
pendulum. Tension adjustments in the muscles increased the stiffness of these supports
and increased the ability of the pendulum to sustain larger applied loads without
tipping or falling. Henceforth, the foundation of biomechanical stability was rested
on the concept of potential energy (PE). Potential energy was explained to have two
basic forms. Both these forms were applicable to the inverted pendulum paradigm. In
the first form, the inverted pendulum by virtue of its mass above the datum line (line
of ground reference) possesses potential energy (Potential energy = mass x gravitational
constant height). In the second form, the concept of PE is extended to elastic bodies
that may possess this energy by virtue of any elastic deformation brought about by
the application of a load on that body. Accordingly, deformation of an elastic body
stores potential energy in the system. This energy is recovered when the load is removed;
like what happens when an elastic band is stretched, and PE is stored in the system
as a result of the stretch. The first form of PE describes the notions of ‘energy
wells’ and the idea of ‘minimum’ potential energy. If we place a ball into a bowl,
a shallow and flat-bottom bowl, the ball is said to be stable because if one were
to apply a small perturbation force to the ball, it rolls up the side of the bowl
but then comes to rest again in the position of least PE—the bottom of the bowl. Put
in another way, a system is thought to exist in a greater state of stability that
has a comparatively smaller PE. Thus, a ball in a steep well is more stable, with
the steepness of the walls of the well imparting the ‘stiffness’ of the system.
In context of the spine, the objective in creating stability with this analogy is
to create a ‘bowl-shaped’ PE surface, or an energy well ([Fig. 2 ]). Two-dimensional bowls (as in diagrams) allow motion in a single plane (like a
hinged skeletal joint). Some ball and socket joints can rotate in 3 planes (3 degrees
of freedom) that would require a 4-dimensional bowl to mathematically represent the
joint movements. Accordingly, spinal joints that rotate, shear, or translate add more
degrees of freedom to their movements. Conceptually a 30-dimensional bowl allows us
to examine movements of the lumbar spine. In clinical terms, different anatomical
structures maintain the structural integrity of the spine; each anatomical entity
may be understood to represent the ‘height’ of the bowl for each dimension. In other
words, the greater the stiffness, the greater the steepness of the sides of the mathematical
bowl, and, therefore, more stable is the joint. Accordingly, increased stiffness is
understood to impart enhanced stability to the spine. Accordingly, an active muscle
(acting against gravity) not only creates tendon force but also produces a stiffer
system. It follows that the greater this activation, the greater is the stiffness.
The spine joints possess intrinsic joint stiffness by virtue of the several ligaments
and capsular structures that increases the stiffness characteristics toward the boundary
of the range of joint motion, while the muscles control stiffness in the mid-range
of joint motion. In other words, a more stable system would undergo more limited displacement
than a less stable system on application of the same magnitude of loading. In biomechanical
terms, spine instability is mostly understood as a system demonstrating increasingly
pronounced (and uncontrolled) displacement in response to the same magnitude of perturbation
[[Fig. 1 ]]. Simple biomechanical instability is, thus, thought to be brought about essentially
and solely by this loss of spine stiffness.[5 ]
[19 ] Mechanical stability is the ability of a structure to return to its original state
after the application of a pertubation. A structure that buckles locally under a load
or pertubation is thought to be unstable. The human spine is unstable under even a
very low compressive loading (80N for the lumbar spine). Therefore, spine systems
are not stable enough without the participation of spinal musculature and the spine
stabilizing systems.
Fig. 1 Common measure of stiffness and static stability as displayed by the load displacement
relationship. Application of the same magnitude of load (L) results in a greater displacement
(d2 ) in a relatively unstable system (U) than the displacement (d1 ) in a relatively more stable system (S). This relationship is often equated unequivocally
to quantify and compare stiffness and stability of static and dynamic spine systems.
Biomechanical characterization of stability (stiffness) and instability (loss of stiffness)
using this model may not correlate to the absence or presence of pathological back
pain, respectively. Adapted from Pope and Panjabi.[7 ]
The Next Level of Complexity: Anatomical Instability
In anatomical terms, however, the spine is a more complex structure than the inverted
pendulum model forwarded to explain its integral stability. The lumbar spine is made
up of five distinct and anatomically and functionally independent motion segments.
