Isthmic Spondylolisthesis: Reduction vs. In-Situ Fusion?

Isthmic Spondylolisthesis is an extremely common cause of lumbar symptomatology and remains one of the most common indications for lumbar reconstruction. Symptomatic patients present with low back pain and/or lower extremity neurologic symptomatology. Conservative care consists of physical therapy, exercise, maintaining normal body weight, adhering to proper body mechanics, and steroid injections of varying types.

Isthmic Spondylolisthesis is characterized by bilateral pars interarticularis defects which separate the posterior column from the remaining motion segment. Therefore, the normal stabilizing function of the facet joints is lost and the upper vertebral body tends to slide forward on the lower segment. Fibrocartilaginous debris develops at the pars defects as the body attempts to heal the defect. Foraminal narrowing develops as the Spondylolisthesis worsens.

The vast majority of patients with isthmic Spondylolisthesis present at the L5/S1 level. A small minority of patients present with bilateral L4 pars defects which can allow an L4/L5 Spondylolisthesis to develop. Rarely, isthmic Spondylolisthesis can develop in the remaining lumbar motion segments. There are reported cases of multilevel isthmic defects.

Studies have revealed that isthmic Spondylolisthesis is a developmental abnormality with genetic predisposition. Approximately 6% of white men from the United States exhibit the abnormality as adults. Rates are lower among US blacks but much higher in American Eskimos and Navajo Indians. A man from the United States with isthmic Spondylolisthesis will genetically transmit a 25 % incidence of isthmic Spondylolisthesis to his male offspring. There is a marked increased incidence of spina bifida occulta in patients with isthmic Spondylolisthesis.

Neurologic Compression in Isthmic Spondylolisthesis
Many symptomatic patients with isthmic Spondylolisthesis develop neurologic symptomatology. Neurologic compression in isthmic Spondylolisthesis is multifactorial and can be classified as follows:

1. Compression of the exiting nerve root at the pars interarticularis defect

2. Foraminal stenosis

3. Compression of the L5 roots within the lumbosacral ligament

4. Tension on the roots within the canal preparing to exit at the next most inferior level (at the vertebral body stepoff such as the S1 roots at the posterior- superior border of the S1 body in an L5/S1 Spondylolisthesis)

5. Cauda equina compression

The vast majority of L5/S1 isthmic Spondylolisthesis patients who develop neurologic symptoms develop L5 nerve root pain and/or dysfunction. These L5 root symptoms develop primarily due to root compression associated with the fibrocartilaginous debris at the pars interarticularis defect, as well as with the foraminal stenosis which occurs when the Spondylolisthesis develops. Surgical decompression of the L5 roots via pars defect débridements and foraminotomies at the time of an in-situ fusion can reliably be expected to relieve neurologic symptoms. As one would expect, patients with L4/L5 isthmic Spondylolisthesis typically develop L4 root symptoms.

Additional compression of the L5 roots can be seen in L5/S1 isthmic Spondylolisthesis as the root passes underneath the lumbosacral ligament (see Figs. 1-4). The lumbosacral ligament was first described by Danforth and Wilson in 1925 [4]. Cadaveric studies have revealed an incidence of lumbosacral ligaments in 46%--100% of cadaveric specimens [1,8,12,13]. There are reports of symptomatic relief of L5 radiculopathy via lumbosacral ligament decompression in patients who had undergone routine surgical treatment of their Spondylolisthesis (L.L. Wiltse 1990, J.J. Regan 2002, personal communication) [18]. Kostuik believes that routine division of the lumbosacral ligament should be done when reduction of high-grade Spondylolisthesis is undertaken (J.P. Kostuik 2002, personal communication).

 

Figure 1: Right-anterior oblique view of the lumbosacral ligament and its attachments. On the left side, note one division of the L4 root merging with the L5 root distal to the lumbosacral ligament. (From [13]) Figure 2: Attachments of the lumbosacral ligament to the L5 vertebral body, L5 transverse process, and sacral ala. (From [13]) . Figure 3: Depiction of a compressed L5 root by the lumbosacral ligament as well as osteophyte formation along the anterior-lateral aspect of the L5/S1 disc space. (From [13])

Figure 4:
A dissected cadaveric specimen illustrating compression of the
L5 root underneath the lumbosacral ligament. (From [13])

Further compression of neural tissue occurs within the spinal canal at the level of the posterior-superior aspect of the lower vertebrae, such as at the posteriorsuperior aspect of the S1 body in an L5/S1 Spondylolisthesis. This step-off causes compression of the cauda equina in general, as well as specific compression of the S1 nerve roots. High-grade Spondylolisthesis is typically necessary for the development of cauda equina-type symptomatology. There are multiple reports of cauda equina symptomatology developing in patients with Spondylolisthesis who are treated conservatively as well as in patients who undergo in-situ fusion without reduction [11,15,17].

Backup, 2-2002, Aesculap AG & Co. KG Tuttlingen