Biomechanics of the spine. Part I: Spinal stability

G Model EURR-6097; No. of Pages 9 ARTICLE IN PRESS European Journal of Radiology xxx (2012) xxx–xxx Contents lists available at SciVerse ScienceDirect European Journal of Radiology journal homepage: www.elsevier.com/locate/ejrad Review Biomechanics of the spine. Part I: Spinal stability Roberto Izzo a,∗ , Gianluigi Guarnieri a , Giuseppe Guglielmi b , Mario Muto a a b Neuroradiology Department, “A. Cardarelli” Hospital, Napoli, Italy Department of Radiology, University of Foggia, Foggia, Italy a r t i c l e i n f o Article history: Received 3 July 2012 Received in revised form 21 July 2012 Accepted 23 July 2012 Keywords: Spine Biomechanics Spinal stability CT MR a b s t r a c t Biomechanics, the application of mechanical principles to living organisms, helps us to understand how all the bony and soft spinal components contribute individually and together to ensure spinal stability, and how traumas, tumours and degenerative disorders exert destabilizing effects. Spine stability is the basic requirement to protect nervous structures and prevent the early mechanical deterioration of spinal components. The literature reports a number of biomechanical and clinical definitions of spinal stability, but a consensus definition is lacking. Any vertebra in each spinal motion segment, the smallest functional unit of the spine, can perform various combinations of the main and coupled movements during which a number of bony and soft restraints maintain spine stability. Bones, disks and ligaments contribute by playing a structural role and by acting as transducers through their mechanoreceptors. Mechanoreceptors send proprioceptive impulses to the central nervous system which coordinates muscle tone, movement and reflexes. Damage to any spinal structure gives rise to some degree of instability. Instability is classically considered as a global increase in the movements associated with the occurrence of back and/or nerve root pain. The assessment of spinal instability remains a major challenge for diagnostic imaging experts. Knowledge of biomechanics is essential in view of the increasing involvement of radiologists and neuroradiologists in spinal interventional procedures and the ongoing development of new techniques and devices. Bioengineers and surgeons are currently focusing on mobile stabilization systems. These systems represent a new frontier in the treatment of painful degenerative spine and aim to neutralize noxious forces, restore the normal function of spinal segments and protect the adjacent segments. This review discusses the current concepts of spine stability. © 2012 Elsevier Ireland Ltd. All rights reserved. 1. Introduction The spine is a complex multi-articular system controlled by the muscles which supports the head and trunk during posture and movements and encloses and protects the spinal cord, nerve roots and, at cervical level, the vertebral arteries. The normal function of the spine presupposes its stability. Apart from the protection of nervous structures, spine stability is the basic requirement for the transfer of power forces between the upper and lower limbs, the active generation of forces in the trunk, the prevention of early biomechanical deterioration of spine components and the reduction of the energy expenditure during muscle action [1,2]. The literature reports a number of biomechanical and clinical definitions of spinal stability but a consensus definition is lacking. The loss of stability, the instability, is an important often unknown cause of back pain particularly at lumbar level. Mobile stabilization systems aim to neutralize noxious forces, restore normal function of the spinal segments and protect the adjacent segments. They represent the new frontier of treatment of degenerative painful spine on which the attention of bioengineers and surgeons has focused. 2. Definitions of stability and instability ∗ Corresponding author at: Neuroradiology Department, “A. Cardarelli” Hospital, Viale Cardarelli 9, 80131 Napoli, Italy. Tel.: +39 0817473116. E-mail addresses: roberto1766@interfree.it (R. Izzo), gianluigiguarnieri@hotmail.it (G. Guarnieri), g.gugliemi@unifg.it (G. Guglielmi), mutomar@tiscali.it (M. Muto). White et al. defined clinical stability as the spine’s ability under physiologic loads to limit patterns of displacement in order not to damage or irritate the spinal cord and nerve roots and to prevent incapacitating deformity or pain caused by structural changes [3]. 0720-048X/$ – see front matter © 2012 Elsevier Ireland Ltd. All rights reserved. http://dx.doi.org/10.1016/j.ejrad.2012.07.024 Please cite this article in press as: Izzo R, et al. Biomechanics of the spine. Part I: Spinal stability. Eur J Radiol (2012), http://dx.doi.org/10.1016/j.ejrad.2012.07.024 G Model EURR-6097; No. of Pages 9 ARTICLE IN PRESS R. Izzo et al. / European Journal of Radiology xxx (2012) xxx–xxx 2 In a similar way the American Academy of Orthopedic Surgeons defined stability as “the capacity of the vertebrae to remain cohesive and to preserve the normal displacements in all physiological body movements” [4]. Any vertebra in each spinal motion segment (MS), the smallest functional unit of the spine (FSU), can perform various combinations of the main and coupled movements during which a number of bony and soft movement restraints guarantee stability. This intrinsic complexity contributes to clinical