The range of motion characteristics of atlantoaxial joints with the "sandwich" deformity: a human cadaveric biomechanical study.

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Tác giả: Jinguo Chen, Xiangyu Hou, Kan-Lin Hung, Huijie Leng, Weishi Li, Yinglun Tian, Shenglin Wang, Nanfang Xu, Ming Yan

Ngôn ngữ: eng

Ký hiệu phân loại: 594.38 *Pulmonata

Thông tin xuất bản: Germany : Neurosurgical review , 2025

Mô tả vật lý:

Bộ sưu tập: NCBI

ID: 58851

 During our clinical work, a special subtype of atlantoaxial dislocation(AAD) was identified, which was combined with atlas occipitalization and C2-3 fusion and was named as "sandwich" AAD.To explore if the biomechanical characteristics between atlantoaxial joints in "sandwich" deformity patients is particular and if there is a relationship between the AAD and the malformations (Chiari malformation and the formation of syringomyelia). A biomechanical study on the atlantoaxial joint by simulating "sandwich" deformity in cadaveric specimens was conducted. Five fresh frozen cadaver spinal specimens (from the occiput to C7) were selected from human donors with no history of spinal trauma and congenital malformations. The C0-1 and C2-3 (C1 pedicle screws combined with occipital titanium, C2 pedicle screws and C3 lateral mass screws) were fixed to develop congenital atlas occipitalization and C23 fusion deformities ("sandwich" deformity). Each specimen was tested two times, firstly under the normal condition and secondly under the "sandwich" condition. Then the range of motion(ROM) between C1 and C2 was measured under different conditions. The results showed that the relative range of flexion-extension motion between C1-2 in the "Sandwich" specimens was significantly greater than that in the normal specimens (P <
  0.05). No significant difference in the relative range of other two motion modes (lateral bending and axial rotation) between C1-2 was observed for the normal and "Sandwich" specimens. The "clamp" mechanism of "sandwich" deformity during flexion and extension might be involved in the pathogenesis of AAD and secondary nervous system damage.
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