Spondyloptosis represents the most advanced and severe degree of spondylolisthesis, when the L5 body is located below the top of S1. The slip angle and the tilt angle vary considerably among different patients. The rarity of this deformity has not permitted the collection of large clinical series, so that rational decisions about treatment have been difficult.

The stability of the lumbosacral junction depends on static factors (spatial orientation of L5 to sacrum, lumbosacral angle, sacral slope, and osteodiscoligamentous complex) and dynamic factors (interaction of neuromuscular system with osteodiscoligamentous complex). The compression forces are supported by the vertebral body and disc; the shear forces are supported by the disc and by posterior bone elements. The pars articularis acts as a bone bridge and is the apparent link between these two regions (1,2).

The progression of spondylolisthesis to a high-grade slip or spondyloptosis is related to the degree of dysplasia of the vertebra and to external factors such as age, growth, weight bearing, and muscle imbalance. The degree of developmental dysplasia associated with lumbosacral kyphosis results in the different types of spondylolisthesis. Spondyloptosis is the final result of developmental high-dysplastic spondylolisthesis associated with ventral translation and lumbosacral kyphosis that was untreated or mismanaged (1,2,3).

The majority of slips do not progress significantly, but some patients progress to high-grade slips and spondyloptosis. Some factors predicting the risk for progression have been identified: i.e., female gender, great growth potential, increased slip angle, trapezoidal L5, domed and vertical sacrum, and sagittal rotation. High-grade slips and younger age are the most significant risk factors for progression (1,3,4,5,6).

The sagittal balance and spinopelvic relationship associated with the degree of vertebral slip are related to progression of the slip. Kyphosis and increased slip angle occur late, and they are as much a result as a cause of progressive high-grade slips. They can be considered to be markers of the risk for spondyloptosis (4,5,6,7).

The increase in lumbar lordosis is present from the early phases as a response compensating for the increased translation and slip angle. Lordosis also increases in the more delayed forms to compensate for sagittal imbalance. Sagittal balance can be achieved by only hyperlordosis, perhaps to anatomic extremes. In situations in which further compensation to
maintain sagittal balance is necessary in addition to lordosis, verticalization of the sacrum occurs. Verticalization of the sacrum is accompanied by contraction of the hamstrings, which promotes caudal rotation of the ischium and anterior rotation of the pelvis in a cephalic direction. These actions occur at the level of the coxofemoral joint and therefore affect posture (hyperlordosis) and gait (crouched or waddling gait), in a manner that characterizes patients with high-degree slip or spondyloptosis (1,4,6,8).

Not all patients with dysplastic posterior elements develop a high-grade spondylolisthesis or ptosis. The morphology of the spine and of the pelvis (inclination of the sacrum, distance between the femoral head and the sacrum) contributes to the cascade of events and is a determinant factor in progression to slip and lumbosacral kyphosis.

The natural history of spondyloptosis is unknown, and its clinical manifestations are not uniform, with different clinical characteristics being observed in different patients.

The clinical picture of patients with spondyloptosis is not uniform: some patients are almost asymptomatic and others present intense symptoms accompanied by a marked degree of functional disability. The symptoms are related to mechanical changes in the lumbosacral region (pain), compression of nervous structures (weakness, numbness, changes in sphincter function), and sagittal imbalance (thoracolumbar fatigue, muscle weakness, gait abnormality) (3,4,5).