The myodural bridge (MDB) is a connective tissue band that connects the suboccipital muscles and nuchal ligament (NL) with the cervical spinal dura mater (SDM) [1,2,3,4,5,6]. It has been recently confirmed as a conserved structure in mammals [7,8,9]. The MDB has a critical role in transmitting tensile force from its muscular and ligamentous components to the SDM, which has an essential role in the etiology of headache and cervicocephalic pain syndrome [10,11,12,13,14]. The rectus capitis posterior minor (RCPmi) was the first suboccipital muscle identified to attach to the dorsal cervical SDM at the posterior atlanto-occipital (PAO) interval [1]. The architecture of muscle, particularly the cross-sectional area (CSA), is a predictor of its force generation [15]. Previous research has focused on the CSA or relative CSA of the RCPmi muscle as biomechanical contributors to cervicocephalic pain syndrome, mild traumatic brain injury (mTBI), and headache syndromes [10,11,12,13, 16]. Several studies have shown that the CSA of adult RCPmi muscles is negatively correlated with the severity of chronic headaches [10,11,12,13, 16]. Fernfindez-de-las-Penas et al [10, 11] have shown that reduced axial CSA of the RCPmi is correlated with symptom severity in patients with chronic tension-type headache (CTTH) and mTBI. Yet, in contrast to these studies, Yuan et al have reported increased sectional area (SA) of RCPmi muscle in patients with chronic headaches [13]. To correctly assess the effect of the RCPmi muscle’ SA on symptom severity in patients with headache syndrome, it is necessary to thoroughly clarify the magnitude of the variations in the SA of the RCPmi muscles in asymptomatic controls. So far, this issue has not yet been comprehensively addressed. Consequently, an assessment of the SA of the RCPmi muscle in asymptomatic controls is essential for an accurate evaluation of the effect of the SA of the RCPmi muscle in symptomatic patients.
Magnetic resonance imaging (MRI) is a powerful noninvasive imaging tool used to detect the SA of the RCPmi muscle. Though two-dimensional (2D) axial MR images are considered optimal for evaluating the SA of the RCPmi muscle, experimental variables, such as selected image level and variable neck posture, can lead to significant error [17, 18]. Because the reduction in slice thickness lessens partial volume effects that may induce inaccuracy of SA measurement, three-dimensional (3D) MRI may facilitate accurate SA measurement of the RCPmi due to its thinner slices and isotropic post-processed reconstruction. In the present study, physiologic CSA was not calculated though it is more commonly used in conventional calculations to determine muscle atrophy or hypertrophy [12, 16,17,18]. A narrow pointed tendon attaches the RCPmi to the tubercle on the posterior arch of the atlas. As it ascends, it broadens before attaching to the medial part of the inferior nuchal line and the occipital bone between the inferior nuchal line and the foramen magnum. The physiological CSA of each fan-shaped RCPmi cannot be accurately calculated due to underlying difficulties in taking the identical measurement plane, which could be influenced by factors such as, selected scanning level, atlanto-occipital interspace distance, and neck posture [17, 18]. Referring to the method described by Yuan et al, the angle between the medial and lateral borders of the RCPmi was measured, and the value was (60.7 ± 4.4)°. Hence, 60° from the midline represented the mean of the orientation in the different subjects. Thirty degrees with the largest RCPmi muscle were set as the optimal angle for a better view of the muscle [13]. Therefore, we measured the maximal SA of the RCPmi muscles on the parasagittal image with a 30° deviation from the median sagittal plane through the mid-posterior arch of atlas and the occipital bone. Nevertheless, to the best of our knowledge, no studies are reporting the maximum SA in the RCPmi muscles using 3D MRI, which could be used to determine the variance in SA of the RCPmi muscle for related pathologic studies.
Multiple studies have confirmed the binding of the NL attachment to the cervical SDM via the PAO and posterior atlantoaxial (PAA) intervals [3, 5, 19]. In 2014, Zheng’s study confirmed that the local enhancement of the NL emanated from the posterior border of NL projecting forward and upward to the cervical dura mater, which she termed as the to be named ligament (TBNL) [20]. The TBNL may participate in cervicogenic pain syndrome by bridging the dorsal extensor musculature of the cervical spine to the pain-sensitive dura mater. In 2017, Yuan et al found that 11.43% of the RCPmi muscles gave off muscular bundles that merged and terminated at the TBNL whose morphology was influenced by this additional connection [21]. Yet, whether this physical connection from the RCPmi to the TBNL affects the maximum SA of the RCPmi muscle remains unclear.
The SA of RCPmi muscle has been suggested as a potential contributor to headache and cervicogenic pain symptoms; hence, the first aim of this study was to determine the anatomical SA of the RCPmi muscle using 3D T2-weighted MR imaging. The RCPmi and TBNL are both critical components of MDB, and their anatomic connection indicates the possibility of a correlation between them. The second aim was to investigate the relationship between the maximum SA of the RCPmi muscles with the RCPmi-TBNL attachment. We hypothesized that the RCPmi and TBNL worked together as an MDB complex to fulfill their crucial function; therefore, the maximum SA of the RCPmi muscle is negatively correlated with the RCPmi-TBNL connection.