and imaging difficulties in assessing spinal movement. The loss of stability, instability, is an important, often unknown, cause of back pain particularly at lumbar level. Like stability, instability also lacks a generally accepted definition. White and Panjabi defined instability as “the loss of the ability of the spine under physiologic loads to maintain its patterns of displacement so there is no initial or additional neurologic deficit, no major deformity, and no incapacitating pain” [5]. Pope and Panjabi qualified instability as a loss of stiffness leading to abnormal and increased movement in the motion segments [6]. With instability movement can be abnormal in quality (abnormal coupling patterns) and/or quantity (increased motion) [7]. The location of the dominant lesion in the MS determines the pattern of instability, but as spinal movement is three-dimensional with coupled movements, tissue derangement tends to cause dysfunctional motions in more than one direction. 3. Normal spinal motion Pope and Panjabi and other classic definitions of instability refer to a global increase in spinal movements over the normal limits associated with the occurrence of back and/or nerve root pain [6]. Unfortunately, the definition of “normal or physiological movements” remains a matter of debate as the excessive overlap of the types of movement between symptomatic and asymptomatic subjects makes it difficult to define standard references and to correlate clinical and radiological findings [8]. Within each MS, the FSU including two adjacent vertebrae with interposing soft tissues, a vertebra can perform three translations along and three rotational movements around each of the x-, y-, zcartesian axes of the space and various combinations of main and coupled movements, the latter occurring simultaneously along or around an axis different from that of the principal motion [9]. According to Louis, during flexion–extension the vertebra moves around a transverse rotation axis placed not in the subjacent disc but in the vertebral body below [10]. Both the endplates and the facet joints perform two circumference arcs around the same rotation centre whose location changes according to level, being placed two vertebral bodies below in the superior cervical spine and in the subjacent vertebral body in the inferior cervical, in the dorsal and lumbar spine [10] (Fig. 1). The low position of the rotation centres gives rise to a coupled movement of antelisthesis which varies from a maximum of 2–3 mm at C2–C3 to a minimum of 0.5 up to 1.5 mm from D1 to L5 [10]. Axial rotation and lateral bending are always coupled movements because of the oblique orientation of both the facet joints and muscles. The coupling is most evident at cervical level. While the centre of lateral bending is always located between the facets, the centre of axial rotation varies according to level: in the central body for the dorsal spine, in the spinous processes for the lumbar segment [10]. The key to proper spinal function is the highly nonlinear load/displacement ratio of the FSU because the effort required for movement changes significantly in its various phases [11] (Fig. 2). The physiologic range of motion (ROM) includes a neutral zone (NZ) and an elastic zone (EZ) [11]. The NZ is the initial part of the Fig. 1. Lateral conventional radiograph of the cervical spine in flexion. During flexion–extension the vertebra moves around a transverse rotation axis placed in the subjacent vertebral body. Both the endplates and the facet joints perform two circumference arcs around the same rotation centre whose location changes according to level, being placed two vertebral bodies below in the superior cervical spine and in the subjacent vertebral body in the inferior cervical, in the dorsal and lumbar spine. intervertebral motion on either side of the neutral position where it meets relatively low resistance and the spine exhibits high flexibility owing to the laxity status of capsules, ligaments and tendons (Fig. 2). The NZ is followed by the EZ where the resistance to movement and the slope of the curve increase linearly when the ligaments, capsules, fascias and tendons are subjected to tension requiring more load per unit displacement [11] (Fig. 2). The EZ represents a zone of high stiffness where spinal motion meets significant resistance [11]. Each of the six degrees of freedom of motion any vertebra can perform with respect to other vertebrae has its own range of motion (ROM), neutral zone (NZ) and elastic zone (EZ) [12]. Fig. 2. Load/displacement curve. The load/displacement curve of the spine is not linear. The range of motion of the spinal joints includes an initial neutral zone (NZ) with relatively large displacements at low load and an elastic zone (EZ) that requires more load per unit of displacement because of the tension of capsules and ligaments. Please cite this article in press as: Izzo R, et al. Biomechanics of the spine. Part I: Spinal stability. Eur J Radiol (2012), http://dx.doi.org/10.1016/j.ejrad.2012.07.024 G Model EURR-6097; No. of Pages 9 ARTICLE IN PRESS R. Izzo et al. / European Journal of Radiology xxx (2012) xxx–xxx 3 Fig. 3. Three subsystems control the stability of the spine: the spinal column, the muscles, and the central nervous system. They are strictly related so any acute or chronic damage to one subsystem requires more compensatory work by the others. The biphasic nonlinear