Cervical myelopathy due to calcification of the posterior atlantoaxial membrane associated with generalized articular deposition of calcium pyrophosphate dihydrate: a case report and review of the literature

Cervical myelopathy due to calcification of the posterior atlantoaxial membrane associated with generalized articular deposition of calcium pyrophosphate dihydrate: a case report and review of the literature
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DOI:
10.1007/s00776-014-0631-2
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发表时间:
2015-11
影响因子:
1.7
通讯作者:
K. Mori;S. Imai;K. Nishizawa;Y. Matsusue
K. Mori;S. Imai;K. Nishizawa;Y. Matsusue
中科院分区:
医学4区
文献类型:
--
作者:
K. Mori;S. Imai;K. Nishizawa;Y. Matsusue

文献摘要

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x线检查显示,从C2延伸至C5的混合型OPLL,齿状后钙化,以及C1后弓和C2椎板之间的圆形钙化肿块(图1a)。左膝、肩部和手指也可见钙化病变(图1 b-d)。左膝关节关节液的偏振显微镜分析显示CPPD晶体。计算机断层扫描(CT)清楚显示寰枢后膜卵圆形钙化,齿状后钙化,以及从C2延伸至C5的OPLL。钙化病变在CT上显示为模糊的斑点状图像(图2a, b)。随后的磁共振(MR)成像显示由于寰枢后膜钙化导致脊髓明显受压,在t1和t2加权图像上均为低强度(图3 a-c)。反过来,OPLL引起的下轴脊髓压迫不明显(图3 a-c)。t2加权图像上脊髓强度的变化也在C1/2水平被发现(图3b)。考虑到所有这些发现,我们将颈椎病归因于寰枢后膜的钙化,并进行了后路减压手术。在双侧暴露C1/2后,我们采用C2椎板部分切除术切除寰枢后膜,包括左侧钙化病变,同时我们能够保留C1后弓。在手术中,病变被小心地从硬脑膜上剥离。在退化的寰枢后膜内证实了白垩白色沉积物(图4a)。减压后尽可能重建从C2处剥离的伸肌。组织病理学检查显示,变性纤维组织内的钙化颗粒被巨噬细胞包围(图4b)。钙化颗粒茜素红S阳性(图4c)。此外,拉曼
On X-ray examination, mixed-type OPLL extending from C2 to C5, retro-odontoid calcification, as well as a round calcified mass between the posterior arch of C1 and the lamina of C2 were noted (Fig. 1 a). Calcified lesions were also found in the left knee, shoulders, and fingers (Fig. 1 b–d). Joint fluid analyses of the left knee joint by polarization microscopy revealed CPPD crystals. Computed tomography (CT) clearly demonstrated oval calcification of the posterior atlantoaxial membrane, retro-odontoid calcification, as well as OPLL extending from C2 to C5. A calcified lesion was visualized as vague spotty images on CT (Fig. 2 a, b). Subsequent magnetic resonance (MR) imaging demonstrated overt compression of the spinal cord due to calcification of the posterior atlantoaxial membrane, which was low intensity on both T1-and T2-weighted images (Fig. 3 a–c). In turn, subaxial spinal cord compression due to OPLL was not evident (Fig. 3 a–c). A change in the intensity of the spinal cord on T2-weighted images was also identified at the level of C1/2 (Fig. 3 b). Taking all of these findings into account, we attributed cervical myelopathy to the calcification of the posterior atlantoaxial membrane and posterior decompression surgery was performed. After bilateral exposure of C1/2, enblock extirpation of the posterior atlantoaxial membrane including the left calcified lesion was performed with partial laminectomy of C2, whereas we were able to preserve the posterior arch of C1. At the surgery, the lesion was carefully dissected from the dura matter. Chalky white deposits within the degenerated posterior atlantoaxial membrane were confirmed (Fig. 4 a). Extensor muscles dissected from C2 were reconstructed after the decompression as much as possible. Histopathological examination revealed that calcified granules within degenerated fibrous tissue were surrounded by macrophages (Fig. 4 b). The calcified granules were Alizarin red S positive (Fig. 4 c). Furthermore, Raman