Pathophysiology of Thoracic Spondylosis, Radiculopathy, and Myelopathy


Summary of Key Points

  • The thoracic spine has unique biomechanical and physiological features, creating a relatively rigid transition zone flanked by more mobile cervical and lumbar regions.

  • The thoracic spinal cord is less prone to dynamic compression than the cervical spinal cord, but is also less tolerant to compression and vascular ischemia.

  • Its limited dorsal mobility makes the thoracic spinal cord vulnerable to ventral compressive pathology, despite adequate space dorsally.

  • Spinal cord compression can be attributed to a variety of ventral or dorsal degenerative pathologies.

  • Imaging techniques used to assess thoracic myelopathy vary based on etiology and the presence of regional instrumentation.

  • Prognosis is generally favorable for most causes of thoracic myelopathy.

  • Surgical approaches vary depending on whether thoracic spondylosis involves myelopathy, radiculopathy, or just back pain.

Although degenerative changes in the thoracic spine are somewhat ubiquitous among adult patients, particularly in the middle-aged and elderly, specific patterns of degeneration may lead to clinically relevant pathology. Clinically relevant pathology is present with either the spinal cord or nerve root compression, malalignment or progressive deformity, or unacceptable pain because of an unmitigated pain generator. In this chapter, we will explore the expected degenerative changes that occur in the thoracic spine and highlight common clinical conditions that stem from the degenerative, spondylotic changes.

Thoracic spondylosis results from a degenerative cascade that affects the bony elements of the spine and the soft tissue structures, including the ligamentum flavum, intervertebral disc, facet capsules, and spinal ligaments. The thoracic spine is unique in regards to its anatomical location and constraints. The thoracic spine is supported by, and its motion is limited by, the rib cage, and has the most significant amount of motion in the axial plane. Although symptomatic degenerative pathology in the thoracic spine is much less frequently diagnosed, it may result in severe symptoms and progressive neurological deficits.

Spondylosis of the thoracic disc presents with an atypical and infrequent characteristic clinical presentation that makes diagnosis challenging. The pathological structures should be carefully evaluated by the clinician, and are crucial to identifying the source of disease. Commonly, management and surgical treatment will involve addressing the disc herniation, facet degeneration, or disorders of ligament ossification. This chapter aims to outline and review the pathophysiology of the thoracic spine and its unique characteristics and traits, along with its most commonly seen pathological processes.

Anatomic Consideration of the Thoracic Spine

An introduction to the anatomical structures involved in thoracic spondylosis and related conditions is presented in this chapter.

The thoracic spine supports the associated rib cage and thorax, protects vital organs, and plays a critical role in the pulmonary and cardiovascular systems. The 12 thoracic vertebrae maintain a slightly kyphotic alignment within the spinal column. The first seven vertebrae bear true ribs, with their origin at the costovertebral and costotransverse joints of the vertebrae and insertion, along with the sternomanubrial complex. The 8th, 9th, and 10th thoracic vertebra bear false ribs, which are differentiated by their insertion onto shared costal cartilage of the anterior rib cage. The 11th and 12th vertebrae bear floating ribs. Each thoracic segment consists of a loadbearing vertebral body with intervening intervertebral discs above and below. Ventrally, along the anterior boundary of the vertebral body, runs the continuous anterior longitudinal ligament (ALL), and posteriorly the less robust posterior longitudinal ligament (PLL). Whereas the ALL limits spinal extension, the PLL limits flexion, and pathological changes in these regions can restrict motion in the thoracic spine. A posterior vertebral arch surrounds the spinal canal in the thoracic spine, with prominent transverse processes and spinous processes. Thoracic pathology is observed less frequently than pathology in other regions; indeed, Kalichman et al. noted that, among 250,000 to 500,000 individuals in the United States with symptomatic spinal stenosis, less than 1% of these cases occurred in the thoracic spine.

The normal alignment of the thoracic spine is in kyphosis, with its magnitude proportional to the pelvic incidence and lumbar lordosis. In addition to the intrinsic stability contributed by the facet joints, the intervertebral disc, and the intrinsic spinal ligaments, the thoracic spine is stabilized by its articulation with the bony and ligamentous structures of the rib cage, with muscular support from the erector spinae and abdominal musculature maintaining sagittal balance. The intervertebral discs are thin, and the vertebral motion segment center of rotation in the sagittal plane lies within the posterior third of the disc space. These discs support the majority of the spinal column’s weight, with the annulus fibrosus as a primary stabilizer in all planes. Prominent and long spinous processes provide a long lever arm upon which the intrinsic segmentally innervated multifidus muscles apply stabilizing forces.

Superior and inferior articular processes form the synovial facet joint and are morphologically shorter and less rigid than other joints. The coronal orientation of these facets facilitates rotation and truncal lateral flexion. Forward flexion and extension are limited compared with the lumbar spine, where the facets are more sagittally directed. The coronally oriented thoracic facets provide stability, as a greater force is necessary to destabilize the thoracic spine compared with sagittally oriented lumbar facet joints. The vertebral canal is narrowest in the thoracic region, with studies indicating that it is smallest at the T4 or T5 level.

