Treatment of Disk and Ligamentous Diseases of the Cervical Spine

Published on 14/03/2015 by admin

Last modified 14/03/2015

Print this page

This article have been viewed 1025 times

CHAPTER 278 Treatment of Disk and Ligamentous Diseases of the Cervical Spine

Vladimir Y. Dadashev, Gerald E. Rodts, Jr.

Cervical spondylosis is defined as a chronic degenerative process involving the cervical spine. Clinical syndromes such as radiculopathy and myelopathy often require surgical intervention. In this chapter the important anatomy and degenerative pathology seen in the cervical spine are reviewed. The more important concepts in clinical evaluation, diagnosis, and management are summarized.

Historical Background

Although the association of cervical spondylosis with radiculopathy and myelopathy is now well understood, it was not until the 19th century that a causative relationship between anatomic compression of neurological structures and the clinical development of neurological symptoms became apparent. It was Sir Victor Horsley who first presented the results of his surgical experience in treating seven patients with caries (tuberculosis) and trauma of the cervical spine at the Annual Meeting of the Surgery Section of the British Medical Association on August 25, 1895. Decompressive laminectomy resulted in significant improvement of the symptoms in the series of patients that he presented. After that report, the most commonly used surgical approach to the cervical spine was the posterior midline, and it was primarily used for nondegenerative pathologies. Semmes and Murphy in 1943 were the first to report the development of cervical radiculopathy from a unilateral ruptured disk. Subsequently, Frykholm, Spurling, and Scoville reported their surgical experience with posterior cervical hemilaminotomy and foraminotomy for cervical radiculopathy. Robinson and Smith and subsequently Cloward reported their results with the anterior approach to the treatment of cervical spondylosis and its causative pathologies. The concept of cervical spondylosis was shaped by our understanding of cervical pain, radiculopathy, and myelopathy.

Anatomy AND Pathophysiology

Pathophysiology of Spondylosis

Knowledge of normal cervical spine anatomy is critical for understanding the pathologic processes that affect it. Cervical spondylosis results from progressive biomechanical stress and strain and can be compounded by repetitive trauma. The process involves noninflammatory disk degeneration (amphiarthrodial joint without a synovial membrane) and is accompanied by facet joint osteoarthritis (zygapophyseal diarthrodial joint lined with a synovial membrane), as well as pathologic changes of the posterior longitudinal ligament and ligamentum flavum such as hypertrophy, laxity, ossification. A normal disk is composed of the nucleus pulposus, which is a water-rich gel (as a result of proteoglycan aggrecan molecules that attract and entrap water) in the center of the disk, and the annulus fibrosus, which is the fibrous outer portion of the disk. The annulus fibrosus is made of type I collagen and is organized into individual sheets called lamellae that are oriented at a 60-degree angle. The very outer lamellae, also called Sharpey’s fibers, are anchored directly into the bony matrix at the periphery of each vertebral body, just outside the cartilaginous vertebral end plate. Also of note, in a healthy cervical spine, the height of the vertebral body is slightly greater anteriorly. Such a vertebral body angle, in addition to the flexible disk, ensures the naturally lordotic sagittal curvature with the center of the axial loading plane within the middle column.

As part of normal aging, degenerative biochemical changes occur in hydrophilic proteoglycan molecules that result in loss of adsorbed water. This eventually leads to a decrease in viscoelasticity of the nucleus pulposus and a reduction in its overall volume and disk height. As a result, the stress under an axial load is translated to the annulus fibrosus and it bulges, with eventual wear and tear causing thinning and further fibrosis. The weakened lamellae allow the fibrotic nuclear material to dissect through the fibers and disrupt the attachment of Sharpey’s fibers to the edges of the vertebral body bone. Subsequently, this process stimulates reactive bony growth and is the origin of early osteophyte formation. In a more acute scenario, dissection of nuclear material through the weakened annulus causes disk herniation. The recent literature shows that the delamination process of the annulus during progressive cervical disk herniation occurs within the lamellae rather than between them, without evidence of any annulus rupture or failure.¹