behaviour of the spinal joints probably meets two opposed needs: to allow movements near the neutral posture with as little muscle effort as possible and to ensure stability at the end of joint excursion [11]. To depict the load–displacement curve of the spinal motion segments, Panjabi created the analogy of the ball in a bowl and compared the NZ to the bottom of a glass in which a ball can move quite freely, and the extremities of the movement, the EZ, to the steeper walls of a cup on whose inclination the ball climbs meeting an increasing resistance [13] (Fig. 2a). A stable column would have the shape of a narrow wine glass, whereas an unstable column could be compared to a large soup bowl [13]. According to a mechanistic hypothesis of spinal pain in asymptomatic subjects, the NZ and ROM are normal and contained within the limits of the pain free zone (PFZ) [13]. The NZ is thought to increase over the PFZ limits in an unstable spine [13]. Severe disc collapse, osteophytosis, surgical fusion and muscular training all improve spinal stiffness reducing the NZ and freeing the spine from pain. 4. Spine stabilization Stability implies a suitable relationship between the NZ and EZ [11]. NZ size, particularly, although a small portion of the ROM, proved to be the most sensitive parameter to define both traumatic and degenerative spinal instability as it increases earlier and more than the ROM and EZ [11,14]. Given the key function of the NZ observed in tests on cadaveric specimens and in animals, Panjabi re-defined instability as the reduced ability by the stabilizing systems of the spine to maintain the neutral zones of the FSUs within physiological limits so that deformity, neurological deficit or disabling pain do not occur [11]. In this definition the quality of movement becomes more significant than the global increase in joint excursion in diagnosing instability. Spinal stability is ensured by a stabilization system consisting of three closely interconnected subsystems [12] (Fig. 3): (1) the column or passive subsystem, (2) the muscles and tendons or active subsystem, (3) the unit of central nervous control. In the passive subsystem bones, disks and ligaments fulfil an intrinsic structural role and directly control the EZ near the extreme parts of normal movement [12]. Bone, disks, ligaments and joint capsules also contain mechanoreceptors which act as transducers, sending a continuous flow of proprioceptive information on loads, motions and posture from each FSU to the central nervous system (CNS) that, in turn, replies via an appropriate and coordinated feedback muscular action [12,15,16] (Fig. 4). Fig. 4. The subsystems controlling spinal stability are functionally related. A continuous stream of proprioceptive information starting from the spinal mechanoreceptors muscle and tendons inform the CNS on the position, load and movement of each FSU. The CNS, in turn, answers through an appropriate and coordinated muscular activity. The active subsystem and the CNS essentially control the neutral zone of FSU movement where resistance is low [12]. Degeneration or any traumatic lesion to the bony and soft components of the spine tend to expand the ROM and the NZ putting a greater demand on the muscles and nervous systems in order to preserve or restrict the segmental instability [12]. 5. Passive stabilization During ordinary daily activities the spine normally supports vertical loads of 500–1000 N, over twice the body weight, and with lifting, up to 5000 N, near 50% of final failure load [17]. The intrinsic structural role and passive stabilization of the spine depend on: - vertebral architecture and bone mineral density, disc-intervertebral joints, facet joints, ligaments, physiological curves. 5.1. Vertebral architecture and mineral density The load-bearing ability of the vertebral body depends on its size and shape, the integrity of the trabecular system and bone density. The vertebral body mainly consists of spongy bone with a threedimensional honeycomb structure similar to airplane wings that yields the best strength/weight ratio [10]. The progressive increase in body size downward in the spine is the only physiological answer to increasing weight loads with average strength ranging from 2000 N in the cervical segment up to 8000 N in the lumbar spine [18]. The cancellous bone of any vertebral body has four main trabecular systems with a constant orientation [10]: - a vertical system extending between the endplates which accepts and transmit vertical loads; - a horizontal system travelling in the posterior arch and joining the transverse processes; - two curved oblique systems, superior and inferior, start from the endplates and cross in the peduncles to end in the spinous and Please cite this article in press as: Izzo R, et al. Biomechanics of the spine. Part I: Spinal stability. Eur J Radiol (2012), http://dx.doi.org/10.1016/j.ejrad.2012.07.024 G Model EURR-6097; No. of Pages 9 4 ARTICLE IN PRESS R. Izzo et al. / European Journal of Radiology xxx (2012) xxx–xxx Fig. 5. (a and b) The vertical compressive loads are first accepted by vertical trabecular columns which transmit forces between the endplates. However the vertical struts alone would tend to bow (a). Their bowing is restrained by the presence of horizontal lamellae which join the vertical struts and by tension favour the radial dispersion of forces conferring resilience to the vertebral body (b). joint processes. Their function is to withstand the horizontal shear stresses ensuring the neural arch to the body. Axial loads are initially accepted by vertical trabecular struts whose bowing is restrained by the tension of the horizontal lamellae which thereby favour the horizontal dispersion of the vertical loads conferring resilience to the cancellous bone (Fig. 5). With respect to spongy bone the body cortical shell, although highly resistant, has much lower elasticity. The resistance of spongy bone also strongly depends on mineral density (BMD). Bone loss in osteoporosis results in a disproportionate exponential reduction of resistance: a bone loss of 25% leads to a reduction of resistance of about 50% [19]. In the mechanical model of cancellous vertebral bone consisting of vertical columns joined by horizontal lamellae (Fig. 6a), the resistance of the columns decreases by the square of increasing length and by the square of decreasing cross section. During the early stages of osteoporosis the resorption of the horizontal lamellae causes a progressive relative elongation of the vertical columns (Fig. 6b) while the thinning of the columns themselves in more advanced stages leads to a summation of the two processes (Fig. 6c). A strong and continuous correlation between spinal BMD and fracture risk has been established, without a defined threshold value for BMD under which vertebral failure will occur [19]. A vertebra can be affected by fatigue after repetitive loading forces individually less than would be required in case of a single load application. Vertebral fatigue begins as focal osseous microdamage which extends until final failure. Bone resorption in osteoporosis is not homogeneous but mainly involves the anterior half of vertebral bodies [20]. In the elderly, because of degenerative disc collapse, the forces are no longer evenly distributed on the endplates and the posterior facets assume much more of the load during erect standing posture. This relative stress-shielding of the anterior bodies is thought to favour local bone loss and weakening as, according to Wolff’s law, bones adapt their mass and architecture in response to the magnitude and direction of forces habitually applied to them [21]. According to the “mechanostat” theory bones weaken when peaks strain and dynamic deformations fall below a given threshold [22]. When the relative off-loading standing posture is followed by spinal flexion a very high increase in stresses (up to 300%) occurs on the weakened anterior bodies [21]. The very high loading disparity could favour the collapse of anterior bodies with wedging and explains why this region is frequently the site of osteoporotic fracture, and how forward bending movements often precipitate the injury [21]. The regional alterations of trabecular architecture by limiting the variation in global bone density could reduce the capacity of dual-energy X-ray absorptiometry (DEXA) of whole bodies to evaluate fracture risk. One study of intact spines found that the best way to predict the strength of lumbar vertebral bodies and to identify vertebrae at risk of osteopenic fracture in a wide age range (19–79 years) was the product of BMD and the endplate area using CT data [23]. Vertebral body fractures modify the mechanical properties of the injured vertebra as well as the adjacent disc and vertebra. Endplate deflection provokes depressurization of the adjacent disc nucleus with a secondary shift of compressive stresses both on the annulus, mainly posterior to the nucleus, and the neural arch. Vertebral augmentation by percutaneous vertebroplasty aims to reverse these effects restoring the stiffness and strength of an injured painful vertebral body, normal pressure in the adjacent disc and load-sharing between vertebral body and arch [24]. Stabilization and pain relief are greatest in case of macroscopic intravertebral instability (vacuum cleft phenomenon and its changes during flexion–extension) [25]. Luo et al. determined how the volume of cement injected affects stress distribution inside the fractured vertebra and between the affected vertebra, adjacent vertebra and disc in cadaveric motion segments [26]. While just a small volume of cement (13% of volumetric body filling) was sufficient to reduce the abnormal endplate deflection and normalize intradiscal pressure distribution under load, larger quantities of cement (25% of averaged filling) were needed to fully stabilize the injured trabecular bone and equalize stress distribution between vertebral body and neural arch [26]. Nevertheless, the altered biomechanics of load transfer to the adjacent vertebra can increase the risk of new adjacent fractures perhaps through a “stress-riser” effect. A retrospective analysis of a cohort of 147 patients treated with vertebroplasty or kyphoplasty found that the most predictive factors among all of possible risk factors for adjacent refracture such as age, gender, BMD, location of treated vertebra, amount of bone cement injected, collapse degree, pattern of cement distribution, treatment modality, cement leakage into the disc space, were Please cite this article in press as: Izzo R, et al. Biomechanics of the spine. Part I: Spinal stability. Eur J Radiol (2012), http://dx.doi.org/10.1016/j.ejrad.2012.07.024 G Model EURR-6097; No. of Pages 9 ARTICLE IN PRESS R. Izzo et al. / European Journal of Radiology xxx (2012) xxx–xxx 5 Fig. 6. (a–c) The load-bearing capacity of vertebral bodies heavy depends on the vertical trabecular struts joining the endplates (a). The resistance of a column decreases by the square of increasing length and by the square of decreasing cross section. During osteoporosis both processes occur with progressive elongation of the columns provoked by the resorption of the horizontal lamellae (b) and the thinning of the columns themselves (c). It results a disproportionate exponential reduction of bone resistance and load bearing capacity. cement leakage into the intervertebral disc space (which highly concentrates the load stresses) and evolving osteoporosis [27]. 