3.2 Degenerative disease of the thoracic spine

Degenerative changes of the thoracic spine are common, and are probably universal by the age of 50. In most cases these are asymptomatic beyond some loss of physical height and an increase in thoracic kyphosis. Two main clinical entities exist: thoracic disc herniation and thoracic spinal stenosis.

This was first described in association with paraplegia. In practice, many thoracic herniations are asymptomatic. The difficulty is to find those that are clinically significant. This is made more difficult by the wide range of presenting symptoms.

As diagnostic imaging has progressed, surgical treatment for patients with severe persistent symptoms has also improved. Using a conventional laminectomy, it is difficult to obtain adequate disc removal without manipulation of the spinal cord. Over a third of patients were left with persistent symptoms or worsened neurological deficits when laminectomy alone was used. Since the 1980s, new techniques such as anterior (transthoracic) and lateral extracavitary decompression and expanded posterior approaches such as costotransversectomy or transpedicular resections have improved results and reduced complications. Advances in thoracoscopic techniques have led to reports of video-assisted minimally invasive approaches to the anterior thoracic spine.

The annual incidence of symptomatic thoracic herniations has been estimated at one per million of the population (much less frequent than in the cervical or lumbar regions). A prevalence of 15–37% has been documented by both autopsy and imaging. Surgically treated thoracic herniations comprise only 0.15–4% of all disc surgeries.

Ninety-five per cent of thoracic disc herniations occur at or below the T6–T7 vertebral level. The remainder occur at any level. They mainly occur in the fourth and fifth decades in both sexes and require special care.

About 50% of cases are said to be traumatic. Recent research suggests that lumbar disc herniations are mainly of genetic origin, but no such research has been done on thoracic discs. Intradisc calcification is seen in up to 50% of patients. Scheuermann’s kyphosis has been noted as an associated diagnosis. Neurological deficits secondary to these lesions are probably due to a combination of vascular disturbance and direct mechanical compression of the spinal cord. Approximately two-thirds of herniations are central, with the balance occupying a paracentral or lateral position. Intradural disc herniations have also been described.

Symptomatic thoracic disc herniations can be associated with a variety of initial complaints. The array of attributed local and radiating pain symptoms can result in lengthy delays in diagnosis. Patients may present with prior workup and treatment for disorders including cholecystitis, renal colic, cardiac disease, endometriosis, and lumbar disc disease.

Neurological abnormalities are predictably limited to the lower extremities or bowel and bladder function. Upper motor neuron signs in the lower extremities such as clonus and Babinski reflexes may be found, particularly in patients with gait abnormalities, lower-extremity weakness, or bowel and bladder complaints. A concordant level of change in sensitivity to pinprick may be identified. Abdominal reflexes may be absent. Differential diagnosis in patients with myelopathic symptoms should include systemic causes of upper motor neuron weakness, such as multiple sclerosis or amyotrophic lateral sclerosis. These can occur concomitantly with a thoracic disc herniation, and will contribute to a poor neurological outcome with surgical treatment.

Plain radiographs should be obtained on all patients. These may demonstrate abnormalities such as disc calcification or narrowing of a disc space. Changes associated with Scheuermann’s disease, such as end-plate irregularities, Schmorl’s nodes, and vertebral body wedging, may also be present.

Computed tomography (CT) myelograms or magnetic resonance imaging (MRI) are definitive investigations. The frequent occurrence of thoracic disc herniations in asymptomatic patients requires careful correlation of clinical complaints with the radiological findings.

Identification of level is essential for patients being considered for surgical treatment, and this is not easy. This can be done either by a sagittal MRI showing both the sacrum and the herniation on a single cut, or by an anteroposterior topogram reconstructed from the CT scan to demonstrate the ribs at each level, allowing a precise count of thoracic and lumbar vertebrae. This is a critical aspect of presurgical preparation.

The treating physician must establish that surgery holds a reasonable expectation of improvement for the patient (Box 3.2.1).

