1.Myelography in the Assessment of Degenerative Lumbar Scoliosis and Its Influence on Surgical Management.
George MCKAY ; Peter Alexander TORRIE ; Wendy BERTRAM ; Priyan LANDHAM ; Stephen MORRIS ; John HUTCHINSON ; Roland WATURA ; Ian HARDING
Korean Journal of Spine 2017;14(4):133-138
OBJECTIVE: Myelography has been shown to highlight foraminal and lateral recess stenosis more readily than computed tomography (CT) or magnetic resonance imaging (MRI). It also has the advantage of providing dynamic assessment of stenosis in the loaded spine. The advent of weight-bearing MRI may go some way towards improving assessment of the loaded spine and is less invasive, however availability remains limited. This study evaluates the potential role of myelography and its impact upon surgical decision making. METHODS: Of 270 patients undergoing myelography during 2006–2009, a period representing peak utilisation of this imaging modality in our unit, we identified 21 patients with degenerative scoliosis who fulfilled our inclusion criteria. An operative plan was formulated by our senior author based initially on interpretation of an MRI scan. Subsequent myelogram and CT myelogram investigations were scrutinised, with any additional abnormalities noted and whether these impacted upon the operative plan. RESULTS: From our 21 patients, 18 (85.7%) had myelographic findings not identified on MRI. Of note, in 4 patients, supine CT myelography yielded additional information when compared to supine MRI in the same patients. The management of 7 patients (33%) changed as a result of myelographic investigation. There were no complications of myelography of the total 270 analysed. CONCLUSION: MRI scan alone understates the degree of central and lateral recess stenosis. In addition to the additional stenosis displayed by dynamic myelography in the loaded spine, we have also shown that static myelography and CT myelography are also invaluable tools with regards to surgical planning in these patients.
Congenital Abnormalities
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Constriction, Pathologic
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Decision Making
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Humans
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Magnetic Resonance Imaging
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Myelography*
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Scoliosis*
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Spine
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Weight-Bearing
2.Cell clusters in intervertebral disc degeneration:an attempted repair mechanism aborted via apoptosis
Polly LAMA ; Jerina TIWARI ; Pulkit MUTREJA ; Sukirti CHAUHAN ; Ian J HARDING ; Trish DOLAN ; Michael A ADAMS ; Christine Le MAITRE
Anatomy & Cell Biology 2023;56(3):382-393
Cell clusters are a histological hallmark feature of intervertebral disc degeneration. Clusters arise from cell proliferation, are associated with replicative senescence, and remain metabolically, but their precise role in various stages of disc degeneration remain obscure. The aim of this study was therefore to investigate small, medium, and large size cell-clusters. For this purpose, human disc samples were collected from 55 subjects, aged 37–72 years, 21 patients had disc herniation, 10 had degenerated non-herniated discs, and 9 had degenerative scoliosis with spinal curvature <45°.15 non-degenerated control discs were from cadavers. Clusters and matrix changes were investigated with histology, immunohistochemistry, and Sodium dodecyl sulphate polyacrylamide gel electrophoresis (SDS-PAGE). Data obtained were analyzed with spearman rank correlation and ANOVA. Results revealed, small and medium-sized clusters were positive for cell proliferation markers Ki-67 and proliferating cell nuclear antigen (PCNA) in control and slightly degenerated human discs, while large cell clusters were typically more abundant in severely degenerated and herniated discs. Large clusters associated with matrix fissures, proteoglycan loss, matrix metalloproteinase-1 (MMP-1), and Caspase-3. Spatial association findings were reconfirmed with SDS-PAGE that showed presence to these target markers based on its molecular weight.Controls, slightly degenerated discs showed smaller clusters, less proteoglycan loss, MMP-1, and Caspase-3. In conclusion, cell clusters in the early stages of degeneration could be indicative of repair, however sustained loading increases large cell clusters especially around microscopic fissures that accelerates inflammatory catabolism and alters cellular metabolism, thus attempted repair process initiated by cell clusters fails and is aborted at least in part via apoptosis.