Adjacent segment disease in the lumbar spine following different treatment interventions
Abstract Background context Adjacent segment disease (ASD) is symptomatic deterioration of spinal levels adjacent to the site of a previous fusion. A critical issue related to ASD is whether deterioration of spinal segments adjacent to a fusion is due to the spinal intervention or due to the natural...
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Published in | The spine journal Vol. 13; no. 10; pp. 1339 - 1349 |
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Main Authors | , , , , , , , |
Format | Journal Article |
Language | English |
Published |
United States
Elsevier Inc
01.10.2013
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Subjects | |
Online Access | Get full text |
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Summary: | Abstract Background context Adjacent segment disease (ASD) is symptomatic deterioration of spinal levels adjacent to the site of a previous fusion. A critical issue related to ASD is whether deterioration of spinal segments adjacent to a fusion is due to the spinal intervention or due to the natural history of spinal degenerative disease. Purpose The purpose of this review is to summarize the recent clinical literature on adjacent segment disease in light of the natural history, patient-modifiable risk factors, surgical risk factors, sagittal balance, and new technology. Study design This review will evaluate the recent literature on genetic and hereditary components of spinal degenerative disease and potential links to the development of ASD. Methods After a meticulous search of Medline for relevant articles pertaining to our review, we summarized the recent literature on the rate of ASD and the effect of various interventions, including motion preservation, sagittal imbalance, arthroplasty, and minimally invasive surgery. Results The reported rate of ASD after decompression and stabilization procedures is approximately 2% to 3% per year. The factors that are consistently associated with adjacent segment disease include laminectomy adjacent to a fusion and a sagittal imbalance. Conclusions Spinal surgical interventions have been associated with ASD. However, whether such interventions may lead to an acceleration of the natural history of the disease remains questionable. |
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Bibliography: | ObjectType-Article-2 SourceType-Scholarly Journals-1 ObjectType-Feature-3 content type line 23 ObjectType-Review-1 |
ISSN: | 1529-9430 1878-1632 |
DOI: | 10.1016/j.spinee.2013.03.020 |