It is our opinion that centrally located herniations with neurological deficits are best treated via an anterior thoracotomy approach. Adequate exposure for complete decompression of the spinal cord is difficult to achieve via a costotransversectomy or a transpedicular approach, particularly for calcified disc herniations, which can extend intradurally. These issues may contribute to the somewhat lower numbers of patients with complete neurological recovery and pain relief following posterior decompressions than for those undergoing transthoracic excision.

Identification of level is essential for patients being considered for surgical treatment. It is not always easy to identify the correct level from images. This can be done either by a sagittal MRI showing both the odontoid process and the herniation on a single cut, or by an anteroposterior topogram developed with the CT scan to demonstrate the ribs at each level, allowing a precise count of thoracic and lumbar vertebrae.

Haemothorax and pneumothorax are recognized potential complications of a transthoracic approach.

While stenosis of the lumbar spinal canal and intervertebral foramen is well recognized, thoracic spinal stenosis remains a comparatively rare entity. Like lumbar stenosis, thoracic spinal stenosis occurs when degeneration produces enlargement of structures surrounding the dural sac, with secondary compression of the neural structures. Compression may be posterior, from the ligamentum flavum and facet joint capsules, or anterior, from the intervertebral disc or posterior longitudinal ligament. Patients with congenitally narrow canals are particularly at risk for developing these problems.

Spinal stenosis may be developmental or acquired through degenerative processes. It may also occur at a stress riser above a previous spinal fusion (iatrogenic).

Symptoms may vary from those of lumbar spinal stenosis due to the potential involvement of the spinal cord. However, lumbar spinal stenosis must still be considered in the differential diagnosis, as these patients may present with similar complaints and lumbar stenosis is much more common.

Sensory abnormalities of the lower extremities occur in virtually all patients, often in a stocking or other non-dermatomal distribution. Some patients demonstrate a thoracic sensory level. Activity-related lower-extremity pain or dysaesthesia is reported by the majority of patients, and 30–40% have bowel and bladder dysfunction. In one series, lesions above T9 tended to show spastic paresis whereas those with lesions in the region of T11–T12 have a flaccid paralysis.

Approximately 50% of patients demonstrate spasticity in the lower extremities, although there appear to be somewhat higher rates of paresis. This may be due to concomitant lumbar stenosis, with a secondary loss of lower-extremity reflexes.

Diagnosis is confirmed by myelogram/CT scan or by MRI. It is important to determine whether the primary compression is due to anterior structures (e.g. ossification of the posterior longitudinal ligament or a herniated disc) or posterior structures (ligamentum flavum and facet capsule hypertrophy). As with a herniated thoracic disc, accurate determination of the spinal levels involved is critical. Complete three-dimensional imaging of the lumbar spine should be performed to ensure that a more caudal lesion is not present.

Observational treatment may be sufficient for patients with myelopathy without incapacitating claudication or weakness. However, in most of the patients we have diagnosed with this condition, weakness and gait abnormality with or without lower extremity claudication is already present. We believe that these patients should be offered surgery aimed at decompression of the spinal cord.

The decision of whether to proceed with anterior or posterior decompression depends on the location of the spinal cord compression. Most of the patients described in the literature have posterior compression due to hypertrophy of the posterior structures, which can be treated by laminectomy. Careful technique is required, with the use of a burr to thin the posterior bone. The remaining soft tissue is then gently elevated off the dura with curettes and a small pituitary rongeur. Use of Kerrison rongeurs should be limited to the 1- to 2-mm punches in the areas adjacent to the facets and lateral to the cord. The decompression must be wide enough to include the medial aspects of the facet joints and must include all potentially compressive levels. Fusion of these patients is not generally required because of the stability provided by the thoracic cage.

Patients with anterior compression should be treated with anterior transthoracic decompression of involved segments.

All series are small. About 70–80% will experience improvement or good resolution of neurological symptoms with adequate decompression. Patients can develop recurrent symptoms despite initially successful surgical treatment. This can be due to recurrent bone formation at the operated level or degeneration at additional spinal levels. Therefore, these patients require regular follow-up with reimaging of appropriate levels for recurrent symptoms.