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颈椎间盘退变疾病

Cervical Degenerative Disc Disease

作者信息

Margetis Konstantinos, Dowling Thomas J.

机构信息

Icahn School of Medicine at Mount Sinai

Long Island Spine Specialists

Abstract

Degenerative disc disease (DDD) of the cervical spine typically develops equally in the aging population regardless of patient sex. Patients most commonly present with pain; when isolated or in combination with other neurological symptoms, pain may necessitate surgical intervention. Treatment options range from nonoperative measures to surgical options, such as decompression, arthroplasty, and instrumented fusion. This section examines the anatomy, natural history, etiology, pathophysiology, evaluation, and treatment options for patients with cervical DDD. The cervical spine, spanning from C1 to C7, offers remarkable function and mobility. The upper cervical segments—C1 (the atlas, which articulates with the occiput) and C2 (the axis)—are uniquely structured to allow extensive motion, with primary rotation occurring at the C1–C2 joint and flexion-extension at the occiput–C1 joint. Surrounding or contained within these vertebrae are critical structures, including the spinal cord, nerve roots, major blood vessels, the trachea, and esophagus. The intervertebral disc (IVD) is located from the C2–C3 level down, aiding in cervical spine mobility and stabilization. In contrast to the thoracic and lumbar vertebrae, the cervical vertebrae have a unique bony prominence called the uncinate process, which articulates with the adjacent level to form the joint of Luschka or uncovertebral joint. This joint helps to reinforce the IVD and provides additional stability and motion. The IVD is an intricate structure composed mainly of 2 parts, the peripherally located annulus fibrosus and the centrally located nucleus pulposus, which are responsible for its load distribution function. The anterior and posterior longitudinal ligaments reinforce the IVD. The annulus fibrosus of the intervertebral discs is mostly of type I collagen in layers (lamellae), proteoglycans, glycoproteins, elastic fibers, and extracellular matrix (ECM) secreting cells. These collagen layers are uniquely positioned to form a strong shell for the inner contents, the nucleus pulposus. The nucleus pulposus has a gel-like consistency composed mainly of water, which decreases with age (90% at birth and 70% by the age of 60). The remaining minority of the nucleus pulposus contents comprises type II collagen and proteoglycans. Aggrecan is a critical proteoglycan in the nucleus pulposus, which, when bound to hyaluronic acid, helps retain water within the nucleus pulposus, allowing for load resistance. After the first year of life, the IVD becomes the largest avascular structure in the body. Most of the nutrition is delivered via metabolite diffusion from the vertebral endplates. Over time, the IVD loses its water content and proteoglycan supply, resulting in a more fibrotic consistency of the nucleus pulposus and subsequent fissuring as the vertebral endplates calcify with age. There are different types of nucleus pulposus herniations. If the nucleus pulposus herniates but remains contained by the annulus, it is called disc protrusion. However, the nucleus pulposus can also penetrate through injured annular fibers, and nucleus pulposus contents can extrude through a defect in the annulus, referred to as a disc extrusion. Furthermore, nucleus pulposus fragments can be separated from the extruded disc material, yielding disc sequestration. The degenerative process of the cervical spine is classified into 3 distinct stages: dysfunction, instability, and stabilization. Dysfunction occurs between the ages of 15 and 45. During this stage, radial and circumferential tears can occur in the annulus, accompanied by facet joint localized synovitis. Instability can occur in individuals between the ages of 35 and 70. This stage is characterized by inner disc disruption, progressive resorption, and degeneration of the facet joints. This condition leads to the final stage of the process, stabilization, which typically occurs after age 60. Here, hypertrophic bone develops around the facet joints as well as the disc, promoting a stiff and possibly ankylosed spine. Interestingly, each spine segment may be at a different stage of degeneration. One level could complete the dysfunction stage, while another could begin the stabilization phase. Disc herniations appear to occur due to the dysfunction and instability phase; spinal stenosis occurs due to the late instability stage and early stabilization stage due to the bony overgrowth and disc space narrowing. Consequently, patients may present with a combination of disc herniations and spinal stenosis affecting different levels of the cervical spine. The C5–6 segment is most commonly affected because of the cervical spine’s biomechanical stress and mobility patterns. When discussing the natural history of cervical DDD and treatment options, symptomatic individuals can experience an array of symptoms, from intermittent or constant pain, along with possible neurological symptoms, without pain. Patients generally receive nonoperative treatment when experiencing nonprogressive pain and/or minimal neurological issues. If surgery is indicated, it is typically elective and can be delayed to achieve symptomatic improvement. However, an exception is patients diagnosed with cervical myelopathy, who should have more urgent surgical treatment to avoid neurological deterioration. The proper diagnosis and treatment for spondylolytic cervical myelopathy can be extremely challenging, especially in patients with or even without ongoing axial neck pain with possible radiculopathy. One must also be aware that 20% of patients with cervical stenosis may also have lumbar stenosis. While many patients may have a straightforward diagnosis with a thorough history and physical examination accompanied by confirmatory imaging modalities, there is a significant subset of patients who have pain without experiencing neurological findings, aside from possible sensory changes, and whose imaging may not easily correlate with physical exam findings. In such cases, additional diagnostic modalities should complement a thorough history and physical examination to ensure an accurate diagnosis. Therefore, a systematic assessment is essential for effectively diagnosing and treating these patients.

