\n\n
正常椎间盘由中央的髓核和外周的纤维环构成,完全处于椎间隙边界内,近端和远端为终板包裹,外周处于椎体隆起外缘内,没有骨赘。
\n\n1.椎间盘受损早期:椎间盘髓核中蛋白多糖减少,使保持水分的功能减弱,导致其生物力学性能改变。使纤维环的胶原纤维变性,纤维环排列紊乱,出现裂纹和断裂,使纤维出现裂隙。
\n\n2.椎间盘突出:在外力作用下可诱发髓核从此裂隙向后方突出。同时纤维环缺乏良好的血运,故断裂的纤维环难以愈合。
\n\n3.椎间盘骨赘形成:椎体和终板的反应性骨组织修复,使软骨下骨硬化和骨赘形成。当椎间盘高度下降,颈椎出现不稳,成纤维细胞活跃发生机化并继而骨化,最后形成凸向椎体前方或后方椎管内的骨赘。
\n\n4.椎间关节骨赘形成:同时颈椎的关节由于异常负载软骨先行退变,逐渐亦累积软骨及软骨下骨产生创伤性关节炎,引起颈项痛和颈椎运动受限。
\n\n在椎间盘和椎骨退变的基础上,连接颈椎的前、后纵韧带、黄韧带及项韧带发生松弛引致颈椎失稳,继而增生。肥厚,进而减少了椎管和椎间孔容积。
\n\n\n\n \n\n上述椎间盘退变及继发病理改变进展到一定程度,可影响脊髓、神经和椎动脉,产生相应症状。
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