Stiffness in the lumbar spine is achieved by a complex interaction between passive
ligaments and muscular activity being controlled by the nervous system.[20 ]
[21 ]
[22 ] Spine biomechanists, like McGill and Cholewicki, have proposed to extend the Bergman's
‘elastostatic’ concept of spinal stability to a more dynamic context of ‘in-vivo’ spine movement.[21 ]
[23 ] Some of the research, however, has recently moved away from the reductionist approach
(studying the spine as isolated components) of stability to an analytical approach
to study spine stability as a dynamic system and concept. This approach has emphasized
the importance of neuromuscular control of the spine stiffness, precise and timely
neural control of spinal muscles (motor-control) that can control segmental stability
of joints through selective muscle activation.[24 ]
[25 ] Accordingly, striking an optimal balance between simultaneously active groups of
muscles, the synergists (affecting a joint moment in a particular direction) and antagonists
(initiating movement in the opposite direction), has been proposed to be a critical
issue in successfully orchestrating a desired movement in a motion segment and at
the same time, preventing injury to the spinal structures. However, this issue becomes
more complicated as multiple muscles cross one or more spine segments at diverse planes
and in different directions across a motion segment. Therefore, it becomes necessary
for the full complement of the spine musculature to work coherently to achieve stability.
Over or under performance of muscle with inappropriate activation, amplitude, or timing
can produce instability or unstable behavior of the spine, even in a minimally loaded
spine. However, Cholewicki et al and others have reported that in most situations,
only a modest amount of stiffness is required to stabilize a spine joint.[21 ]
[26 ]
[27 ] According to them, maximal joint stiffness can be achieved during muscle contractions
with as low as 25% of a maximum isometric contraction of the paraspinal muscles. On
the other hand, overactivation of muscle may impose pathological loading on the joint
and may result in impedance of motion and injury. Gardener-Morse et al have reported
that activity in the multifidus (MF) muscle is sufficient to maintain lumbar stability
and stiffness with moderate loading of the lumbar spine.[28 ]
[29 ] Studies by this group have shown in a mathematical model that the relatively smaller
MF muscles contribute maximally to lumbar spine stiffness, whereas the longer and
more superficial erector spinae (ES) muscles affect movement of the spine in space.[30 ] Punjabi et al have proposed that the midrange of spine segmental motion is regulated
by the motor-control system through muscle activation that ensures appropriate stability
of the segment [[Fig. 2 ]]. This mid-zone of motion in individual spine joints has been designated as the
‘neutral-zone’. Movements in any degree of freedom in this ‘conceptual’ zone encounter
minimum resistance from the structural components connecting the motion segment, including
the muscles. Spine joints demonstrate passive stiffness characteristics that increase
toward the end-range of the joint motion by engaging the ligaments and bony joint
articulations (passive tissues/system). It has been proposed that within the neutral-zone,
the role of the motor system is to first add sufficient stiffness and ensure joint
stability via muscle activation before torque generation.[22 ] Spine injury may result in losses of such normal motor-control patterns, losses
in normal passive stiffness, and resultant aberrant joint motion. In the scenario
of an injury accompanied by a loss of passive tissue stiffness (passive elements),
both magnitude and pattern of muscular stiffness need to be altered to achieve stability
(active stiffness). Several spine rehabilitative measures propose addition of a modest
amount of muscle-induced ‘extra’ stiffness to attain stability in the spine. Importantly,
Cholewicki et al have reported that sufficient stability of the lumbar spine in the
neutral position can also be achieved in most people with modest levels of co-activation
of the muscles forming the abdominal wall (below 10% of maximum isometric contraction).[21 ] An injury resulting in losses in passive tissue stiffness in the disc or ligaments
may present with joint laxity (increased neutral-zone) that necessitates higher levels
of muscle activation to achieve increased stiffness required to ensure sufficient
stability, after such loss. As McGill puts it: “…functionally, a patient must be able
to maintain sufficient stability during necessary daily activities: …tasks of daily
living are not compromised by insufficient strength but rather points to the importance
of endurance,” indicating that lower levels of sustained muscle co-contraction of
the synergists, and hence low levels of stiffness, are required to operate the spine
for daily activities.[21 ]
[31 ] However, the one-fits-all explanation of spine instability has been proven to be
doubtful.[20 ]
[32 ]
Fig. 2 The energy well concept of spine stability (a, b, c and e). This example demonstrates
the system (b) to be more stable than system (a) due to the lower potential energy
associated with the system (b). The steepness of the walls in (b) represents greater
stiffness of the system, and, therefore, it is thought to impart greater stability
to the ball. Therefore, a greater force will be required to roll the ball off the
well (b) than in (a). System (c) is the most stable and robust of the three examples.