5.2. Disc-intervertebral joints Owing to its peculiar structure, the disc has both the tensionresisting properties of a ligament and the compression-resisting properties typical of joint cartilage. The disc behaves as a ligament allowing for and controlling the complex three-dimensional movements of the spine: vertical compression and distraction, flexion–extension, lateral bending and axial rotation. The outermost fibres of the annulus are the first controller of the abnormal micro-movements of a normal MS: experimental discectomies cause a significant increase in movements, especially flexion–extension [28]. With the nucleus behaving like a pressured cylinder, the disc is also the main shock absorber of mechanical stresses transmitted during motions to the skull and brain. When the disc is submitted to symmetric loads the nucleus transmits loads in all direction pushing away the endplates, while, in case of eccentric loads, tends to move toward the region of lower pressure, where the annulus fibres are put under tension. Bending movements induce maximum tensile and compressive loads on the opposing sides of the outermost annulus layers along with bulging on the compression side and stretching on the tensile side. During axial rotation the disc experiences torsional shear stresses with half of the annulus fibres engaged (parallel to rotation direction) until eventual delamination. The biomechanical behaviour of the normal young nucleus is homogeneous and isotropic, equal in all its parts and all directions: whatever the spatial position of the spine the load is transmitted evenly on the endplates avoiding any focal concentration [29]. By contrast, in the degenerated disc the nucleus loses its normal fluid-like properties and loads asymmetrically assuming a solidlike behaviour. In contrast to the nucleus, the fundamental biomechanical property of the annulus is its high anisotropy in tension reaching up to a 1000-fold increase in the tensile modulus along the alignment of the collagen fibres [29,30]. The tensile circumferential properties of the annulus are also inhomogeneous, the anterior annulus being stiffer than the posterior annulus and the outer annulus stiffer than the inner ring [31]. When the normal disc is loaded tensile circumferential loads are generated in the annulus because of the pressurization of the nucleus and the resistance of its fibres to stretching and bulging under axial compression. With the degenerative depressurization of the nucleus, annulus fibres are no longer pushed outwards but loaded in compression. The changes in tensile properties occurring with disc aging and degeneration are relatively small in comparison to the morphological changes. The nucleus pulposus mainly works in the NZ bearing low axial loads while the stiffer annulus fibrosus accepts a larger proportion of the highest loads [32]. Under Please cite this article in press as: Izzo R, et al. Biomechanics of the spine. Part I: Spinal stability. Eur J Radiol (2012), http://dx.doi.org/10.1016/j.ejrad.2012.07.024 G Model EURR-6097; No. of Pages 9 ARTICLE IN PRESS R. Izzo et al. / European Journal of Radiology xxx (2012) xxx–xxx 6 very high compressive loads the first structure to fail is usually the endplate rather than the disc [33]. The water content and thickness of the disk continuously change during normal daily activities under the opposite influences of hydrostatic and osmotic pressures [34]. Under load the high hydrostatic pressure leads to a gradual release of water out of the disc whose thickness diminishes until it is counterbalanced by the osmotic pressure exerted by proteoglycans whose concentration increases progressively [34]. In the recumbent position the reprevailing osmotic pressure again recalls water back into the disc. In the degenerating disc the reduced hydrostatic pressure of the nucleus displaces compressive loads on the internal annulus that folds inward with an increase in shearing stresses which favour the fissures and delamination for both structural fatigue and impaired cellular response. Fracture of the endplate and Schmorl herniation drastically reduce the disc pressure accelerating the degeneration and destruction of the annulus. 