Spondylolysis and Spondylolisthesis in Children and Adolescents: I. Diagnosis, Natural History, and Nonsurgical Management

Cavalier, Ralph; Herman, Martin J.; Cheung, Emilie V.; Pizzutillo, Peter D.

doi:10.5435/00124635-200607000-00004

Cited by 124 publications

(161 citation statements)

References 30 publications

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“…The resulting lumbar stenosis may cause L5 nerve radiculopathy as well as bowel and bladder dysfunction from compression of sacral nerve roots. Children and adolescents with dysplastic spondylolisthesis are more likely to carry greater risk of progressive deformity and subsequent neurologic injury than do patients with isthmic or acquired spondylolisthesis (4). Indeed, patients with dysplastic spondylolisthesis, such as patients II-3, III-2, XA-12, and XA-30 in this study, are notably more likely to require surgical treatment.…”

Section: Discussionmentioning

confidence: 81%

“…Dysplastic spondylolysis (i.e., Wiltse-Newman type I) represents a type of congenital defect of vertebral pars interarticularis in the upper sacrum and lower lumbar, commonly affecting L5 (1). This type of spondylolysis is not rare, comprising 14-21% of cases in a large sample population (4). Among 605 pediatric patients who underwent surgical treatment for spondylolisthesis in multisurgeon centers from 2004 to 2007, 10% of them were affected by dysplastic spondylolysis (5).…”

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confidence: 99%

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Dysplastic spondylolysis is caused by mutations in the diastrophic dysplasia sulfate transporter gene

Cai

Liu

Cai

et al. 2015

Proc. Natl. Acad. Sci. U.S.A.

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Spondylolysis is a fracture in part of the vertebra with a reported prevalence of about 3–6% in the general population. Genetic etiology of this disorder remains unknown. The present study was aimed at identifying genomic mutations in patients with dysplastic spondylolysis as well as the potential pathogenesis of the abnormalities. Whole-exome sequencing and functional analysis were performed for patients with spondylolysis. We identified a novel heterozygous mutation (c.2286A > T; p.D673V) in the sulfate transporter gene SLC26A2 in five affected subjects of a Chinese family. Two additional mutations (e.g., c.1922A > G; p.H641R and g.18654T > C in the intron 1) in the gene were identified by screening a cohort of 30 unrelated patients with the disease. In situ hybridization analysis showed that SLC26A2 is abundantly expressed in the lumbosacral spine of the mouse embryo at day 14.5. Sulfate uptake activities in CHO cells transfected with mutant SLC26A2 were dramatically reduced compared with the wild type, confirming the pathogenicity of the two missense mutations. Further analysis of the gene–disease network revealed a convergent pathogenic network for the development of lumbosacral spine. To our knowledge, our findings provide the first identification of autosomal dominant SLC26A2 mutations in patients with dysplastic spondylolysis, suggesting a new clinical entity in the pathogenesis of chondrodysplasia involving lumbosacral spine. The analysis of the gene–disease network may shed new light on the study of patients with dysplastic spondylolysis and spondylolisthesis as well as high-risk individuals who are asymptomatic.

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Section: Discussionmentioning

confidence: 81%

mentioning

confidence: 99%

Dysplastic spondylolysis is caused by mutations in the diastrophic dysplasia sulfate transporter gene

Cai

Liu

Cai

et al. 2015

Proc. Natl. Acad. Sci. U.S.A.

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“…It is estimated to occur naturally in approximately 6 % of the population, increasing in prevalence from birth to approximately age 22. Physical activities that accentuate the natural lumbar lordosis through required hyperextension and rotational loads are thought to be a cause of pars defects, spondylolysis, and, potentially, spondylolisthesis [ 25 ]. A "stress reaction" refers to the incomplete bone disruption and sclerosis one might see on CT or the intraosseous edema on MRI, at the pars, lamina, or pedicle.…”

