Abstract

Bertolotti syndrome is a diagnosis given to patients experiencing low-back pain due to a lumbosacral transitional vertebra (LSTV). LSTVs cause altered biomechanics at the lumbosacral junction, predisposing these patients to degenerative disease. It has been proposed that these patients have additional non-osseous variation such as ligamentous differences in the lumbar spine. The iliolumbar ligament, which attaches from the iliac crest to the transverse process of L4 and L5, plays a significant role in reducing lumbar motion in all six degrees of freedom; therefore, altered ligament anatomy can have a significant impact on stability. The purpose of this study was to examine the iliolumbar ligament complex in patients with Bertolotti syndrome and anatomically normal controls to determine if underdevelopment of the iliolumbar ligament complex is seen in Bertolotti syndrome. This is a retrospective analysis of patients with Bertolotti syndrome and anatomically normal controls who received care at the authors' institution between 2010 and 2020. Axial thickness of the iliolumbar ligament at the L5 vertebral level was assessed via MRI. Results were compared between the defective and normal side within unilaterally affected (Castellvi types IIa and IIIa) Bertolotti syndrome patients, between defective sides in bilaterally affected Bertolotti syndrome patients (Castellvi types IIb, IIIb, and IV), and between the affected side in Bertolotti syndrome patients and the corresponding location in normal controls. A total of 173 patients were included in the study, 102 with Bertolotti syndrome and 71 controls. Among the Bertolotti patients, 49 had left LSTVs, 29 had right LSTVs, and 24 had bilateral LSTVs. For patients with unilateral defects, defective side ligaments were thinner than ligaments on the normal side (p < 0.05). For bilateral LSTVs, ligament thickness on each side was considered statistically equivalent (p < 0.05) and not significantly different from that in controls. Bertolotti syndrome correlates to significant underdevelopment of the iliolumbar ligament corresponding to the side of the LSTV as compared to the ligament on the contralateral side. In patients with bilateral LSTVs, no difference in the iliolumbar ligament compared to that in controls was seen. Developmental changes in the iliolumbar ligament may further exacerbate the altered lumbosacral biomechanics seen in patients with unilateral LSTV, whereas bilateral LSTVs may still allow normal development of the ligament complex. Further research should be done to examine the discrepancies seen in this study.

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