5.3. Facet joints Facet joints fulfil two basic functions: - control of the direction and amplitude of movement, - sharing of loads. According to the three-column model of Louis, the weight of the head and trunk is transmitted first on two columns placed on the same frontal plane, the atlantooccipital lateral joints, then, from C2 to L5, on three columns arranged like a triangle with an anterior vertex [10]. The anterior column is composed of the superimposing bodies and discs, the two posterior columns of the vertical succession of the facet joints. Normally between the three columns there exists a balanced and modular action for which the posterior facets accept from 0% up to 33% of the load depending on posture, but in case of hyperlordosis, high and prolonged weight loading and disc degeneration the percentage can rise to 70% [35]. Like the vertebral bodies the increasing size of the facet joints downward compensates the increasing functional demand. The spatial symmetry of the facets is an essential requirement for correct functioning: every significant asymmetry predisposes to instability and premature degeneration of the facets and discs. Long-standing remodelling and destabilization of the facet joints along with degenerative changes in posterior ligaments lead to degenerative spondylolisthesis with sagittal orientation of the facet joints acting as a predisposing factor [36]. Patients showing narrow inferior articular processes and facet joint spaces visible on AP radiographs or with narrow facet joint angles on axial MR-CT scans are likely to develop degenerative spondylolisthesis [37]. Facet joint angles greater than 45◦ relative to the coronal plane were found to have a 25 times greater likelihood of developing degenerative slippage [38]. An estimated 15–40% cases of chronic low back pain cases are thought to be caused by lumbar facet joints due to joint capsule mechanical stresses and deformation with activation of nociceptors [39]. Pain induced by pressure originating in the facets and/or posterior annulus of the lumbar spine may be relieved by using interspinous processes spacers. 5.4. Ligaments The ligaments are the passive stabilizers of the spine. The stabilizing action of a ligament depends not only on its intrinsic strength, but also and to a greater extent on the length of the lever arm through which it acts, the distance between the bony insertion, Fig. 7. Owing to kyphosis the vertebrae of the dorsal spine are located distant from the body sagittal balance vertical axis which joins the external auditory canals and the centre of femoral heads passing through the C7–D1 and L5–S1 interspaces. Eccentric ventral and lateral axial loads and bending moments create which concentrate the stresses on the anterior parts of the bodies favouring their collapse and wedging. The larger the kyphosis, the greater the distance between vertebral bodies and the body balance axis and the greater the ventral concentration of stresses. the point of force application, and the IAR of the vertebral body, the fulcrum located in the posterior body around which the vertebra rotates without moving at any given moment during any movement. A very strong ligament with a short lever arm may contribute to stability less than a less strong ligament working by a longer lever arm that gives it a mechanical advantage (Fig. 7). The interspinous and supraspinous ligaments being located far away from the IAR and working with a long lever arm oppose spinal flexion more than the flava ligaments having a shorter lever arm [40]. Being very close to the spinal IAR and intrinsically less resistant, the posterior longitudinal ligament has a dual mechanical disadvantage. 5.5. Physiological curves Sagittal curves are acquired and represent the evolutionary response to the needs of the standing position and biped gait with little energy expenditure [41]. Dorsal kyphosis is the only sagittal spinal curve present at birth. Cervical and lumbar lordoses develop with head rising and standing and walking, respectively. Both in normal individuals and in pathologic conditions sagittal spine curves are regulated by pelvic geometry expressed by different parameters, namely pelvic incidence (PI), sacral slope (SS) and pelvic tilt [41,42]. PI is a fixed morphologic parameter which after birth remains unchanged in each subject: any sagittal balance change is obtained because of the adaption of other positional parameters [42]. After lumbar or thoracolumbar burst fractures local kyphosis can be compensated by hyperlordosis caudad and, if necessary, hypokyphosis Please cite this article in press as: Izzo R, et al. Biomechanics of the spine. Part I: Spinal stability. Eur J Radiol (2012), http://dx.doi.org/10.1016/j.ejrad.2012.07.024 G Model EURR-6097; No. of Pages 9 ARTICLE IN PRESS R. Izzo et al. / European Journal of Radiology xxx (2012) xxx–xxx cephalad, but within the limits dictated by pelvic geometry. In order to maintain the trunk centered over the femoral heads, an increased SS leads to increased lumbar lordosis and dorsal kyphosis in both normal and pathologic conditions. The concept of maintenance of global spinal balance is helpful in guiding treatment choices in spinal traumas. Sagittal spinal curves also increase the resistance to vertical loads up to 17 times by directing deformations into pre-ordered directions which can be quickly controlled by the fast intervention of muscle contraction. The physiological curves of the spine also affect the response to traumatic forces. Owing to the kyphosis, the vertebrae in the thoracic spine are distant from the body’s anterior–posterior balance axis (passing through the external auditory canals, the interspaces C7-D1 and L5-S1 and the centre of the femoral heads) and are subjected to eccentric loads. Eccentric axial loads, anterior to vertebral IAR, create lever arms and bending moments in a ventral or lateral direction which concentrate the stresses on the anterior part of the bodies favouring the occurrence of wedge compression fractures, while all the elements posterior to the vertebral IAR move away from each other [43] (Fig. 7). In the lordotic segments vertical vector forces run near or through the IAR of the vertebrae, without creating any leverage or rotation. The forces are more evenly distributed on the endplates: according to Newton’s third law, equal and opposite forces act on the endplates favouring central or burst fractures [43]. 