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Thoracic disc prolapse …
- Updated 01.21.2024
- Released 11.22.1999
- Expires For CME 01.21.2027
Thoracic disc prolapse
Introduction
Overview
Thoracic intervertebral disc disease is a rare source of pain and neurologic dysfunction, and it is not as well known to most clinicians as lumbar or cervical disc disease. Thoracic disc disease has been described as causing many different symptoms without a discrete clinical syndrome. Although back pain is usually the most common presenting symptom, many other presentations have been described that are often misleading. The author of this article provides an updated overview of the disease, including presentation, presumed mechanisms of injury, and updated diagnosis and management principles, both surgical and nonsurgical.
Key points
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• Thoracic disc disease is an often-missed diagnosis in patients with neurologic deficits. | |
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• MRI is the key imaging modality for diagnosis of disc prolapse and cord compression. For patients who have contraindications for MRI scans, CT myelogram is an acceptable alternative. Noncontrast CT may be critical in demonstrating the degree and location of calcification in the disc rupture. | |
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• Surgical management of the offending disc fragment or decompression of the spinal cord can lead to recovery of neurologic function. | |
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• New, minimally invasive techniques of thoracic discectomy have been developed. |
Historical note and terminology
Thoracic intervertebral disc disease is a rare source of pain and neurologic dysfunction compared to cervical and lumbar pathologies (35; 31; 54). Spinal cord injury from ruptured thoracic disc was first reported in 1838 (43). In 1911 Middleton and Teacher reported a patient who “felt something crack in his back” while lifting a heavy plate, which forced him to bed. He progressed to flaccid paraplegia later that day and died 16 days later of urinary tract infection. An autopsy of the patient showed a T11 to T12 herniated disc with spinal cord compression (61). Microscopic examination revealed hemorrhage, necrosis, and thrombosed vessels in the spinal cord. Since then, there have been numerous reports of clinically significant herniated thoracic discs as causes of pain and neurologic abnormality in patients.
Although the potential for a devastating acute paraplegic manifestation of thoracic disc herniation exists, it is often difficult to decide if an operative intervention is necessary, even when thoracic disc disease is discovered. The rib cage provides an "internal brace" that impedes onset or progression of thoracic disc herniation, whereas no such protection is available to the cervical or lumbar spine.
Clinical manifestations
Presentation and course
Lack of discrete clinical syndrome associated with thoracic disc herniation and rarity of the condition make it difficult for clinicians to diagnose this disease process, and it is often misdiagnosed or missed completely. The most common initial symptom of thoracic disc herniation is back pain, reported by 57% to 76% of patients (03; 85). The history of trauma is variable, reported in 37% of symptomatic patients (85). A review by Linscott and colleagues found an inciting event to be identifiable in 49% of cases (51). The most common events reported were lifting/twisting, falling, or other trauma. Another possible presenting sign and symptom of the disease is myelopathy with long tract signs suggesting spinal cord compression. In the Linscott and Heyborne study of 78 cases, weakness on initial exam was found in 42% of patients (36% had lower extremity weakness), and sensory changes and reflex abnormalities were seen on exam in 37% and 33% of patients, respectively (51).
The spinal level of thoracic disc herniation determines the type of clinical syndrome presented in those patients who are symptomatic. In general, symptomatic patients with the offending disc at the upper thoracic spine, namely at T1 to T2 level, present with interscapular pain radiating to the lower neck or unilateral shoulder or arm. Patients can also present with pain, paresthesias, and numbness radiating into the axilla and medial aspect of the arm and forearm (01). Although uncommon, a presentation of a C7 to T1 or T1 to T2 herniated disc is Horner syndrome, resulting from interruption of preganglionic sympathetic fibers to the head and neck (29; 52; 46; 36). Another case report in the literature described a T2-3 disc herniation presenting as chest pain, mimicking a cardiac origin, in a young athlete (10).
