Dr. Kevin Yip

Dr Kevin Yip
Orthopaedic Surgeon
MBBS(UK), FRCS(EDIN), FAM(SING), FHKCOS(ORTHO)

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Anatomy and Biomechanics

A good background in the anatomy and clinical biomechanics of the thoracolumbar spine will provide the basis for understanding the mechanisms of injury and the principles of management. The majority of thoracolumbar spine injuries arising from low-velocity sports usually are less catastrophic than some of the athletic injuries involving the more vulnerable cervical spine.

The thoracic spinal cord is protected by the relatively larger and less mobile thoracic vertebra and rib cage. The spinal cord has outer white matter, which contains the myelinated nerve fibers that form the ascending sensory and descending motor tracts. The gray matter within the spinal cord contains the cell bodies of the nerve roots and is vulnerable to irreversible damage if compressed.

The cord ends with the conus medullaris at the level of the L1 vertebra. The spinal nerves, which arise from the cord, usually can re-innervate after a compression injury similar to a peripheral nerve after a compression injury. The cauda equina is a collection of spinal nerves below the level of the conus. The cord and spinal nerve roots are suspended in cerebrospinal fluid contained within the dura mater.

The human body has 12 thoracic and 5 lumbar vertebrae, which consist of the vertebral bodies that support the trunk and the neural arch that protects the neural elements. Transverse and spinous processes act as lever arms to attach the stabilizing muscles and ligaments. The thoracic vertebrae provide attachment of the supporting rib cage at the costovertebral and costotransverse junctions.

This buttressing by the “nonfloating” ribs on the neural arch may protect the posterior half of the thoracic vertebral body from axial loading, thus explaining the relatively small incidence of burst fractures in the T1 to T10 levels.

The vertebrae articulate with each other by means of a fibrocartilagenous intervertebral disc, two facets joints, and numerous intervertebral ligaments. The avascular disc has an outer, fibrous annulus and an inner, gelatinous nucleus pulposus. The end plates are hyaline cartilage that distributes the pressure of axial loading and allows the diffusion of nutrients into the discs from the adjacent subchondral bone.

The disc annulus has innervation only to the outermost layer. This explains the asymptomatic, degenerative tears of the inner annulus layers and the severe pain and reflex spasms that occur with outer annular tears and disc herniations, even when the nerve roots are not being compressed.

The facets are synovial joints on the posterior neural arch that are oriented along the coronal plain in the thoracic spine and the more sagittal orientation in the lumbar spine. This orientation of the thoracic spine facets is more suitable for flexion and rotation, whereas the lumbar facets may allow relatively more flexion and extension as well as lateral bending.

The area of bone that connects the lamina to the pedicles and is between the superior and inferior facets is called, appropriately, the pars interarticularis. This portion of the bony neural arch forms the roof of the neural foramina for the exiting nerve roots.

A defect in the pars is known as a spondylolysis. This pseudoarthrosis may become painful when compressed between the inferior facet of the cephalad vertebra and the superior facet of the vertebra caudal to the pars involved. The soft tissue of the defect may be a fibrous or a pseudosynovial junction, which may enlarge and compress the exiting nerve root beneath it.

Spondylolisthesis is the forward translation of one vertebral body over another. In athletes, it usually is related to a spondylolysis, because the supporting posterior facets have lost the osseous continuity with the vertebral body. In the older population, degeneration of the facets may lead to an unstable forward translation despite having an intact pars interarticularis. This condition is known as a degenerative spondylolisthesis.

The intervertebral ligaments and thoracolumbar musculature receive the least clinical attention but are the most responsible for providing dynamic stability. These well-innervated soft tissues also are the structures involved in the majority of symptomatic spinal injuries, which can be classified as minor strains or sprains.

The anterior longitudinal ligament resists hyperextension, whereas the intraspinous,supraspinous, and facet capsular ligaments resist hyperflexion forces. The ligamentum flavum, which connects the adjacent lamina, is unique in that it contains elastin fibers that allow a tension spring action instead of the fixed-length rope restraints of other ligaments containing predominately collagen fibers .

The musculature of the thoracolumbar spine can be divided into three groups: superficial, intermediate, and deep. The superficial group consists of the trapezius, latissimus dorsi, the levator scapulae, and the rhomboids, and it helps to stabilize the shoulder girdles. The intermediate muscles of the back consist of the serratus posterior, both superior and inferior, that assist in respiration.

The deep muscles of the spine are known as the intrinsic muscle; these include the erector spinae and transversospinalis group of muscles. The intrinsic muscles stabilize the local vertebrae for movements such as extension, rotation, and lateral bending of the spine.

The abdominal muscles of the thoracolumbar spine can be divided into the anterior and posterior groups. The abdominal muscles along with the diaphragm help to stabilize the mobile lumbar vertebra. The rectus abdominis, external oblique, internal oblique, and transversus abdominis muscles form the anterior lateral group. The posterior group includes the psoas, iliacus, and quadratus lumborum muscles.

White and Panjabi have defined clinical instability as “the loss of ability of the spine under physiological loads to maintain relationships between vertebra in such a way that there is either damage or subsequent irritation to the spinal cord or nerve roots.

In addition there is development of incapacitating deformity or pain due to structural changes.” Clinical instability may result from trauma, degeneration, surgery, or pathologic disease, such as neoplastic or infectious conditions. White and Panjabi also have developed a checklist for thoracic and thoracolumbar instability.

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