Section: Spondylolysis and Spondylolisthesismentioning

confidence: 99%

Spine Injuries in Tennis Players

McAnany

Patterson

Hecht

2016

Contemporary Pediatric and Adolescent Sports Medicine

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“…W hile lumbar spondylolysis in the general adult population may reach as high as 5%-7% in select studies, 3,6,7,12,16,19,31,32,38,45,46,67 the actual incidence of spondylolysis in pediatric patients presenting with axial low-back pain may approach 50%.…”

Section: Neurosurg Focus 43 (2):e6 2017mentioning

confidence: 99%

“…

FOCUS

Neurosurg Focus 43 (2):E6, 2017W hile lumbar spondylolysis in the general adult population may reach as high as 5%-7% in select studies, 3,6,7,12,16,19,31,32,38,45,46,67 the actual incidence of spondylolysis in pediatric patients presenting with axial low-back pain may approach 50%.3,36 Numerous prior studies have described the presentation and management of lumbar spondylolysis, most commonly presenting at L-5 in up to 95% of cases and followed by L-4 in 5%-15%. 12,36,37,56 The vertebral segments of greatest lordosis and flexibility in the lumbar spine are the L4-5 and L5-S1 motion segments, where the points of greatest facet overhang occur and the greatest biomechanical forces are applied to the posterior elements.

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mentioning

confidence: 99%

Minimally invasive direct pars repair with cannulated screws and recombinant human bone morphogenetic protein: case series and review of the literature

Ghobrial

Crandall

Lau

et al. 2017

Neurosurgical Focus

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OBJECTIVEThe objective of this study was to describe the use of a minimally invasive surgical treatment of lumbar spondylolysis in athletes by a fluoroscopically guided direct pars screw placement with recombinant human bone morphogenetic protein–2 (rhBMP-2) and to report on clinical and radiographic outcomes.METHODSA retrospective review was conducted of all patients treated surgically for lumbar spondylolysis via a minimally invasive direct pars repair with cannulated screws. Demographic information, clinical features of presentation, perioperative and intraoperative radiographic imaging, and postoperative data were collected. A 1-cm midline incision was performed for the placement of bilateral pars screws utilizing biplanar fluoroscopy, followed by placement of a fully threaded 4.0-mm-diameter titanium cannulated screw. A tubular table-mounted retractor was utilized for direct pars fracture visualization and debridement through a separate incision. The now-visualized pars fracture could then be decorticated, with care taken not to damage the titanium screw when using a high-speed drill. Local bone obtained from the curettage was then placed in the defect with 1.05 mg rhBMP-2 divided equally between the bilateral pars defects.RESULTSNine patients were identified (mean age 17.7 ± 3.42 years, range 14–25 years; 6 male and 3 female). All patients had bilateral pars fractures of L-4 (n = 4) or L-5 (n = 5). The mean duration of preoperative symptoms was 17.22 ± 13.2 months (range 9–48 months). The mean operative duration was 189 ± 29 minutes (range 151–228 minutes). The mean intraoperative blood loss was 17.5 ± 10 ml (range 10–30 ml). Radiographic follow-up was available in all cases; the mean length of time from surgery to the most recent imaging study was 30.8 ± 23.3 months (range 3–59 months). The mean hospital length of stay was 1.13 ± 0.35 days (range 1–2 days). There were no intraoperative complications.CONCLUSIONSLumbar spondylolysis treatment with a minimally invasive direct pars repair is a safe and technically feasible option that minimizes muscle and soft-tissue dissection, which may particularly benefit adolescent patients with a desire to return to a high level of physical activity.

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Spondylolysis and Spondylolisthesis in Children and Adolescents: I. Diagnosis, Natural History, and Nonsurgical Management

Cited by 124 publications

References 30 publications

Dysplastic spondylolysis is caused by mutations in the diastrophic dysplasia sulfate transporter gene

Dysplastic spondylolysis is caused by mutations in the diastrophic dysplasia sulfate transporter gene

Spine Injuries in Tennis Players

Minimally invasive direct pars repair with cannulated screws and recombinant human bone morphogenetic protein: case series and review of the literature

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