The graph in (d) shows the characteristics of displacement in response to segmental
loading across a flexion-to-extension task through the available range of motion (ROM).
Note that the displacement response is increased (in proportion to loading) around
the center of the graph (called the neutral zone = NZ), and decreases toward the extremes
of the ROM, outside the NZ (at the elastic zones). The graph (e) represents the ROM,
NZ perspectives in the energy well example. This review discusses the evidence and
potential implications of the dynamicity of task-dependent changes incurred in the
shape and segments of the curve (d), as observed in physiological adaptations and
in spine disorders. Adapted from Reeves et al.[1 ]
Is There Any Agreement between the Two Definitions?
The question then is, what could be a clinically meaningful definition for spine instability
that is compatible with its biomechanical counterpart? What kind of biomechanical
behavior in the motion segments would qualify and quantify as spine instability in
situations in which the loss of stiffness of the spine follows deficiencies in motor
control or loss of passive restraints of spine motion from an injury, presenting as
back pain? From a clinical viewpoint, instability of the spine occurs when an applied
force or perturbation produces displacements in a motion segment greater in magnitude
than observed in a normal spine with the same perturbation. Panjabi proposed that
the active subsystem (muscles), passive subsystem (ligaments and bones), and the neural
control (innervation) subsystems controlled spinal stability with precise inter-subsystem
interactions. He hypothesized that the motor-control system played an important role
in controlling motion in the neutral-zone.[22 ]
[33 ] Accordingly, spine segmental instability based on this model was defined as “a significant
decrease in the capacity of the stabilizing systems of the spine to maintain the size
of intervertebral neutral zones within the physiological limits, so that there is
no neurological dysfunction, no major deformity, and no incapacitating pain.” The
neutral-zone concept has been defined as a mid-portion of the total physiologic range
of intervertebral motion. The total physiologic range has been divided into a neutral
zone (movement surrounding the neutral position) and an elastic zone (outside the
two ends of the neutral zone; stopping at the end of range of motion [ROM]). Motion
within the elastic zone occurs without considerable internal resistance. Extending
this concept of visualizing vertebral motion into different segments, Panjabi's proposal
of biomechanical spine instability has objectively defined changes in the neutral
zone in spinal derangements. He considered segmental instability to be an abnormal
movement of one vertebra on the adjacent vertebra secondary to an increase in the
size of the intersegmental neutral zone involved. Evidently, clinical presentation
of instability demonstrates observable signs and symptoms in patients that match signs
of disruption in of one or more of their spinal stabilization subsystems and with
an increase in the size of the neutral-zone, on clinical examination. Accordingly,
based on the data on normal segmental motion observed from cadaveric spines in-vivo imaging, and experimental studies, lumbar instability in the clinical setting is
diagnosed by a sagittal intervertebral translation of > 4 mm or > 15% of the vertebral
body width, observed in an end-range flexion-extension X-ray film. Greater than 15-degree
rotation at any of the L1 to L4 segments, or > 20-degree at the L4-L5, and > 25-degree
rotation at L5-S1 segments have been demarcated as unstable limits with end-range
rotation radiography. The challenge with the elastostatic definitions and even some
parts of dynamic spine stability concepts is that these definitions present a static
characterization of the spine. One may ask if spine stability subsystems do only resist
biomechanical perturbations that could potentially damage the passive anatomical structures
of the spine or does the complex motor-control system selectively manipulates maneuverability
of the segments in expense of its stiffness (and stability) in a task dependent manner?
Is There a Necessity for an Agreement between Clinical and Biomechanical Stability?
As a part of this critique, we will attempt to take an overview of observations made
by investigators like Hasan, who challenges the very construct of conventional spine
stability. Hasan's observations from spine motor-control literature suggest that response
to perturbations in many common situations, in fact, ‘assist’ rather than ‘resist’
the perturbation and, therefore, are potentially ‘destabilizing’ in nature.[24 ]
[25 ] In classical mechanics, instability in a system leads to an infinite and ‘unbounded’
perpetuation of the perturbation. Considering conventional definitions of linear control
systems non-applicable to the spine due to diverse material properties shared by nerves,
muscles, and tendons (biological system), Hasan proposes that spine motor control
may not enforce stability in the strictest sense of a quick resistance to a perturbation.
This absolute resistance, according to him, may not be necessary for successful control
of movement—or even of posture. He proposes that a potentially ‘destabilizing’ state
in the spine may be desirable when maneuverability is important to facilitate position
maintenance and to enable negotiating an impending or ongoing movement. Additionally,
other than responses to external perturbations, it is noteworthy to mention that anticipatory
adjustments to internal perturbations also may not necessarily resist motion. In short,
frank instability may be desirable when high maneuverability is necessary.
