Abstract

Substantiated degeneration of rectus capitis posterior minor muscle in Chiari malformation I based on multimodal observations: a prospective cohort study.

Bao, Mingbin (M);He, Yunsen (Y);Liu, Li (L);Tao, Ye (Y);Huang, Qinjiang (Q);Zhang, Mengjun (M);Liu, Ping (P);Zhang, Zhou (Z);Liao, Yongli (Y);Qin, Xiaohong (X);Li, Wei (W);Wu, Bo (B);

 
     

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Neurosurg Rev.2025 Apr 22;48(1):377.doi:10.1007/s10143-025-03534-w

Abstract

BACKGROUND: The primary pathophysiological mechanism of Chiari Malformation Type I (CMI) is the disruption of cerebrospinal fluid hydrodynamics (CSF-HY) at the craniocervical junction (CVJ), and numerous studies have indicated that the rectus capitis posterior minor (RCPmi) significantly promotes CVJ-CSF-HY. Consequently, RCPmi might have a significant role in the pathophysiological mechanisms underlying CMI, although no relevant studies have been conducted previously. Therefore, this article employs multimodal MRI neuroimaging to investigate the function of RCPmi in CMI patients, while also critically reviewing previous controversies regarding RCPmi research findings in other populations.

METHOD: This study included a total of 89 subjects, consisting of 45 patients with CMI and 44 healthy controls. Bilateral RCPmi muscle volumes and fatty infiltration (FI) levels were assessed using 3D-MRI-T1 sequences. Simultaneously, diffusion tensor imaging (DTI) data were utilized to extract fractional anisotropy (FA), apparent diffusion coefficient (ADC), as well as the number and length of the muscle fiber tracks. Mann-Whitney U tests, Kruskal-Wallis tests, and independent samples T-tests were conducted to evaluate differences in bilateral RCPmi volume and related metrics between CMI patients and healthy controls. Furthermore, a critical review and summary of all previous research data regarding the morphology of the RCPmi were conducted.

RESULT: The volume of RCPmi in CMI patients was significantly smaller than that in the healthy control group (p < 0.05), and there was also significant fat infiltration (p < 0.05). The FA, ADC, as well as the number and length of muscle fiber tracks in CMI patients were significantly higher than those in the healthy control group (p < 0.05).

CONCLUSION: (1) CMI patients exhibited significant atrophy and FI in bilateral RCPmi compared to healthy controls, and the resulting functional decompensation may affect CVJ-CSF dynamics. (2) The FA and ADC values of the bilateral RCPmi in CMI patients were significantly elevated, suggesting the potential presence of denervation damage. Future research should employ methods such as electromyography, pathology, and molecular biology to validate the pathological and functional impairments of RCPmi and their impact on the normal physiological functions of the craniovertebral junction, aiming to provide new insights for the clinical treatment of CMI.

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