Abstract
Introduction: Thickened ligamentum flavum (LF) is a major contributor to the clinical syndrome of lumbar canal stenosis (LCS). The patho-mechanisms responsible for this phenomenon remain unclear. Cysts adjacent to facet joints (FJ) in the spine are regarded as rare entities that may uncommonly contribute to LCS. Inaccurate pathological interpretation and unawareness of a key anatomical feature has generated erratic terminology and confusion about their origin.
Methods: Twenty-seven consecutive patients with radiologically confirmed central canal or lateral recess stenosis underwent lumbar laminectomy for neurogenic symptoms. Surgical specimens comprising en bloc excision of LF and medial inferior facet (to retain LF and FJ relationships) were examined microscopically following staining with haematoxylin-eosin and Miller’s elastic stain. Controls were facet/LF specimens from 89 cadaver lumbar spines.
Results: Mean LF thickness was 8.9 mm (+/− 0.3 mm SEM) at the operated levels and 2.9 mm (+/− 0.3 mm) at the non-operated, adjacent levels (p < 0.01). Twenty-eight synovial cysts (8 bilateral, 12 unilateral) were present at a single level in 20 (74%) patients. Synovial cysts per spine level were: L1/2 = 0; L2/3 = 3; L3/4 = 7; L4/5 = 16; L5/S1 = 2. The cyst levels all showed advanced osteoarthritis and LF degeneration. Ten patients (50 %) with cysts had pre-existing degenerative spondylolisthesis (DS). Only 5 patients had pre-operative radiological apperances of unilateral facet cysts. Therefore 82 % of our observed synovial cysts were microscopic or occult. The synovial cysts communicated with the FJ via a bursa-like cleft within the LF, and their linings of synoviocytes and other cells contained fragments shed from the articular surface. The control cadaver specimens revealed that a synovial bursa or intra-ligamentous out-pouching from the synovial cavity was present in 90% of normal LF at L4/5 and was up to 12 mm in length. This intra-ligamentous synovial recess, either wholly or partially lined by synoviocytes, was only present in 55% of specimens at L1/2 with a maximum length of 5 mm. Several other juxtafacet cyst types were observed in the experimental group and a novel classification based upon pathological findings is presented.
Discussion: Para-facetal intraspinal cysts are common in degenerative lumbar spinal stenosis. DS is also a frequent finding but is statistically unrelated to cyst formation (Chi-square: p=0.187). We have found that debris from osteoarthritic facet joints enters a bursa-like cleft within the LF where it becomes incorporated into the wall where it excites a granulomatous reaction leading to blockage and synovial cyst formation. The existence of this channel has not been reported previously. We suggest that microscopic synovial cysts contribute significantly to the ligamentous thickening seen in LCS. We also present a novel classification of juxtafacet cysts based on our pathological findings.
Correspondence should be addressed to Dr Owen Williamson, Editorial Secretary, Spine Society of Australia, 25 Erin Street, Richmond, Victoria 3121, Australia.
