Spine center for neuroorthopaedics, spinal cord injuries and scoliosis, RKH Orthopedic Clinic Markgröningen gGmbH, Markgröningen, Germany.
Arch Orthop Trauma Surg. 2024 May;144(5):1969-1976. doi: 10.1007/s00402-024-05275-9. Epub 2024 Mar 30.
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.
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.
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.
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.
本研究提出了一个小枕骨后直肌（RCPmi）异常的新病因，该异常是 C0-C1-C2 复合体矢状面失稳的原因，重点是确定 RCPmi 双侧是否缺失或萎缩。
一位 36 岁男性患者，出现反复颈部疼痛（VAS 8/10）和左手整个手部刺痛感，持续了六个月，无明显神经功能缺损。未报告放射状手臂疼痛。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 水平脊髓病。随后进行了后路 C0-1 复位和椎板切除术。
RCPmi 的先天性缺失或萎缩，导致 C1 结节后方缺乏向上向后的牵引力，导致 C1 后弓发育不良。因此，扁形 C1 后弓失去了 C2 后弓的支撑和整个患者 36 年生命过程中所需的向上向后的牵引力。这种逐渐失去支撑和牵引力导致 C1 后弓逐渐向 C2 后弓的前侧移位，导致 C0/1 关节在矢状面的旋转半脱位。最终导致 SCS 和脊髓病。从出生到现在，排除了创伤因素，在上颈椎、颈部肌肉和韧带中未发现典型的退行性改变。
在本病例中，我们不仅报道了 RCPmi 的萎缩或缺失作为 C0-C1-C2 复合体非创伤性矢状面失稳的新病因，还发现了 RCPmi 的新功能。RCPmi 对 C1 后弓的向上向后的牵引力对于正常 C1 前后径的发育至关重要。