Symptomatic patients with midthoracic spine (T3 to T8) herniations complain of back pain over the level of the disc pathology. Radicular pain associated with these levels consists of radiating pain, dysesthesia, or numbness wrapping around the chest wall in distribution of the nerve root being compressed. In the lower thoracic spine, presenting symptoms can mimic visceral symptomatology including cholecystitis, pancreatitis, renal lithiasis, duodenal ulcer, acute abdomen, and lower back problems. Chronic abdominal pain or segmental paresis of the abdominal wall can be a presenting sign in a patient with lower thoracic disc disease (94; 84). Laterally positioned disc ruptures may impact the spinal cord minimally but produce nerve root irritation causing an isolated unilateral intercostal neuralgia without myelopathy. Typically, the upper thoracic root will be compressed in its axilla such that a T7-8 lateral rupture will irritate the T7 root as it exits under the T7 pedicle and out the foramen. Numbness in addition to pain may or may not result as there is usually overlap of sensory innervation in the thoracic region from adjacent dermatomes.
In more malignant forms of thoracic disc herniation in the midthoracic or lower thoracic spine, patients can present with Brown-Sequard or anterior spinal artery syndrome. With disc compression of the lateral aspect of the spinal cord, patients can present with dissociated contralateral pain and temperature sensory loss with loss of ipsilateral proprioception and motor function. The blood supply to the midthoracic spinal cord is tenuous, and because of this, midline compression by thoracic disc can lead to anterior spinal artery syndrome (or anterior cord syndrome), resulting in paraplegia with loss of pain and temperature bilaterally but preserved posterior column function (76). Angiographic improvement in anterior spinal artery flow was shown to correlate with neurologic recovery in a 54-year-old woman following surgical decompression of a T8 to T9 thoracic disc rupture (81). Venous congestion of the thoracic cord leading to myelopathy due to disc compression has also been described (78). Conus medullaris syndrome results from disc herniation of the lower thoracic spine, resulting in saddle anesthesia, loss of lower autonomic functions such as bowel, bladder, and sexual functions, and absent reflexes. These symptoms may occur in conjunction with pain or suddenly without pain. A Chinese group reported 13 cases of patients seen over a 5-year period with disc herniation in the T11 to L1 region, presenting with foot drop, presumably from compression of the lower motor neuron in the conus affecting tibialis anterior function. Twelve of the 13 cases recovered with surgery (20). Painless myelopathy may also occur with subtle gait stiffness or spasticity and signs of iliopsoas weakness, with the patient complaining about the inability to climb stairs or rise from a chair (11). Approximately 30% of patients present with abnormal bowel, bladder, and sexual functions (03). Patients can also present with symptoms of neurogenic claudication (62) and with complaints of pain, numbness, and weakness in the lower extremities after walking a short distance. Cord compression syndromes were the initial complaint in 9% to 41% of patients with thoracic disc disease (85).
Spontaneous intracranial hypotension has been reported from an intradural thoracic disc herniation resulting from a cerebrospinal fluid leak from intradural penetration of disc (73; 34; 97; 44; 12). T-MRI evaluation for thoracic disc herniation is now part of the routine work-up for intracranial hypotension (27; 21). Another MRI finding is the black outlining of the lower cerebellum and brainstem seen on T2 imaging characteristic of superficial siderosis, a condition of pial hemosiderin deposition from chronic subarachnoid bleeding from intracranial hypotension. Thoracic CT myelography may demonstrate a significant CSF leak through the ventral dura, as described by the University of Pittsburgh group in the case of a young man with intracranial hypotension causing subdural hematomas (39). The leak was caused by a T1-2 ventral osteophyte initially failing blood patch but responding to anterior discectomy with fusion and microsurgical dural repair. Rarely, intradural thoracic disc herniation may clinically mimic motor neuron disease (ALS) when associated with intracranial hypotension and superficial siderosis (45; 97; 44; 12; 17).