It is, however, not clear from extant literature if transient instabilities contribute
to improved maneuverability or are just inconsequential outcomes of the motor-control
system's response to unexpected perturbations. Crisco & Panjabi reported in 1990 on
stability of trunk equilibrium, proposing the requirement of a certain minimum stiffness
at the trunk.[34 ] Some researchers also have separated the concept of equilibrium from stability and
have suggested that a spine system may be mechanically stable even if not intrinsically
in equilibrium.[35 ] Similar studies have reported that magnitudes of muscle co-contractions change depending
upon varying levels of loads held at different trunk heights with outstretched hands
even at the same horizontal distance away from the body. This indicates that stability
requirements are constantly adjusted in terms of joint stiffness, without changing
the equilibrium requirements of joint moments in the system. Though some reports have
proposed that a certain degree of stiffness is a prerequisite for spine stability,
some others have questioned the fundamentals of stability, arguing that some observers
have adopted too stringent views on stability thereby constraining the growth of each
of the different variables that constitute the energy state of the entire system.
It has also been proposed that probably not all variables in a biological system are
important enough to be stabilized for a voluntary point-to-point movement. Its only
factors that influence the direction and extent of the hand movement may be worthy
of stabilization, and neither the movement duration nor the time course of individual
joint angles and torques decided stability requirements in the system.[24 ] Interestingly, it is suggested that motor coordination may not have a preplanned
movement trajectory. Motor controls are set dynamically as task goals are specified
and executed moment-to-moment, accounting for a cost function that depends on the
calculation of the task error with minimization of the effort.[36 ] Literature on human motor control is not very clear on whether and when the motor
control system acts to ensure or to decline stability in the interest of maneuverability.
Hasan proposes that the motor control system responds to a sudden perturbation in
the system by a pattern of muscle activity that mimics an ‘accustomed voluntary movement’,
oblivious of stability considerations. Accordingly, responses to sudden mechanical
perturbations may temporarily assist rather than resist the perturbation and a runaway
motion induced by this short-term instability is resisted by voluntary intervention.
This argument demolishes the purported role of afferent feedback in motor-control
and its role in the negative feedback in biological control systems. Therefore, the
simple explanation of co-contraction of mutually antagonist muscles to resist every
perturbation by increasing joint stiffness, may not always be applicable. In context
of the spine, the system would rather rely on the instability set in by the perturbation
and use the resultant inertia of the body to slow down a falling movement. This mechanism
would then allow enough time for a voluntary, corrective recovery response that eventually
checks the fall. With these observations, some observers have seriously doubted the
role of stretch-reflex mediated stability mechanisms that are triggered in the muscle
as a motor-control response to resist any applied perturbation.[24 ] According to Hasan, these responses may not even be desirable at times and may,
in fact, precipitate or exacerbate clinical instability. A perturbation is initially
accompanied by stretching (or shortening) of the muscle around a joint. This change
in muscle length is associated with an increase (or decrease) in muscle contraction.
This force-response to the change in length occurs as an intrinsic property of the
muscles without lag or temporal delays due to short nerve conduction and muscle response
times. This force-response is different from general muscle activity per se and is
independent of the motor-control system's response to perturbation. Continuation of
this passive stretch in the muscle initiates a second response in muscle force mediated
via the stretch-reflex. According to Hassan's observations, a stretch-reflex may not
be able to ensure stability if the lag property of muscle, nerve conduction delays,
and properties of tendon compliance delays the response.[37 ] Authors have argued that, for instance, if an extension-moment affected by the spindle
reflex action at a primary joint (subjected to a flexion perturbation) arrives late,
it may bring about further instability of the joint toward the extensor side. Further,
the authors hypothesize that both short or long latency reflex action using a continuous
feedback system may have greater destabilizing effects than ensuring stability resulting
with such delays. It may thus seem that motor-control systems do not necessarily work
to ensure stability. Hence, the question arises as to whether motor control system
can ensure stability in the first place.
The spine kinematic research fraternity commonly agrees that motor-control of the
spine may exist as a passive control system provided by the non-contractile tissues
around the spine skeletal joints and the active muscle system helping to decelerate
or accelerate motion in spine segment to negotiate complex trajectories of movement.
