The exact mechanism of neurologic dysfunction in thoracic disk disease remains unclear. However, most believe that mechanical compression is a key factor. Stenosis, whether central or lateral, is a radiographic/pathoanatomic finding. In thoracic stenosis, the herniation is more often central than lateral. The imaging studies of choice to diagnose thoracic stenosis are magnetic resonance imaging (MRI) or computed tomography (CT). Both will show a narrowing of the spinal canal, exiting nerve root, or both. Etiology is uncertain because patients with these radiographic findings do not necessarily exhibit symptoms; therefore, additional mechanisms must also play a role. For example, neural vascular insufficiency has been thought of as a contributing etiology of stenosis, but presently available imaging techniques cannot detect this. The area between T4 and T9 has an especially tenuous blood supply and is vulnerable to injury. Moreover, the space available for the cord in the thoracic spinal canal is smaller compared to the cervical and lumbar regions, making any compression potentially more significant than other areas of the spine. Myelopathy and radiculopathy remain a clinical diagnosis and imaging studies showing neural compression are insufficient for making a diagnosis. The multifactorial nature of the etiology remains to be elucidated.

By default, detecting and addressing the areas of neural compression remains the mainstay of treatment in thoracic disk disease. Wide decompression with removal of osteophytes, hypertrophied ligamentum, and overgrown facets are important. Thoracic disk herniations can compress the spinal cord as well as exiting nerve roots in the foramina. Recognition of the location of compression is critical to effectively and appropriately treating the herniation.

Compression of the T2–T12 thoracic nerve roots usually does not cause any clinically apparent deficits as the motor innervation is to the intercostal muscles. Bandlike radicular pain wrapping around the chest is a more common complaint. When herniations are in the midthoracic spine, patients can mistake this pain for abdominal pain or even a heart attack. In animal studies, compression of a nerve root alone may cause anesthesia but it is not enough to cause pain (dysesthesia). Exposure to chemical factors, such as irritants from a damaged disk might potentiate nerve root irritation. This “irascible” nerve root is more susceptible to symptomatic nerve compression. As such, oftentimes removal of even small
disk herniations with little evidence of compression may relieve pain symptoms. Myelopathy by itself is usually not painful, but often patients present with either axial mechanical pain or radicular pain symptoms.

The spinal canal can be compressed not only by disk herniations, but also by many other structures. Hypertrophy and buckling of ligamentum flava may encroach on the posterior spinal canal. Facet hypertrophy and osteophyte formation can also cause both spinal canal and nerve root compression. Facet synovial cysts often form in degenerative spines and may be the culprit of stenosis. More rare cases such as ossification of the posterior longitudinal ligament (OPLL) and Scheuermann’s disease have also been reported to causes.

Thoracic disk herniations can be classified based on location, consistency, or level. Most authors describe the location as central, paracentral, foraminal, or far
lateral. Approximately 80% of herniations are central or paracentral. Central herniations are most likely to cause spinal cord compression and myelopathy, and least likely to cause radicular pain. Paracentral herniations lie off the midline of the disk and can cause spinal cord compression, nerve root compression, or oftentimes both. Foraminal and far lateral herniations cause isolated nerve root compression (Fig. 17.3). Location of the herniation oftentimes dictates the surgical procedure and approach needed for surgical treatment.

Herniated disks can also be classified by the presence of calcifications: hard versus soft disks. Calcified disks are more likely to be symptomatic than noncalcified disks. They are also often associated with adhesions between the disk and the dura, making discectomy much more difficult and increase the risk of complications. Intradural herniations have also been reported, which often present with significant neurologic deficit. CT myelography is the study of choice rather than MRI if this is suspected.

The level of herniation is another important way to classify herniations. Upper thoracic herniations are rare, whereas herniations around the thoracolumbar junction (T11–T12, T12–L1) are more common. In fact 75% of herniations occur between T8 and L1. With the most common level being T11–T12. It is thought that the transition between the mobile lumbar spine and the stiffer thoracic spine leads to accelerated degeneration at those levels and makes the disk prone to herniation. The change in orientation of the facets may also play a role with T11–T12 joint being more coronally oriented with less resistance to torsional force than the sagittal- oriented T12–L1 facet joints. Importantly, compression at the conus level (T11–L1) may lead to bowel and bladder deficits, with little other symptoms.

Stenosis denotes a narrowing of the spinal canal that is not related to a soft disk herniation. Stenosis can be either central or foraminal narrowing, and can be developmental or acquired. Developmental stenosis is usually idiopathic and represents a congenital narrowing of the spinal canal from short pedicles. This narrowing predisposes patients to neurologic dysfunction from even minor insults. This predisposition alone is not enough to cause symptoms. Congenital stenosis can also be seen in genetic conditions such as achondroplasia. Acquired stenosis is often related to the end stages of the degenerative process in the spine with osteophytes and facet/ligamentum hypertrophy as the culprits.

OPLL or ossification of the yellow ligament (OYL) can also cause acquired stenosis. This is more common in the Asian population and adhesions between the ossified ligament and dura is common. Surgical excision can be very demanding in these patients and fraught with complications such as dural tear and paralysis.

Degeneration of the thoracic spine without neural involvement is common and usually asymptomatic. There are no formal classification systems to organize thoracic spondylosis. With the thoracic ribs serving as additional stabilizers, instability or spondylolithesis is very uncommon in the thoracic spine without a history of trauma.

The clinical presentation of thoracic disk disease is variable, and dependent on the location and size of the eliciting lesion. The most common initial symptoms are the following:

Initial symptoms should be distinguished from complaints at presentation, which can be more severe and include bladder symptoms in 30% of patients and motor or sensory symptoms in 61% (Table 17.1).

Pain can be axial or radicular. Radicular pain usually presents as a bandlike pain wrapping around the chest or abdomen of the patient. The level of the complaint may correlate with a dermatomal pattern of the nerve being affected, although most patients exhibit T10 findings regardless of the level of disease. Most patients report exacerbation of pain by coughing and sneezing. Radicular complaints down the arms or legs are uncommon.

Pain from thoracic disk diseases can also be referred to other areas of the body. Herniations in the midthoracic spine may be referred to the chest and abdomen,
mimicking coronary artery disease or gastrointestinal pain. Herniations in the lower thoracic spine may radiate to the groin and flank, and can be confused with inguinal hernias and renal calculi.