The thoracic spine’s alignment is kyphotic and is often measured from T3 or T4 to T11 or T12, because of the difficulty of obtaining radiographs of the vertebral bodies above T3. Normal thoracic kyphosis may range from 20 degrees to greater than 50 degrees in asymptomatic adult patients. Expected values for thoracic kyphosis are proportional to lumbar lordosis. A minimal lumbar lordosis translates to a decreased lower thoracic curve, whereas an increased lumbar lordosis corresponds with a decreased pelvic incidence. As aging leads to a loss of disc height, the severity of kyphosis increases in most patients. In some patients, symptomatic or subclinical compression fractures and loss of extensor muscle strength also contribute to increased kyphosis.

The geriatric population (patients >65 years old) tends to display greater thoracic kyphosis, with increased segmental kyphosis occurring in the lower thoracic spine. Osteoarthritis of the aging thoracic spine on lateral radiographs will present with anterior and lateral lipping and osteophyte formation with narrowing disc spaces and wedging of midthoracic vertebrae.

Degenerative changes of the thoracic discs with aging are poorly understood beyond longitudinal studies examining radiographic changes over time. The vascularity of the thoracic spinal cord contributes to this pathophysiology, as blood supply in this region is more variable and tenuous than in the cervical or lumbar region. The intrinsic blood supply of the thoracic cord is derived from one anterior and two posterior longitudinal arterial trunks, with the midline anterior trunk giving off central penetrating arterial branches. Compression of radicular feeders, venous engorgement, or elongation of the laterally oriented terminal branches can lead to decreased perfusion. Okada et al. followed 103 men over 10 years and noted progressive thoracic disc degeneration among 63%, with smoking and cervical spine degeneration being significantly associated. The disc height is relatively smaller in the thoracic spine compared with the lumbar spine, but the annulus fibrosus posteriorly is thicker and more durable.

The intervertebral discs play a significant role in the biomechanical and motion properties of the thoracic spine. Thoracic disc height is generally less than that of discs in the lumbar and cervical spine, but the annulus fibrosus is stronger posteriorly. Because the thoracic discs are relatively thin, herniations are rare and often too small to cause symptoms, occurring more commonly in the lower thoracic segments. Thoracic disc herniations can be subdivided by location: central, centrolateral, or lateral in the axial plane, which has clinical relevance in terms of the associated neurological findings, ranging from bilateral myelopathy to unilateral radiculopathy. The majority of thoracic disc herniations are central or centrolateral. Herniations can be soft or calcified, with approximately 30% to 70% of herniations showing some calcification on computed tomography (CT) scan. Denticulate ligaments run longitudinally between the spinal cord and nerve roots and limit posterior displacement of the cord, particularly in the upper and middle portions of the thoracic cord, where they are more robust. The denticulate ligaments may reduce the spinal cord’s ability to float away from a ventral compressive lesion such as a disc herniation, resulting in worse spinal cord deformation and neurological impairment even in the presence adequate space for cerebrospinal fluid (CSF) dorsally. Magnetic resonance imaging (MRI) is highly sensitive in identifying these herniations; however, MRI findings may not correlate to neurological status or symptoms. A CT scan can be used to evaluate the degree of disc calcification and to guide surgical management. Dietze and Fessler recommended CT myelography as a modality to accurately characterize thoracic disc herniations. CT myelography may help identify extradural thecal sac defects adjacent to the disc herniation and soft tissue density mixed with calcification, indicating vertebral end plate osteophytes.

The kyphotic alignment of the thoracic spine causes the spinal cord to lie directly on the posterior longitudinal ligament (PLL) and the posterior aspects of the vertebral bodies and discs. Goh et al. found that increased compression places force on the anterior aspect of the thoracic disc, and that, as such, upper areas are more likely affected by bony changes such as osteophytes. In contrast, degenerative disc changes mainly occur in the lower thoracic spine. Thoracic disc herniation, ossification of the posterior longitudinal ligament (OPLL), tumor, or any other mass may cause significant ventral compression of the cord. Combined with local tethering and limited dorsal migration, this creates stretch and shear, leading to ischemia and irreversible spinal cord injury.

Specific Pathologies

Ossification of the Ligamentum Flavum

The ligamentum flavum is one of the most elastic tissues in the human body, with a tensile failure load of up to 300 N in the lower thoracic spine. It connects two adjacent laminae at the posterior aspect of the spinal canal, extends laterally to the anterior portion of the facet joint, and is separated from the dura by epidural fat. Ossification of the ligamentum flavum (OLF) is an ossified mass in the ligamentum flavum between two adjacent laminae. There is a capsular portion and an interlaminar portion that should be identified. OLF is frequently associated with OPLL. Intrinsic causes include genetic predisposition and dietary factors, and extrinsic causes such as mechanical factors have been postulated. No definite etiology has been confirmed. Repetitive mechanical stress resulting in maximum tensile force in at-risk individuals has been suggested as a contributing factor, and this theory is supported by the fact that OLF most commonly occurs at T10‒T12. Degenerative factors have also been suggested, as aging may play a role. Ossification typically begins from the capsular portion and progresses to the interlaminar portion. Increasing calcification leads to canal stenosis dorsally and dorsolaterally from the associated facet capsule, with ossification resulting in mechanical injury and vascular ischemia to the spinal cord. Patients may present with pain, myelopathy, or both. Conservative treatment is usually unsuccessful, and surgical decompression is performed for myelopathy.

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