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The etiology of development spondylolisthesis is multifactorial, and involves hereditary, traumatic, biomechanical, growth, and morphological factors.
Assessment of global sagittal balance in spondylolisthesis should include a thorough assessment of the alignment of the spine, pelvis, and lower extremities.
Unbalanced pelvis refers to a retroversion of the pelvis (increasing pelvic tilt) and a verticalization of the sacrum (increasing sacral slope) in an attempt to prevent forward global imbalance when the capacity of the spine to compensate for the spondylolisthesis is exceeded.
When the compensation mechanisms from the spine and pelvis are exceeded, patients attempt to maintain a balanced posture through hip and knee flexion.
Decreasing sacral slope is abnormal in high-grade spondylolisthesis, particularly in the presence of an unbalanced pelvis.
The Spinal Deformity Study Group Classification describes six types of developmental spondylolisthesis and relies on the assessment of the slip grade and sagittal balance.
Surgical treatment of developmental spondylolisthesis should aim at preserving/restoring pelvic and global balance.
A complex surgery is not necessary for all patients with spondylolisthesis; the complexity of the surgery should increase as the severity (type) of spondylolisthesis increases.
Formal surgical reduction is generally not required for low-grade spondylolisthesis, but it can be indicated for the subset of patients with slip severity of 40% or more and significant dysplastic changes.
Formal surgical reduction in high-grade spondylolisthesis is strongly recommended when lumbosacral kyphosis is less than 80 degrees, the proximal femoral angle is 10 degrees (or more), or the C7 plumb line is in front of hip axis.
Spondylolysis is a defect in the pars articularis of a vertebra. It can occur independently or in association with spondylolisthesis, most frequently at the level of L5–S1. Spondylolisthesis is the forward displacement of one vertebra with respect to the adjacent caudal vertebra. Spondyloptosis is a 100% translation of one vertebra on the next caudal vertebra.
Marchetti and Bartolozzi have developed a classification system based on the developmental origin vs. the acquired forms of spondylolisthesis, pointing out that some spondylolistheses are associated with bony and soft tissues abnormalities.
Developmental spondylolisthesis divides into two major types (high and low dysplastic), depending on the severity of bony dysplastic changes present in the L5 and S1 vertebrae and on the risk of further slippage. Dysplastic facet joints and spina bifida of L5 and/or S1 are frequent in both types, but in addition:
The high dysplastic type is associated with significant lumbosacral kyphosis (LSK), a trapezoidal L5 vertebra, hypoplastic transverse processes, and sacral doming with verticalization of the sacrum.
The low dysplastic type is associated with a relatively normal lumbosacral profile, a rectangular L5 vertebra, preservation of a flat upper end plate of S1, and no significant verticalization of the sacrum.
Acquired spondylolisthesis is secondary to trauma, surgery, a pathologic disease, or a degenerative process: the traumatic form can be owing to either an acute fracture or a stress fracture. Typically, a stress fracture occurs in young athletes and is distinct from the developmental type of spondylolisthesis.
This chapter focuses on developmental spondylolisthesis, the most frequent type of spondylolisthesis seen in children, adolescents, and young adults. The purpose of the chapter is to focus on the implications of sagittal balance of the human body as it applies to this disorder and to demonstrate how this knowledge can help to better understand pathophysiology, classification, and treatment.
Developmental spondylolisthesis in children occurs predominantly at L5–S1 (87%), but also at L4–L5 (10%) and L3–L4 (3%). Although many authors have searched for a spondylolytic lesion at birth, a pars defect has never been reported in a newborn. In a prospective study that initially recruited 500 first-grade children, Fredrickson et al. found a prevalence of spondylolysis of 4.4% at 6 years old, 5.2% at 12 years old, 5.6% at 14 years old, and 6% in adulthood. Thus spondylolysis/listhesis is intimately linked to the standing posture. Tardieu et al. have studied how sagittal balance is acquired during bipedal gait acquisition by comparing neonatal and adult pelvises in three dimensions. During gait acquisition, the relationship between the sacrum and acetabula is modified through the mobility and malleability of the sacroiliac joints, as indicated by very significant changes in pelvic incidence (PI) values. Before walking, hip flexion and anterior vertebral flexion induce an anterior location of the trunk center of gravity. After walking, femoral extension and lumbar lordosis induced by muscular actions increase sacral slope and PI, creating a backward displacement of the center of gravity behind the femoral heads, a basic characteristic of human standing posture that will set and control all spinopelvic relationships from childhood to adulthood.
