The occipitoatlantal capsular ligaments are the primary stabilizers of the occipitoatlantal joint in the craniocervical junction: a finite element analysis.

OBJECTIVEThere is contradictory evidence regarding the relative contribution of the key stabilizing ligaments of the occipitoatlantal (OA) joint. Cadaveric studies are limited by the nature and the number of injury scenarios that can be tested to identify OA stabilizing ligaments. Finite element (FE) analysis can overcome these limitations and provide valuable data in this area. The authors completed an FE analysis of 5 subject-specific craniocervical junction (CCJ) models to investigate the biomechanics of the OA joint and identify the ligamentous structures essential for stability.METHODSIsolated and combined injury scenarios were simulated under physiological loads for 5 validated CCJ FE models to assess the relative role of key ligamentous structures on OA joint stability. Each model was tested in flexion-extension, axial rotation, and lateral bending in various injury scenarios. Isolated ligamentous injury scenarios consisted of either decreasing the stiffness of the OA capsular ligaments (OACLs) or completely removing the transverse ligament (TL), tectorial membrane (TM), or alar ligaments (ALs). Combination scenarios were also evaluated.RESULTSAn isolated OACL injury resulted in the largest percentage increase in all ranges of motion (ROMs) at the OA joint compared with the other isolated injuries. Flexion, extension, lateral bending, and axial rotation significantly increased by 12.4% ± 7.4%, 11.1% ± 10.3%, 83.6% ± 14.4%, and 81.9% ± 9.4%, respectively (p ≤ 0.05 for all). Among combination injuries, OACL+TM+TL injury resulted in the most consistent significant increases in ROM for both the OA joint and the CCJ during all loading scenarios. OACL+AL injury caused the most significant percentage increase for OA joint axial rotation.CONCLUSIONSThese results demonstrate that the OACLs are the key stabilizing ligamentous structures of the OA joint. Injury of these primary stabilizing ligaments is necessary to cause OA instability. Isolated injuries of TL, TM, or AL are unlikely to result in appreciable instability at the OA joint.

Signal changes of the alar ligament in a healthy population: a dispositional or degenerative consequence?

OBJECT The alar ligaments (ALs) are vital for stabilizing the craniocervical junction. In terms of morphology, their appearance varies and is visible on MRI. Dark signal of the AL on proton-density (PD)-weighted images is generally considered the norm, but the etiology of frequently observed signal hyperintensities is poorly understood. Using spectral fat suppression, signal hyperintensities can be differentiated into fat- and nonfat-related hyperintensities (NFH). Although signal hyperintensities have no evident association with whiplash-associated disorder, age-related degeneration has often been theorized. Therefore, this study investigates the signal intensities of the ALs on 3.0-T MRI with special reference to age. Expanding thereon, the authors investigated the relationship between signal hyperintensities and patient characteristics, such as height, weight, and sex. METHODS Sixty-six healthy volunteers were scanned using 3.0-T PD-weighted MRI, including spectral fat suppression of the craniocervical junction. The study population was separated into 2 groups (old vs young) using 2 approaches: dichotomization at the median age (40.0 years) and the calculated threshold (28.5 years) using receiver operating characteristics (ROC). The AL was independently characterized with respect to continuity, course, shape, signal intensity, and graduation of homogeneity by 2 experienced neuroradiologists. Signal intensity was differentiated into fat-related hyperintensity and NFH. Univariate and multivariate logistic regression models were employed to investigate the relationship between patient characteristics and signal intensities. RESULTS Two different AL patterns were observed: inhomogeneous (33.3%) and homogeneous (66.7%). The latter pattern was mostly surrounded by a small dark rim (56.8%). Fat could be identified in 15.9% of all ALs (21 of 132 patients), and NFH was identified in 17.4% of all ALs (23 of 132 patients). Here, 28.5 years was the preferred threshold, demonstrating a relatively high sensitivity for dichotomizing the population based on the ROC of NFH. The most relevant factor for having NFH was being older than the calculated threshold (odds ratio [OR] 3.420, p = 0.051). Fat-related hyperintensities occurred significantly more frequently in men than women (OR 0.110 and p = 0.007 for women; OR 9.075 and p = 0.007 for men). Height was the second most significant factor: for every 1-cm increase, the odds of having fat lesions increased by approximately 10% (OR 1.102; p = 0.017). CONCLUSIONS This study shows that AL signal hyperintensities are substantially influenced by age, sex, and height in healthy individuals. Regarding fat-related hyperintensities, the most relevant factors proved to be sex and height. The odds of detecting NFH increased almost significantly after a relatively young age (> 28.5 years) and were remarkably more frequent in individuals older than 28.5 years. The authors caution presumptions equating signal alterations with age-related deterioration. Instead, they suggest that dispositional factors such as sex and height are more relevant in the AL constitution. Signal alterations in ALs naturally occur in healthy symptom-free individuals, underscoring the importance of cautiously interpreting such lesions on posttraumatic MRI scans.