Abstract：
OBJECTIVE: This study presents an abnormality of the musculus rectus capitis posterior minor (RCPmi) as a new etiological factor for nontraumatic sagittal plane instability in the C0-C1-C2-complex, with a focus on identifying the absence or atrophy of RCPmi on both sides.
METHODS: A 36-year-old male patient presented with recurring neck pain (VAS 8/10) and tingling paresthesia in the entire left hand over a six-month period, without significant neurological deficits. Radiated arm pain was not reported. Imaging examinations revealed sagittal plane instability in the C0-C1-C2-complex, spinal canal stenosis (SCS), and myelopathy at the C1 level. Subsequently, a dorsal C0-1 reposition and fusion with laminectomy were performed.
RESULTS: The congenital absence or atrophy of RCPmi, leading to the lack of cephalad-rearward traction on the C1-tuberculum-posterius, induced a developmental failure of the C1 posterior arch. Consequently, the oblate-shaped C1 posterior arch lost support from the underlying C2 posterior arch and the necessary cephalad-rearward traction throughout the patient\'s 36-year life. This gradual loss of support and traction caused the C1 posterior arch to shift gradually to the anterior side of the C2 posterior arch, resulting in a rotational subluxation centered on the C0/1 joints in the sagittal plane. Ultimately, this led to SCS and myelopathy. Traumatic factors were ruled out from birth to the present, and typical degenerative changes were not found in the upper cervical spine, neck muscles, and ligaments.
CONCLUSIONS: In this case, we not only report the atrophy or absence of RCPmi as a new etiological factor for nontraumatic sagittal plane instability in the C0-C1-C2-complex but also discovered a new function of RCPmi. The cephalad-rearward traction exerted by RCPmi on the C1 posterior arch is essential for the development of a normal C1 anterior-posterior diameter.
METHODS: A 36-year-old male patient presented with recurring neck pain (VAS 8/10) and tingling paresthesia in the entire left hand over a six-month period, without significant neurological deficits. Radiated arm pain was not reported. Imaging examinations revealed sagittal plane instability in the C0-C1-C2-complex, spinal canal stenosis (SCS), and myelopathy at the C1 level. Subsequently, a dorsal C0-1 reposition and fusion with laminectomy were performed.
RESULTS: The congenital absence or atrophy of RCPmi, leading to the lack of cephalad-rearward traction on the C1-tuberculum-posterius, induced a developmental failure of the C1 posterior arch. Consequently, the oblate-shaped C1 posterior arch lost support from the underlying C2 posterior arch and the necessary cephalad-rearward traction throughout the patient\'s 36-year life. This gradual loss of support and traction caused the C1 posterior arch to shift gradually to the anterior side of the C2 posterior arch, resulting in a rotational subluxation centered on the C0/1 joints in the sagittal plane. Ultimately, this led to SCS and myelopathy. Traumatic factors were ruled out from birth to the present, and typical degenerative changes were not found in the upper cervical spine, neck muscles, and ligaments.
CONCLUSIONS: In this case, we not only report the atrophy or absence of RCPmi as a new etiological factor for nontraumatic sagittal plane instability in the C0-C1-C2-complex but also discovered a new function of RCPmi. The cephalad-rearward traction exerted by RCPmi on the C1 posterior arch is essential for the development of a normal C1 anterior-posterior diameter.
摘要：
目的：这项研究提出了小后直肌炎（RCPmi）的异常，作为C0-C1-C2复合体非创伤性矢状面不稳定的新病因，重点是确定两侧RCPmi的缺失或萎缩。
方法：一名36岁男性患者在6个月的时间内表现为反复出现的颈部疼痛（VAS8/10）和整个左手感觉异常刺痛，没有明显的神经缺陷.没有报告放射性手臂疼痛。影像学检查显示C0-C1-C2复合体矢状面不稳定，椎管狭窄（SCS），和C1水平的脊髓病。随后，进行背侧C0-1复位和椎板切除术融合。
结果：RCPmi的先天性缺失或萎缩，导致C1-结节-后部缺乏头向后牵引，引起C1后弓的发育失败。因此,在患者36年的整个生命中，扁圆形C1后弓失去了底层C2后弓的支撑和必要的头向后牵引。这种逐渐失去的支撑和牵引使C1后弓逐渐向C2后弓的前侧移动,导致矢状平面中C0/1关节中心的旋转半脱位。最终,这导致了SCS和脊髓病。从出生到现在都排除了创伤因素,在上颈椎没有发现典型的退行性改变，颈部肌肉,和韧带。
结论：在这种情况下，我们不仅报道了RCPmi的萎缩或缺失是C0-C1-C2复合体非创伤性矢状面不稳定的新病因，而且还发现了RCPmi的新功能。RCPmi在C1后弓上施加的向后牵引力对于正常C1前后直径的发展至关重要。
方法：一名36岁男性患者在6个月的时间内表现为反复出现的颈部疼痛（VAS8/10）和整个左手感觉异常刺痛，没有明显的神经缺陷.没有报告放射性手臂疼痛。影像学检查显示C0-C1-C2复合体矢状面不稳定，椎管狭窄（SCS），和C1水平的脊髓病。随后，进行背侧C0-1复位和椎板切除术融合。
结果：RCPmi的先天性缺失或萎缩，导致C1-结节-后部缺乏头向后牵引，引起C1后弓的发育失败。因此,在患者36年的整个生命中，扁圆形C1后弓失去了底层C2后弓的支撑和必要的头向后牵引。这种逐渐失去的支撑和牵引使C1后弓逐渐向C2后弓的前侧移动,导致矢状平面中C0/1关节中心的旋转半脱位。最终,这导致了SCS和脊髓病。从出生到现在都排除了创伤因素,在上颈椎没有发现典型的退行性改变，颈部肌肉,和韧带。
结论：在这种情况下，我们不仅报道了RCPmi的萎缩或缺失是C0-C1-C2复合体非创伤性矢状面不稳定的新病因，而且还发现了RCPmi的新功能。RCPmi在C1后弓上施加的向后牵引力对于正常C1前后直径的发展至关重要。