Spondylolysis has not been reported in quadrupeds, only in bipeds. Furthermore, there are only rare cases reported in humans before walking age. Evolution from the quadrupedal to the bipedal posture in primates and humans has been allowed by progressive and very significant changes in the shape and position of the pelvis and spine and of their supporting ligaments and muscles. A quadruped has no lumbar lordosis and a more longitudinal and narrow pelvis. In sharp contrast, a human has a well-developed lumbar lordosis and a much “rounder” pelvic shape, a situation that has gradually evolved in primates along with the transition to bipedal posture. These changes in shape and morphology of the pelvis are crucial to the understanding and management of developmental spondylolisthesis, a disorder that is closely linked to the bipedal posture and associated with activities involving a lordotic effect on the lumbar spine, such as gymnastics.
Although the exact etiology of developmental spondylolisthesis remains unknown, it is most likely multifactorial because various hereditary, traumatic, biomechanical, growth, and morphological factors have been proposed to play a role.
Many authors believe that spondylolisthesis is related to an autosomal dominant genetic predisposition with incomplete penetrance. Accordingly, there is an increased prevalence of spondylolisthesis in members of the same family, ranging from 19% to 69% in first-degree relatives of children with spondylolisthesis. High-grade spondylolisthesis has also been reported in identical twins.
Several authors believe that spondylolysis can be caused by repetitive microtrauma resulting in a stress fracture of the pars interarticularis. In the case of spondylolisthesis without an isthmic defect, elongation of the posterior elements can be seen after healing of the pars defect that was initially associated with an anterior translation of L5. The pars articularis is submitted to high shear, compressive, and tensile loads during flexion and extension movements, and is the weakest region of the posterior neural arch. Accordingly, there is an increased prevalence of spondylolysis and spondylolisthesis among athletes participating in sports involving repetitive alternate flexion-extension loading of the spine, such as gymnastics.
Under normal conditions, the facet joints at L5–S1 support the majority of the shear force, whereas the L5–S1 disc supports most of the compression force. In spondylolysis, the facet joints are not functional, as the pars defect creates a disassociation between the L5 body and the facet joint. Therefore, most of the shear stresses at L5–S1 are transferred to the disc, which predisposes to degeneration of the disc and subsequent spondylolisthesis. In addition, forward displacement of the body of L5 distracts the pars defect, as the posterior elements of L5 remain strongly attached to the posterior ligaments and erector spinae muscles. With progression of the spondylolisthesis there is a further decrease in disc stiffness and increase in stresses across the lumbosacral junction. Variable amounts of dysplasia involving the facets, laminae, and end plates are always present in developmental spondylolisthesis and further disturb the normal posterior bony hook/catch at the lumbosacral junction.
The morphology of the sacrum and pelvis and the relationship to each other modulate the geometry of the lumbar spine and, consequently, the mechanical stresses at the lumbosacral junction. Subjects with abnormal sacropelvic morphology seem predisposed to altered mechanical stresses in the lumbar spine and lumbosacral junction and appear to be at higher risk of developing spondylolysis and spondylolisthesis.
Progression of spondylolisthesis mainly occurs during skeletal growth and is far less likely after skeletal maturity. The severity of slip at the initial presentation is the main risk factor for progression, but progression is less likely when the slip percentage is less than 40%.