Early reactive bone growth ultimately causes osteophyte spur and ridge formation, which leads to infolding and peeling of the posterior longitudinal ligament from the bone and secondary hypertrophy and ossification. In addition, the loss of disk space height causes initial straightening of the normally lordotic sagittal curvature of the cervical spine. As the center of axial loading shifts anteriorly, a cycle of further degeneration contributes to the chronic compressive vertebral body changes that eventually result in a kyphotic deformity.² These changes lead to abnormal cervical spine biomechanics and subsequently to hypertrophy or laxity of the facet joint and ligamentum flavum. The cervical spine hypermobility or instability is pathologically stabilized by osteophyte bar formation and uncovertebral joint degeneration. Multiple studies have demonstrated a significant decrease in mobility with advanced age.³ In a more recent study by Miyazaki and colleagues, magnetic resonance imaging (MRI) was performed on patients with degrees of spondylosis ranging from very mild to very severe.⁴ The early degenerative process affected the mobility of the functional spinal unit, which changed from a normal disk to a more unstable phase with increased mobility. As the degeneration entered later phases, the motion segment stabilized and became more ankylosed. The C4-5 and C5-6 segments were shown to contribute most of the total angular mobility, but their contribution to total angular mobility decreased significantly after severe degeneration. This degenerative cascade eventually leads to neuroforaminal or spinal canal stenosis, or both.

Pathophysiology of Pain

Patients can have clinically significant neurological symptoms or objective findings during any of the aforementioned stages. Symptoms can range from mild axial neck pain to severe cervical myelopathy. Even though the actual source of pain in cervical spondylosis is controversial, there is consensus that it originates from degeneration of the cervical disk or facet joint (or both).⁵ Multiple studies have demonstrated very rich innervation, both somatic and autonomic, of the cervical intervertebral disk and facet joint.

As the cervical nerve root exits the neuroforamina, it splits into ventral and dorsal rami, which are the source of somatic, proprioceptive, and nociceptive input. The small branches (somatic root) of the ventral ramus join the vertebral nerve (autonomic root) to form the sinuvertebral nerve. The vertebral nerves are formed by the gray rami communicantes, which are branches of the sympathetic trunk and the stellate ganglion. The sinuvertebral nerve arborizes superiorly and inferiorly as it enters the cervical canal through a neuroforamen and supplies the posterior aspect of the annulus (up to the posterior third), the posterior longitudinal ligament, and the dura. The anterior longitudinal ligament and anterior annulus are innervated by the sympathetic trunk and recurrent branches of the gray rami communicantes. It is reasonable to conclude that an annular tear can cause increased afferent output that can be the source of axial neck pain. Moreover, Bogduk and coworkers have proposed that intervertebral disks, especially when under significant stress, can be the source of pain even without obvious annular rupture or herniation.⁶ An internal annular rupture would suffice because it can cause enough inflammatory changes as it encroaches on the deep and rich innervation of the annulus fibrosus.

In addition to the cervical disk being a source of axial neck pain, the cervical facet joint can also be an important source. The dorsal rami of the cervical nerve roots supply most of the innervation to the facet joints, which are rich in mechanoreceptors and nociceptive nerve endings. Studies by Dwyer and associates have confirmed that stimulation of the facet joint produces a clinically distinguishable, characteristic pattern of pain that enables the construction of pain charts.⁷ Practitioners can use these charts to isolate the symptomatic joint in patients with cervical zygapophyseal pain. Some authors believe that facet joint pain could be of primary importance, especially in neck pain associated with whiplash injury.⁸