摘要

颈椎间盘退变疾病在老年人群中通常无论患者性别均会发生。患者最常见的症状是疼痛。疼痛或伴有其他神经症状时,可能需要手术干预。治疗选择范围从非手术措施到减压、器械融合,或椎板成形术或器械辅助二者联合使用。本章将探讨其解剖结构、自然病程、病因、病理生理、评估及治疗选择。颈椎,即C1至C7,具有卓越的功能和活动范围。上颈椎,C1(寰椎,与枕骨相连)和C2(枢椎)高度特殊化,因其关节面方向可实现显著的活动范围(旋转、前屈、后伸和侧屈),其中旋转范围更大。颈椎相邻结构包括脊髓、神经根、血管以及气管和食管。椎间盘从C2 - C3水平开始向下分布,有助于颈椎的活动和稳定。与胸椎和腰椎不同,颈椎有一个独特的骨性突起,称为钩突,它与相邻节段形成钩椎关节或Luschka关节。该关节有助于加强椎间盘,并提供额外的稳定性和活动度。椎间盘是一个复杂的结构,主要由两部分组成,外周的纤维环(AF)和中央的髓核(NP),它们负责椎间盘的负荷分布功能。前纵韧带和后纵韧带加强了椎间盘。椎间盘的纤维环主要由分层的I型胶原蛋白、蛋白聚糖、糖蛋白、弹性纤维和分泌细胞外基质(ECM)细胞组成。这些胶原层独特地排列形成一个坚固的外壳,包裹内部的髓核。髓核具有类似凝胶的质地,主要由水组成,随着年龄增长而减少(出生时约90%,60岁时约70%)。髓核其余的少数成分由II型胶原蛋白和蛋白聚糖组成。髓核中的一种关键蛋白聚糖是聚集蛋白聚糖,它与透明质酸结合时,有助于将水保留在髓核内,从而具备抗负荷能力。出生后的头几年,椎间盘成为体内最大的无血管结构。大部分营养物质通过椎体终板的代谢物扩散来供应。随着时间推移,椎间盘不仅开始失去水分,其蛋白聚糖供应也会减少,导致髓核纤维化程度增加并随后出现裂隙。随着年龄增长,椎体终板会钙化。有不同类型的髓核突出。如果髓核突出但仍被纤维环包裹,称为椎间盘膨出。然而,髓核也可穿透受损的纤维环纤维,其内容物可通过纤维环的缺损挤出,称为椎间盘突出。此外,髓核碎片可与挤出的椎间盘物质分离,形成椎间盘游离。颈椎退变过程分为三个不同阶段:(1)功能障碍,(2)不稳定,(3)稳定。功能障碍发生在15至45岁之间。在此阶段,纤维环可出现放射状和环状撕裂,并伴有小关节局部滑膜炎。不稳定(阶段2)可发生在35至70岁的个体中。此阶段的特征是椎间盘内部破坏并逐渐吸收,以及小关节退变。这种情况导致该过程的最后阶段,即稳定阶段,最常发生在60岁以后。在此阶段,小关节周围以及椎间盘周围会出现骨质增生,导致脊柱僵硬甚至可能发生强直性脊柱炎。有趣的是,每个脊柱节段可能处于不同的退变阶段。一个节段可能处于功能障碍阶段,而另一个节段可能开始进入稳定阶段。椎间盘突出似乎是功能障碍和不稳定阶段的结果,而椎管狭窄则是晚期不稳定阶段和早期稳定阶段由于骨质过度生长和椎间隙变窄导致的结果。因此,可能会发现一位患者其颈椎节段在不同水平同时存在椎间盘突出和椎管狭窄。由于颈椎的生物力学原因,C5 - 6最常受累。在讨论颈椎间盘退变疾病的自然病程和治疗选择时,有症状的患者可能会经历一系列症状,从间歇性或持续性疼痛,以及可能伴有或不伴有疼痛的神经症状。当患者经历非进行性疼痛和/或轻微神经问题时,通常接受非手术治疗。如果需要手术,通常是择期手术,可以推迟手术,希望症状能有所改善。然而,一个例外是被诊断为脊髓型颈椎病的患者,他们应该接受更紧急的手术治疗以避免病情进展。对于脊髓型颈椎病的正确诊断和治疗极具挑战性,尤其是对于有或甚至没有持续性颈部轴向疼痛并可能伴有神经根病的患者。还必须注意的是,20%的颈椎管狭窄患者可能同时患有腰椎管狭窄。虽然许多患者通过详细的病史、体格检查以及确诊性影像学检查可能有明确的诊断,但有相当一部分患者有疼痛但没有神经学表现(除了可能的感觉变化),其影像学检查结果可能与体格检查结果不易相关联。正是在这种情况下,其他诊断方法应辅助详细的病史和体格检查以进行准确诊断。因此,进行系统评估对于正确和充分地诊断及治疗这些患者至关重要。

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