Thoracic Spinal Stenosis

Published on 11/04/2015 by admin

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Last modified 11/04/2015

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48 Thoracic Spinal Stenosis

Introduction

Stenosis of the thoracic spine is a relatively rare condition when compared to stenosis of the cervical or lumbar spine. Because it is unusual, a full understanding of the condition’s epidemiology and clinical presentation is limited, yet like stenosis in other spinal regions, its causes are numerous. These include ossification of the ligamentum flavum (OLF) (Figure 48-1) or posterior longitudinal ligament (OPLL) (Figures 48-2 and 48-3), herniation of intervertebral discs (Figures 48-4 and 48-5), and spondylosis. Other causes include neoplastic lesions, facet cysts, vascular malformations, and fracture. Stenosis of the thoracic spine typically presents with a variable combination of three main symptoms: back pain, radiculopathy, and myelopathy.

Much of what is known about thoracic stenosis has been derived from the experience of Japanese practitioners. OLF is cited as the most common cause of thoracic spinal stenosis. Although case reports of OLF with thoracic myelopathy in whites and North Americans have been published,12 patients of Asian descent are most frequently affected. Up to 20% of Asians older than 65 years of age have some degree of thoracic stenosis due to OLF.3 Aizawa et al, in a retrospective study of 265 Japanese patients, found OLF to account for more than half of all cases of thoracic myelopathy.4 Middle-aged men had the condition more frequently than women. It is not yet clear why this condition has a gender discrepancy and why it tends to occur in younger patients than those with cervical or lumbar stenosis.

Because OLF and OPLL are unusual among Westerners, much of the European and North American literature focuses on thoracic intervertebral disc disease as the primary etiology of thoracic spinal stenosis. As with OLF and OPLL, thoracic disc herniation is overall an unusual cause of thoracic back pain, radiculopathy, and myelopathy. Studies suggest than it affects males most frequently and tends to occur between the fourth and sixth decades.4

Pathology

A number of anatomical features make the thoracic spinal cord particularly vulnerable to injury. Unlike the cervical region, where the spinal cord takes up approximately 25% of the cross-sectional area of the canal, the thoracic cord constitutes 40% of the canal. Due to this anatomical difference, space-occupying lesions in the thoracic spine may cause more rapid and profound impingement and impairment of the cord. The thoracic kyphosis also creates a relative “bowstring” effect with the spinal cord draped across the posterior longitudinal ligament, the intervertebral discs, and the vertebral bodies. This positions the ventral cord in close apposition to compressive pathology of these structures.

The thoracic spinal cord has a more tenuous blood supply than the lumbar and cervical neurological segments. Ventral perfusion derives from the main feeding vessel, the artery of Adamkiewicz, which variably supplies the thoracic spinal cord. Intrinsic blood supply comes from the midline anterior spinal artery and two posterior vessels that are smaller than their counterparts in other regions of the spine. Intercostal arteries make up the extrinsic blood supply and are smaller and fewer in number than those in the cervical and lumbar spine. This vascular arrangement creates a relative watershed area between T4 and T9 that makes the region vulnerable to ischemic injury.

OLF occurs as a normal part of the aging process and rarely leads to stenosis. Histologically, the normal ligamentum flavum is composed of significant amounts of elastin that, with aging and degeneration, is progressively replaced by collagen, fragments of bone, cartilage, and fibrous tissue.5 Pathologic ossification is characterized by extreme progression of these processes leading to overgrowth and, ultimately, canal and foraminal stenosis. The precise mechanisms of pathologic OLF have not yet been clearly determined. It has been suggested that high mechanical stress of the thoracolumbar junction leads to degeneration of the facets and intervertebral discs, initiating progressive injury of the ligamentum flavum in this region.6 Ossification then proceeds in response to repetitive injury. This may explain why OLF occurs more frequently in the lower thoracic spine. Although plausible, this theory has been questioned because the cervical and lumbar spinal regions are more mobile than the thoracic spine, yet ossification in these locations is less common.7 It is also rare for OLF lesions to extend across multiple levels. Medical comorbidities such as diabetes mellitus, abnormalities in calcium metabolism, hypoparathyroidism, and Paget disease may play a significant role and have been associated with pathologic OLF.8,9 The higher incidence of OLF in the Japanese population clearly suggests a genetic etiology.

OLF associated with thoracic myelopathy most typically occurs in the lower thoracic spine.10 In their epidemiologic study, Aizawa et al found that T11-12 was the most common site of compression, followed by T10-11 and T9-10. When OPLL was the cause, T1-2 was affected most commonly, followed by T2-3 and T3-4.11

As with OLF and OPLL, isolated traumatic injury to thoracic intervertebral discs is rare. The splinting effect of the rib cage as well as the vertical orientation of the thoracic facets serves to reduce the forces on thoracic discs compared to those in the lumbar spine. This is thought to decrease the incidence of discal injury in the thoracic area. Degeneration of thoracic discs due to aging can occur as well, being most common in the fourth through the sixth decades of life, with males affected more frequently than females. Thoracic disc herniation tends to occur in the midline or just lateral to the midline, and predominates in the lower thoracic levels (Figures 48-6 and 48-7).12 Wood et al reviewed 90 MRI scans of asymptomatic patients and demonstrated that, often, thoracic disc herniations exist without symptoms.13 An additional study by Wood et al showed that these herniations do not frequently progress.14

Diagnosis

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