CHAPTER SYNOPSIS:
Spinal stenosis in the thoracic region is a rare condition. Causes for the condition are varied and include generalized skeletal disorders and localized spinal conditions. The diagnosis of thoracic stenosis with associated myelopathy can be difficult to make secondary to the variety of presenting complaints. Diagnosis is made easier with imaging modalities, and surgical treatment options are varied and cause specific. Surgical treatment options for thoracic stenosis as a result of an ossified posterior longitudinal ligament have been widely published, and recent long-term studies have discussed optimal surgical treatment for herniated thoracic discs.
IMPORTANT POINTS:
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Early recognition of thoracic stenosis as a cause of neurologic compromise is a difficult endeavor.
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Neurogenic claudication is an important and recognizable feature of thoracic stenosis.
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Appropriate radiologic studies, including magnetic resonance imaging and computed tomography after myelography, are essential to confirm the diagnosis.
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In the majority of cases, thoracic stenosis is caused by a combination of acquired and developmental origins.
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Operative approach is based on the location of the primary compressive pathologic abnormality in the spinal canal, the total number of stenosed levels, the need for decompression of the lumbar spine, and the overall health of the patient.
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Long-term follow-up of this patient population is critical, and cases of late deterioration after surgical treatment have been reported.
CLINICAL/SURGICAL PEARLS AND PITFALLS:
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Conservative treatment of thoracic stenosis rarely is effective, and in most situations, surgical intervention is performed as early as possible because of the severity of the presenting symptoms.
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Thoracic levels included in surgical decompression are selected based on radiologic evidence of neural element compression that correlates with the clinical symptoms and signs.
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Primary indications for surgery are complete paraplegia, paraparesis, monoparesis, signs of thoracic myelopathy and gait disturbance, hypalgesia of the perineum with sexual dysfunction, and neurogenic claudication with thoracic radiculopathy.
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When a primary compressive pathologic abnormality is present in the posterior spine, a decompressive laminectomy with partial medial facetectomy at all affected levels is performed. When an anterior pathologic abnormality is present, an anterior decompression is performed with resection of the posterior cortex of adjacent vertebral bodies.
VIDEO AVAILABLE:
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Stenosis of the vertebral canal can occur at any level, with resultant compression of the neural elements. Spinal canal stenosis and associated myelopathic symptoms secondary to compression of the spinal canal are known and widely published entities in the cervical and lumbar spine. Upper extremity radiculopathy is a sequela of cervical stenosis, and neurogenic claudication and lower extremity radiculopathy frequently occur as a result of lumbar stenosis.
Stenosis of the thoracic spine is a less encountered entity. Isolated cases of thoracic stenosis have been described in association with skeletal disorders such as achondroplasia, osteochondrodystrophy, Paget disease, diffuse idiopathic skeletal hyperostosis, and renal osteodystrophy. Thoracic stenosis also has been reported in cases of localized spinal conditions such as thoracic spondylosis, ossification of the ligamentum flavum (OLF), and ossification of the posterior longitudinal ligament (OPLL). Pathologic conditions such as herniated thoracic discs and tumor can cause local compression in the thoracic spine and lead to myelopathic symptoms. Stenosis usually is localized to the lower third of the lumbar spine, and neural element compromise almost always is the result of a pathologic abnormality involving both the anterior and posterior neural elements. Figures 12-1 and 12-2 show the images of a woman with metastatic breast cancer to T7 who had signs and symptoms consistent with thoracic myelopathy at presentation.
Thoracic disc herniation accounts for approximately 0.25% to 0.75% of all herniated discs. It affects male and female individuals equally, and occurs more commonly during the third, fourth, and fifth decades of life. A history of trauma is present in 33% to 50% of patients, although the role of trauma in the pathogenesis of the herniation is not well defined. OLF and OPLL frequently are observed in Japan but rarely are reported outside that country. OLF has been reported to occur in up to 20% of Japanese patients who are older than 65 years. Conversely, the frequency rate of OPLL of the thoracic spine is low, 0.8%. Age at presentation ranges from the third to eighth decades of life, and a male predominance has been noted in the patient population. Thoracic OLF most commonly occurs in the lower thoracic spine. The cause of OLF is unknown, and it is thought that the ossification originates from the ligamentum itself. Ossified lesions are composed of lamellar bone with developed Haversian canals. Repeated stress at the thoracolumbar junction has been hypothesized to be the cause of OLF.
The diagnosis of thoracic stenosis can be difficult to make secondary to the variety of patterns of presentation. Palumbo et al. performed a retrospective review of 12 patients treated for thoracic spinal stenosis. Presenting symptoms in that patient population were variable. Pain was present in all 12 patients, and other complaints included muscle weakness, paresthesias in the lower limb and perineum, neurogenic claudication, urinary incontinence, impaired sexual function, and gait disturbance. The caudal end of the thoracic spinal canal contains both the lumbosacral cord enlargement and portions of the lower thoracic through the first sacral nerve roots. Consequently, compression in that area of the canal can involve both the conus medullaris and the caudal nerve roots, and can thus produce mixed upper and lower nerve root lesions. Another proposed cause of the intermittent claudication observed in association with thoracic stenosis is direct neural element compression, transient circulatory impairment, or both.
Essential to correctly diagnosing thoracic stenosis are appropriate radiologic studies. In the past, myelography with oil-soluble contrast medium was used for thoracic visualization. However, that technique was severely limited by the amount of contrast medium needed to achieve visualization. Since 1980, the use of water-soluble contrast media and enhanced axial view computed tomography (CT) has facilitated improved visualization of the thoracic spine. Enhanced CT helps to delineate frequent midline and small defects in the thoracic spine and extradural compression. Therefore, CT performed after myelography has been hailed as the most accurate method of defining compressive pathologic abnormality. Magnetic resonance imaging, in contrast, has been identified as the most effective method of screening for thoracic cord compression. Based on radiographic evaluation of 12 patients, Palumbo et al. found that in the majority of cases, canal compromise resulted from a combination of developmental and acquired stenosis. More specifically, localized spondylosis occurred in association with either developmental canal narrowing or a generalized skeletal disorder. Figure 12-3 shows CT findings typical of canal stenosis. In this case, the stenosis was the result of a fracture-dislocation at T6-7 that resulted from a motor vehicle collision.