Variability in Surgical Treatment of Spondylolisthesis Among Spine Surgeons

Background There are a multitude of treatments for low-grade lumbar spondylolisthesis. There are no clear guidelines for the optimal approach. Objective To identify the surgical treatment patterns for spondylolisthesis among United States spine surgeons. Methods 445 spine surgeons in the United States completed a survey of clinical/radiographic case scenarios on patients with lumbar spondylolisthesis with neurogenic claudication with (S+BP) or without (S−BP) associated mechanical back pain. Treatment options included decompression, laminectomy with posterolateral fusion, posterior lumbar interbody fusion, or none of the above. The primary outcome measure was the probability of 2 randomly chosen surgeons disagreeing on the treatment method. Results There was 64% disagreement (36% agreement) among surgeons for treatment of spondylolisthesis with mechanical back pain (S+BP) and 71% disagreement (29% agreement) for spondylolisthesis without mechanical back pain (S−BP). For S+BP, disagreement was 52% for those practicing 5 to 10 years versus 70% among those practicing more than 20 years. Orthopedic surgeons had greater disagreement than did neurosurgeons (76% vs. 56%) for S+BP. Greater clinical equipoise was seen for S−BP than for S+BP regardless of surgeon characteristics. For spondylolisthesis without mechanical back pain, neurosurgeons were significantly more likely to select decompression-only than were orthopedic surgeons, who more commonly selected fusion. Conclusions Clinical equipoise exists for the treatment of spondylolisthesis. Differences are greater when the patient presents without associated back pain. Surgeon case volume, practice duration, and specialty training influence operative decisions for a given pathologic condition. Recognizing this practice variation will hopefully lead to better evidence and practice guidelines for the optimal and most cost-effective treatment paradigms

CSF rhinorrhea from a transclival meningocele demonstrated with metrizamide CT cisternography Case report

✓ A 63-year-old woman with a 10-year history of intermittent cerebrospinal fluid (CSF) rhinorrhea was found to have a transclival meningocele. After pluridirectional tomography demonstrated a bone defect in the clivus, the diagnosis was established by means of computerized tomography (CT) by comparing the absorption coefficients of a soft-tissue mass within the sphenoid sinus before and after the injection of metrizamide into the lumbar subarachnoid space. An increase of 39 absorption units clearly indicated the movement of CSF from the prepontine subarachnoid space into the sphenoid sinus. This case illustrates the value of metrizamide CT cisternography in the evaluation of patients with CSF rhinorrhea

The "thickened" ligamentum flavum: is it buckling or enlargement?

Thickening of the LF is ascribed to buckling due to DSN. Uncertainty exists as to whether this can occur without DSN. Our primary hypothesis was that facet degenerative changes alone, independent of DSN, can thicken the LF. Our secondary hypothesis was that inflammatory changes surrounding degenerative facet joints may incite thickening. Fifty-two patients were divided into 1 of 3 groups: group 1 (normal lumbar spine, n = 21), group 2 (LF thickening and FH with normal height of the L4-5 disk, n = 18), and group 3 (LF thickening and FH with decreased height of the L4-5 disk, n = 13). LF thickness measured on axial T1WI at the midpoint of the LF length was compared with that in group 1. Facet joints were evaluated for spurring, joint fluid, and cortical irregularity, indicating facet degeneration. Enhancement of the facet joints and LF thickening were also evaluated (n = 2). The Student t test was used to compare groups. Normal LF thickness (group 1) was 3.1 mm, whereas LF thickness averaged 4.9 mm in group 2 and 5.3 mm in group 3 (both P < .001). Patients with asymmetric LF thickness showed greater LF thickness on the side with greater FH. There was more LF enhancement on the side with greater facet degenerative disease. LF thickening can be secondary to facet degenerative changes, independent of DSN. Inflammatory changes may be an inciting factor for LF thickening