MRI-based evidence of rectus capitis posterior minor hypertrophy and its correlation with disease duration in Parkinson's disease.
MRI-based evidence of rectus capitis posterior minor hypertrophy and its correlation with disease duration in Parkinson's disease.
Where did the research take place?
The study site has not been established. Author addresses may differ from where the research occurred.
Dalian, CN · Author affiliation
Department of Anatomy, Dalian Medical University, Dalian, 116044, China.Location evidence
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Original abstract
BACKGROUND: Recent research in Parkinson's disease (PD) has increasingly focused on alterations in cerebrospinal fluid (CSF) dynamics and glymphatic system (GS) function. The myodural bridge (MDB), a structure connecting the suboccipital muscles to the spinal dura mater, is involved in the regulation of CSF dynamics. The rectus capitis posterior minor (RCPmi) is a core component of the myodural bridge complex (MDBC). This study employed magnetic resonance imaging (MRI) to evaluate morphological changes in the RCPmi in PD patients and to explore their potential association with CSF dynamics and disease duration. MATERIALS AND METHODS: This retrospective MRI study included 349 participants: 156 patients with PD and 193 healthy controls (HC). The occiput-C2 angle (OC2A) was measured on mid-sagittal T2-weighted images. Standardized cross-sectional area (CSA) ratios of MDBC constituent muscles (RCPmi, RCPma, OCI) and non-constituent muscles (OCS, RCL) were quantified on axial images. In 51 PD patients with complete disease duration records (range 1-14 years), the correlation between RCPmi CSA and disease duration was analyzed. From the overall cohort, 277 participants with well-defined occipito-atlantal cistern (OAC) morphology (114 PD, 163 HC) were selected for measurement of OAC parameters (D-FM, D-C1, D-C2) and concurrent anteroposterior diameters of the medulla oblongata and upper cervical spinal cord at the corresponding anatomical levels. RESULTS: No significant differences were observed between the PD and HC groups in OC2A or atlas posterior arch CSA (P > 0.05), indicating that subsequent muscle comparisons were not biased by head position or individual anatomical variation. Compared with the HC group, the PD group exhibited significantly larger CSAs of all MDBC constituent muscles (P < 0.05), with the most pronounced difference noted for RCPmi (PD: 1.97 ± 1.35 vs. HC: 1.58 ± 1.07, P = 0.003). No significant differences were found for non-constituent muscles (P > 0.05). Within the PD group, RCPmi CSA showed a moderate positive correlation with disease duration (r = 0.47, P < 0.001). Analysis of OAC parameters revealed significantly larger D-C1 and D-C2 distances in the PD group compared with the HC group (D-C1: 3.96 ± 1.29 mm vs. 3.60 ± 1.29 mm, P = 0.020; D-C2: 2.75 ± 0.88 mm vs. 2.45 ± 0.82 mm, P = 0.004), whereas D-FM did not differ significantly (P > 0.05). Concurrent measurements of neural tissue anteroposterior diameters at the same anatomical levels as the OAC parameters showed no significant differences between PD group and HC group (P > 0.05). CONCLUSION: This study demonstrates selective hypertrophy of the RCPmi in patients with PD, with the degree of hypertrophy significantly correlated with both disease duration and OAC enlargement. These morphological findings provide a cross‑sectional imaging correlate of disease chronicity. The study did not directly measure CSF dynamics or longitudinal disease progression; therefore, any link between RCPmi hypertrophy and CSF function remains hypothetical and requires future functional and longitudinal validation.