What some researches such as Hasan see as black and white evidences in ‘support’ of
or working ‘against’ stability as simple ‘assistive’ or ‘resistive’ responses to a
perturbation, may be oversimplified explanations of the idea of stability as it is
currently understood or misunderstood. Studies in neurophysiology have documented
that just before a voluntary movement, the stretch-reflex response evoked in the agonist
muscles.[38 ] Second, early agonist electromyographic activity for a voluntary movement is increased
in magnitude and is reduced in latency regardless of the effect of the perturbation
on the muscle length.[39 ] Accordingly, this imposed shortening of an agonist muscle via the stretch-reflex
appears to be in contradiction to an action that may potentially resist the impending
perturbation. Some authors comparing data from random trials using perturbation protocols
have reported that stretch-reflex responses may not necessarily be resistive in nature
and may even assist the perturbation depending on the direction of the intended movement.[40 ] Accordingly, it can be argued here that there must be a linking arrangement in the
motor-control system that regulated the interplay and balance between the direction
of propulsion and the control of acceleration. As Hasan puts it, “despite such destabilizing
responses, humans can usually surmount perturbations and accomplish the desired motor
task thanks to later responses of the motor control system including voluntary responses”.[24 ] However, one may argue that what looks as an apparent abandonment of stability by
the neural stabilizing system, may be a motor-control strategy to adopt newer trajectories
of movement. Accordingly, one may also extend the definition of stability from a more
generalized depiction of a system-based definition that surrounds the concept of stiffness,
to the one that encompasses specific task-dependent requirements in the face of impending
or ongoing perturbation.
Some questions, however, persist with the non-reductionist view of stability that
includes the generation of apparent short-term instability arising from purported
functional requirements for long-term stability, following a hierarchical pattern
of muscle activation. Or, for instance, if the ‘assistance’ to a perturbation is uniformly
propagated across all the spine joints or if it demonstrates the same patterns of
muscle activation seen with voluntary spine movements. Also, if the observation that
reflex responses (based on feedback rules) augment perturbations to represent a strategy
that disregards considerations of conventional stability, is it then true that people
having impaired or suppressed reflexes are likely to demonstrate reduced ‘assistance’
to instability, and therefore remain more ‘stable’ during active and objective spine
movements? One may also ask if this reflex feed forward phenomenon, in some sense,
compromised spine maneuverability and predisposed the spinal susceptibility to micro
trauma? Though the view that the motor-control system takes advantage of applied physical
perturbations to enhance the accuracy of voluntary movement tasks make sense, one
needs to closely examine if this induced ‘instability’ introduced by the motor control
system to control spine stiffness and manipulate physiological maneuverability is
intentional and becomes pathological clinical instability once it goes beyond the
operational grasp of the motor control system.
It may be summarized from the above discussion that the biomechanical term spine stability/instability
has often been inaccurately used as a diagnostic term to characterize a subset of
back pain (NSLBP) patients.[41 ] It has very succinctly put as “Stability is an everyday word which has been applied
to the spine in various ways. The diverse concepts of spinal stability and instability
are unified by a wide-spread belief that they are linked to spinal pathology and pain”.[42 ]. Instability in the clinical context designates a condition that not only is thought
to be denoted by excessive vertebral movements in response to applied loads, and suggests
that these excessive displacements result in pain, progressive deformity and risk
of neurologic damage.[8 ]
[43 ]
[44 ] Inspection, palpatory assessment and passive testing of vertebral mobility and pain
with prone instability testing in the clinic, palpation of step-off and straight leg
raise tests form the mainstay of clinical diagnosis of spine instability. The quintessential
radiological assessment of instability being the calculation of static, end-range
inter-vertebral displacement from radiographs in maximum flexion and extension (first
reported in 1944), it is hardy a guess that interpretations of spine stability from
static end-points on dynamic stability of spine segments across their ROM, may be
misleading.[8 ]
[34 ]
[45 ] The mismatch between biomechanical and clinical assessments and criteria for diagnosing
instability in LBP could be related to the absence of an objective, acceptable and
comprehensive definition that satisfies and balances aspects of a distorted load-displacement
relationship, on one hand, and of tissue injury and pain, on the other. Accordingly,
availability of an agreement based on biomechanical quantification of instability
and clinical diagnosis may help to establish standardized thresholds to characterize
dynamic biomechanical instability that correlates to clinical criteria for pain, or
conversely, to specify degrees of clinical instability that correspond to a predefined
magnitude of mechanical instability deleted as changes in the different zones defined
within the dynamic range of joint motion.