Previous studies support the role of a biomechanical weakness in the vertebral growth plate as an important mechanism in slip progression. In the growing child, increased stress in the L5–S1 disc can be associated with bony remodeling through the growth plates, particularly the upper end plate of S1. Involvement of the upper S1 end plate can further contribute to the progression of the spondylolisthesis in a process similar to the progression of Blount disease ( Fig. 23.1 ).
Fig. 23.2 presents the authors’ current point of view on the pathogenesis of developmental spondylolisthesis, in an attempt to incorporate the prominent influence of human standing sagittal balance and unify the various findings previously reported in the literature. In the presence of spondylolysis and bony dysplasia, the mechanical stresses applied at the lumbosacral junction are further altered by the abnormal spinopelvic balance, secondary to the abnormal sacropelvic morphology. Secondary deformation of the L5 vertebral body, sacrum, and pelvis because of bone remodeling through the growth plates, according to the Hueter-Volkman law, also alters the biomechanical loads at the lumbosacral spine, thus contributing to further progression of the spondylolisthesis, in a process similar to the progression seen in Blount disease. Postural changes and compensation mechanisms through modifications in the sagittal balance of the spine, pelvis, and lower extremities further lead to abnormal biomechanical loads, contributing to the development of spondylolisthesis (see Fig. 23.1 ).
In the past two decades, there has been much development in the understanding of developmental spondylolisthesis, as significant new knowledge on sagittal spinopelvic balance has been gained. In 2005, the Spine/Scoliosis Research Society summary statement in the Spine Focus Issue devoted to spondylolisthesis stressed the point that “global sagittal plane alignment is important in both adult and pediatric patients with spondylolisthesis. In patients with high-grade developmental spondylolisthesis, this has provided a compelling rationale to reduce and realign the spondylolisthesis deformity, thus restoring global spinal balance and improving the biomechanical environment for fusion.” Improved understanding of the complex relationship between spondylolisthesis and human standing posture was gained by moving away from concentrating solely on the local L5–S1 junction and focusing instead on the global sagittal picture, using long standing lateral sagittal x-rays of the spine and pelvis, and more recently full-body sagittal radiological images using low radiation technology ( Fig. 23.3 ).
The study of sagittal alignment refers to the evaluation of the relationships between parameters describing the lower extremities, sacropelvis, lumbar spine, thoracic spine, and cervical spine. Globally, there is variability in the position of C7 relative to S1 (global spinal balance), even in the normal population. However, when measured with respect to the femoral heads, global spinal balance is maintained in a narrower range in normal as well as spondylolisthetic subjects. This finding supports the idea that measurement of global sagittal balance should take into account the important contribution of the pelvis and therefore should be achieved relative to the femoral heads. Normally, a subject with adequate global spinal balance should stand with the C7 plumb line located over or behind the femoral heads (see Fig. 23.3 ), which ensures that C7 is not in front of the body’s center of gravity (usually located over the femoral heads to minimize energy expenditure).
In normal individuals, studies have shown that sacropelvic morphology determines sacropelvic orientation, which in turn greatly influences the shape and orientation of the spine, especially lumbar lordosis. This results in an open linear chain linking the head to the pelvis, where the shape and orientation of each successive anatomical segment are closely related and influence the adjacent segment, to maintain the center of gravity over the femoral heads. In lumbosacral spondylolisthesis, abnormal sacropelvic morphology combined with the presence of a local lumbosacral deformity can result in disturbed spinal balance. Using a postural model of sagittal balance showing the relationships between parameters of each successive anatomical segment from the thoracic spine to the sacropelvis, Mac-Thiong et al. have observed that a relatively normal posture was maintained in low-grade spondylolisthesis, whereas posture was abnormal in high-grade spondylolisthesis. For high-grade spondylolisthesis, the sagittal balance was particularly disturbed in the subgroup with an unbalanced pelvis. They also reported that, for most patients with spondylolisthesis, the global spinal balance was relatively constant, regardless of local lumbosacral deformity and particularly alignment of C7 with respect to S1, indicating the predominant influence of the sacropelvis in achieving a normal global spinal balance.
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