There are no specific signs attributable to thoracic disc herniation other than decrease in pinprick sensation over a root level and loss of superficial abdominal reflexes. Epigastric reflex generally tests thoracic roots T5 to T7. The upper abdominal or supraumbilical reflex tests roots T7 to T9. The middle abdominal reflex tests roots T9 to T11. The infraumbilical or suprapubic reflex tests T11 to upper lumbar nerve roots. Although absence of reflexes in the above-mentioned patients is not a significant finding in young patients, especially muscular males, lack of reflex is definitely pathologic (24).
Prognosis and complications
Although the natural history of this disease process is uncertain, in general, the prognosis of thoracic disc prolapse depends on the presentation of the patient at initial evaluation. Given the large number of incidentally discovered thoracic disc herniations and the lack of symptoms in these patients, the prognosis is good in terms of asymptomatic patients not deteriorating neurologically. Prognosis for patients presenting with symptoms is generally good. In a retrospective review of literature, about 80% of patients who presented with pain, sensory deficits, or bowel and bladder deficits improved after surgical intervention. Approximately 65% of patients with motor impairments improved after surgical intervention. The recovery potential in patients with myelopathy, which implies long standing cord compression, is unpredictable.
Clinical vignette
Vignette 1. A 51-year-old presented approximately eight days after becoming paraplegic. She experienced pleuritic type chest pain, nausea, and vomiting. She noted that her legs felt weak, but she was still able to walk. The weakness was more pronounced in her left leg. The patient was diagnosed with pulmonary infection and discharged on antibiotic therapy. Two days after the onset of her pleuritic-like chest pain and symptoms, the patient stated that she could not control her lower extremities or walk. Approximately five days later, the patient noted urinary incontinence and presented to a local emergency room. At this second visit, the patient stated that previous complaints of pleuritic-like chest pain and nausea were resolved.
The patient’s history included the removal of an abdominal mass approximately 13 years earlier. She denied any history of coronary artery disease, hypertension, cardiac arrest, or diabetes; she was not on any type of medication, and she had no allergies. On neurologic examination, the patient was alert and oriented and her speech was normal. The cranial nerves were intact. An MRI showed a severe cord compression at T6 to T7 level.
The patient was admitted to neurosurgery service with a diagnosis of paraplegia with worsening neurologic symptoms. She was immediately prescribed Decadron. A right-sided thoracotomy with a resection of the sixth rib and a T6 to T7 thoracic discectomy were performed. The patient did well postoperatively and was discharged to a rehabilitation center near her home. At a 6-month follow-up, the patient had some myelopathic gait and myelopathy, but the patient’s motor exam was markedly improved. A postoperative MRI at T6 showed complete removal of the disc matter with the return of normal curvature with residual changes where previous cord compression was.
Vignette 2. A 51-year-old man presented with a 9-month history of progressive proximal and distal leg numbness and a slight sense of weakness climbing stairs; he also reported some urinary urgency and hesitancy but without sexual dysfunction. The numbness began in the right foot and spread up to the knee, followed by a similar course of spreading numbness in the left leg. He denied back or leg pain. The only reported trauma was approximately six months prior to the symptoms, when he fell off a boat into the water, landing hard on his back. He owned and worked at a dairy, and his work required occasional heavy lifting.
Examination revealed normal power but slightly increased tone and mildly spastic gait, with increased knee reflexes and ankle reflexes bilaterally. Proprioception was diminished in feet and toes. Light touch sensation was diffusely diminished from the knees down. Percussion of the spine was nontender. Thoracic and lumbar MRI both showed a broad-based T11-12 disc rupture, largely soft but partially calcified, with posterior displacement of the spinal cord and with signal change in the cord above and below the level of compression consistent with edema. A smaller disc rupture at left T7-8 was noted without spinal cord compression and was considered incidental.
Follow-up thoracic CT obtained to determine the consistency of the T11-12 rupture confirmed the partial calcification on the left.