6. Active stabilization According to Panjabi, muscles and tendons provide active stabilization of the spine under the control of the nervous system, ensuring stability primarily in the NZ where the resistance to movement is minimal [12]. Muscle action is needed to stabilize the spine during standing, lifting and bending activities. Without the muscles the spine would be highly unstable even under very light loads [1239]. The muscles may be divided into superficial (rectus abdominis, sternocleidomastoideus) and deep (psoas) flexors and superficial (long) and deep (short) extensors. The function of the superficial, multisegmental muscles differs from that of deep unisegmental muscles. Being small and located very close to vertebral rotation axes, the short muscles (intertransverse, interspinous, multifidus) globally act primarily as force transducers sending feedback responses to the CNS on the movement, load and position of the spine [44]. The long superficial muscles are the main muscles responsible for generating movements. The lumbar erector spinae and the oblique abdominal muscles produce most of the power forces required in lifting tasks and rotation movement respectively, having only limited insertions on the lumbar motion segments, while the multifidus muscle acts as a dynamic stabilizer of these movements [44]. The oblique and transverse abdominis muscles are mainly flexors and rotators of the lumbar spine but stabilize the spine at the same time, creating a rigid cylinder around the spine by increasing intra-abdominal pressure and tensing the lumbodorsal fascia [45]. The complexity of the posterior musculature excludes any possibility of voluntary control upon single units. Out of external forces (gravity), consistent compressive loads exerted on the spine are due to muscle activity which has been assessed by electromyography and mathematical models. The large number of muscles, the complex antagonistic activities, the variability of spine insertion sites and related moment arms hamper the determination of muscle force and its contribution to spinal loading. 7 Fig. 8. In case of damage to ligaments, discs, joint capsules and to the mechanoreceptors they contain, abnormal transducer signals are generated and sent to the CNS causing an altered motor response which, in turn, increases the mechanical stress of bony and joint spinal components and elicits an abnormal feedback response by FSUs and muscles themselves creating a vicious cycle ultimately leading to the development of inflammation, muscle fatigue, and activation of nociceptors with acute and chronic pain. CNS: central nervous system. The CNS receives extensive inputs from all of joints, muscles and tendons of each MS in order to regulate and coordinate in time and space muscle activity (Fig. 4) [12]. In case of acute or chronic damage to ligaments, discs, joint capsules and the mechanoreceptors they contain, abnormal transducer signals are generated and sent to the CNS causing an altered motor response with impaired temporal and spatial coordination [46]. In turn, the altered muscle response increases the mechanical stress of bony and joint spinal components and elicits an abnormal feedback response by FSUs and the muscles themselves (starting from the muscle spindles and Golgi tendon organs) addressed to the CNS, creating a vicious cycle that ultimately leads to inflammation, muscle fatigue, and activation of nociceptors with onset and perpetuation of pain [46] (Fig. 8). Schleip et al. suggest that, as the thoracolumbar fascia is rich in Ruffini and Vater-Pacini corpuscles in all its three layers, fascia damage can be implicated in the genesis of chronic pain through the abnormal stimulation of the CNS [47]. In fact, patients with chronic low back pain show a delayed muscle response and offset in performing voluntary movements, and a reduced postural control compared to asymptomatic subjects [48]. 7. Therapeutic applications and conclusions The difficulty of assessing spinal instability raises many concerns for its treatment. Fusion surgery is based on the classical assumption that instability implies increased motion and if motion is blocked spinal pain is also relieved. The main disadvantages of fusion surgery in degenerative instability remain loss of mobility and curvature with impaired sagittal balance, instrumentation failure and transfer of increased stresses to adjacent motion segments referred to as “transition syndrome” (Fig. 9). Symptomatic adjacent disease at ten years has been reported in 25% and 36% of patients after cervical and lumbar fusion, respectively [49,50]. These problems have led to the development of new mobile stabilization systems which aim to neutralize abnormal forces, restore the normal function of the spinal segments and preserve the adjacent segments. Dynamic stabilizers represent the new frontier of treatment of degenerative painful spine and have been the focus of attention of bioengineers and surgeons in the last 