Pathophysiology of Radiculopathy

The pathologic changes in patients with cervical radiculopathy can be divided into acute and chronic. Acute radiculopathy is usually secondary to soft disk herniation and occurs in a younger patient group. The inflammatory process, which involves a cytokine-mediated response, leads to a decrease in the number of large-diameter myelinated axons. This finding can be seen within the first week ⁹ and results in relatively more prominent motor findings. Chronic radiculopathy, in contrast, usually causes predominantly sensory complaints and is more commonly seen in an older patient group. Chronic radiculopathy is associated with cervical spondylosis. Jancalek and Dubovy showed that changes include thickening of the dura mater and arachnoid membrane around the affected nerve root with associated alteration of the blood-nerve barrier, which eventually leads to nerve root dysfunction as a result of chronic compression.¹⁰

Pathophysiology of Myelopathy

Multiple pathologic processes that eventually lead to similar pathologic cervical cord changes in the white and gray matter can cause cervical myelopathy. Even acute cervical cord injury (despite representing a different mechanism and manifestation) has been shown to result in similar pathologic cord findings as those of indolent cervical spondylosis.¹¹

The pathogenesis of myelopathy in patients with cervical spondylosis should be subdivided into three main components that are responsible for the final cord changes.¹² The first consists of static factors, which are processes that lead to cervical canal stenosis and cord compression. The second consists of dynamic factors caused by repetitive movement of the compressed cord, which is associated with decreased elasticity and susceptibility to stretch-associated injury. The third component is the final cord changes that are seen histopathologically and include vascular rearrangement, arterial- or venous-induced ischemia and infarction (or both), oligodendrocyte apoptosis, and other cytotoxic cell changes.

The static factors that contribute to decreased canal diameter include acquired spondylosis of the disk, facet, vertebral bodies, and ligaments and subsequent loss of the lordotic curvature. In addition, other less common conditions can contribute, such as congenital cervical stenosis, ossification of the posterior longitudinal ligament, and ossification of the ligamentum flavum. Patients with congenital cervical stenosis are initially asymptomatic but eventually progress to severe cord compression and usually become symptomatic by the third decade. The normal sagittal cervical canal diameter has been identified as being approximately 17 to 18 mm. Based on multiple studies, the canal is considered stenotic when smaller than 13 mm,¹³ which is associated with a high risk for the development of cord compression with myelopathic changes.

The dynamic factors resulting in cervical cord injury are multifactorial. First, the movements of a severely compressed cord are restricted. Second, flexion of the spine results in overstretching of the cord. This effect is more severe in the setting of a prominent ventral osteophyte complex or with a kyphotic deformity. Conversely, extension causes posterior cord compression by buckling of the ligamentum flavum and shingling of the laminae. Some studies, including MRI, show both flexion- and extension-induced compression, with extension-associated injury causing more severe compression. Panjabi and White ^13a showed that axial rotation and lateral bending do not cause as significant cord indentations as do sagittal movements. As mentioned earlier, the spondylotic spine can become unstable and result in repetitive cord injury during flexion-extension movements. Furthermore, the spinal cord’s ability to tolerate stretch decreases with age, and thus older adults become extremely susceptible to stretch injury.¹⁴ In animal studies, Shi and Pryor confirmed three types of conduction block resulting from and correlating with the extent of stretch injury in the absence of pathologic variables related to vascular damage¹⁵: an immediate, spontaneously reversible component that may result from a transient increase in membrane permeability that affects ionic distribution; a second component that may be due to perturbation of the myelin sheath and was reversible with the use of a potassium channel blocker; and a third component that was irreversible and resulted from profound axolemmal disruption.

Finally, the last well-described pathogenesis of myelopathy is cord ischemia. Spondylotic cord compression causes the pathologic butterfly pattern of cord ischemia that affects the gray and medial white matter. This pattern is also consistent with a vascular hypoperfusion injury. The compression probably affects flow in the small pial and intramedullary arterioles, as well as the larger anterior spinal artery. Venous congestion may also play a role and lead to venous infarction. All these processes can result in cord cavitation and delayed syringomyelia and are probably similar to traumatic syrinx formation. In further support of this ischemic theory, oligodendrocytes have been shown to undergo apoptosis, similar to the pathologic changes in traumatic cord injury.