10–15 years. The function of interspinous spacers is to provide a posterior shift of motion segment instantaneous axis of rotation (IAR) Please cite this article in press as: Izzo R, et al. Biomechanics of the spine. Part I: Spinal stability. Eur J Radiol (2012), http://dx.doi.org/10.1016/j.ejrad.2012.07.024 G Model EURR-6097; No. of Pages 9 8 ARTICLE IN PRESS R. Izzo et al. / European Journal of Radiology xxx (2012) xxx–xxx Fig. 9. Sagittal midline FSE T2-w scan showing a posterior D12–L1 disc herniation with light compression of spinal cord. One of main drawbacks of the spinal fixations by rigid constructs is the transition syndrome caused by abnormal load stresses converging on motion segments adjacent to fixed segments. Two years after a fixation L1–S1 this middle-aged patient developed dorsal chronic pain. The image is degraded by susceptibility artefacts due to the construct. towards the region of increased stiffness and behind the facets, reducing the compressive loads on the facet joint during standing posture and extension movements [51]. Among the interspinous implants classic single-action rigid or deformable spacers essentially control extension, limiting compressive stresses on the facets and posterior annulus (Fig. 10), while double-action devices couple a tension band to an interspinous device to control both flexion and extension movements and also better decompress the anterior annulus limiting the normal anterior shift of vertebral IAR during spinal flexion (Fig. 6b) [51]. The best indications for interspinous devices are lumbar canal and foraminal segmental stenosis, degenerative spondylolisthesis or retrolisthesis, and Baastrup disease. The indications for discogenic pain control are less defined, but Swanson et al. reported a significant reduction of pressure within the posterior annulus and nucleus of anatomic specimens after application of interspinous devices. This action is expected to relieve pain generating from disc nociceptive nerve endings when stimulated by irregular distribution of internal pressures and abnormal loads. The preservation of movement is crucial to promote the exchange of nutrients and waste products to and from the disc [52]. Dynamic stabilization techniques are globally indicated in the first stages of degenerative disc and facet diseases to prevent or delay more invasive and less reversible approaches with the hope of reversing degenerative processes once they are promptly corrected [51]. Many of these procedures have been developed by radiologists: their minimal invasiveness makes them cheap, safe and reversible [51]. Knowledge of the basic principles of biomechanics can facilitate our understanding of the aetiology of spine diseases and how all the bony and soft spinal components contribute individually and together to ensure spinal stability. This knowledge is mandatory in view of the increasing involvement of radiologists and neuroradiologists in interventional spinal procedures, and the Fig. 10. (a and b) As a consequence of disc degeneration and collapse, higher loads are supported by vertically slipping neural arcs and facet joints (a). The implant of interspinous spacers (IS) shifts the instantaneous axis of rotation (IAR) backwards reducing the pressure between facets and in the posterior annulus, potential sources of acute and chronic pain (b). In case of listhesis the IS can reduce the anterior slippage of the vertebra. Vertical red arrows indicate compression; green arrows tension or distraction. Big red horizontal arrow: degenerative anthelistesis; green horizontal arrow: vertebral realignment. ongoing development of new techniques and devices. Mechanical experiments in human and animal specimens provide much more quantitative information than can be obtained in vivo. Experimental data obtained from MS studies vary widely, first because of the complex structural and material properties of MS substructures (nonlinearity, viscoelasticity, anisotropy, inhomogeneity), their interactions and their changes with aging and degeneration. The key feature of proper spinal MS functioning is the highly nonlinear load/displacement ratio since the effort required for the movement significantly changes in its various phases. Spinal stability implies a suitable relationship between the NZ and EZ [11,13]. Early motion modifications begin and concentrate in the first phase referred to as the NZ, nearest to neutral position. Spinal stability is ensured by a stabilization system consisting of three closely interconnected subsystems: the column or passive subsystem, the muscles and tendons or active subsystem, and the unit of central nervous control [12]. The assessment of spinal instability remains a major challenge for specialists. In an unstable spine movement can be abnormal in quality (abnormal coupling patterns) and/or in quantity (increased motion). Fusion surgery leads to loss of mobility and physiologic curvature and transfer of increased stresses to adjacent motion segments. Dynamic stabilizers provide an intermediate solution between conservative treatment and traditional fusion surgery and often allow a minimally invasive approach and represent a new frontier in the treatment of degenerative painful spine [51]. With the contribution of interventional radiology will be soon available new devices with improved design and with more specific implementations. 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