The patient was counseled regarding the need for surgical intervention, noting no safe nonsurgical treatment for this, and underwent a T11-12 decompressive laminectomy, bilateral facetectomy, and microdiscectomy with T10-12 pedicle screw instrumented fusion. The patient was monitored during surgery with motor and sensory evoked potentials of the upper and lower extremities; the lower extremity potentials improved during the initial posterior decompression and further with microscopic disc removal from either side. The patient had an uneventful postoperative course and was seen at 1 month, 3 months, and finally at 6 months from surgery with postoperative thoracic x-rays showing good alignment and position of pedicle screws.
The patient’s leg numbness and bladder symptoms had resolved at the first postoperative visit, but increased reflexes did not normalize until six months after surgery, at which time he was fully active at work and playing golf as well.
Biological basis
Etiology and pathogenesis
Thoracic disc disease comprises various pathologies of the thoracic disc space. Disc herniation describes extrusion of the nucleus pulposus through a tear in the annulus fibrosus. Depending on the age of the rupture, disc disease can be described as an acutely ruptured disc, degenerated disc disease, or osteophytic disease. An acutely ruptured disc denotes soft disc extrusion out of the confines of the annulus fibrosus. With continued mechanical use and aging, the nucleus pulposus tends to desiccate and break down at the same time that the annulus fibrosus calcifies. This leads to the disc spaces bulging into the spinal canal with calcified ligamentous structures, referred to as degenerative disc disease or spondylosis. With further degeneration of the disc space, bony contact between the two vertebral bodies leads to bone formation at the point of contact. This osteophyte formation may reduce the diameter of spinal canal or nerve root foramen and result in symptoms.
Aging changes the compliance of nucleus pulposus, which is the main material comprising the center of the disc. Elasticity of the surrounding annulus fibrosus and ligamentous structures also degenerates, desiccates, and tears with repeated stresses and strains of daily usage. The rib thorax serves as protection from the harsh stresses and strains experienced by the cervical and lumbar spine. This rib cage of the thorax prevents extreme movement of the thoracic vertebral joint; therefore, disc herniation in the thoracic spine is uncommon as compared to cervical and lumbar disc disease.
The anatomy of the thoracic spine confers unique biomechanical properties. The thoracic spine can be categorized arbitrarily into three regions based on anatomical morphology and biomechanical characteristics. The upper thoracic spine consists of the T1 to T3 vertebral segments. This region shows morphologic features similar to the cervical vertebral segments. The spinal canal exhibits decreasing lateral width with increasing pedicle length. The middle thoracic spine consists of the T4 to T9 vertebral segments. This region is characterized by an almost constant spinal canal cross sectional area and a small ratio of spinal cord-to-canal cross-sectional area. The lower thoracic spine, from T10 to T12 vertebral segments, has anatomical characteristics resembling the lumbar vertebral segments. The lateral width of the canal and the pedicle length increase in this region to reach the canal cross-sectional area approaching the lumbar segment (67). Biomechanically, the upper thoracic vertebral region tends to favor axial rotation and the lower segment has the propensity for flexion and extension movement. Thus, the thoracic spine acts as a biomechanical transition zone between the cervical and lumbar spine. This transitional nature of the thoracic spine confers variability in incidences of disc prolapse along the thoracic spine.
Relative to the cervical and the lumbar spine, the range of movement of the thoracic spine is severely limited due to this anatomic arrangement. Disc space to vertebral body ratio is smaller than that of the cervical and lumbar spine. Facets and joints are aligned in anteroposterior directions such that flexion-extension and rotational movements are severely limited (23). The ribs that encircle the chest wall with the sternum complete the cylindrical structure, which further limits the movement of the thoracic spine and makes disc prolapse much rarer here than in the mobile cervical and lumbar spine. A biomechanical cadaver study found the posterior longitudinal ligament, which, amongst other functions, provides a resistive force to disc herniation, to be strongest in the thoracic spine (91).
Although the thoracic spine is less apt to be involved in disc prolapse, the intrinsic anatomy of the thoracic spinal canal and the thoracic cord itself lends to its predisposition to be a devastating event in which any offending component can cause narrowing of the spinal canal diameter. The vascular supply to the mid- and lower-thoracic region is tenuous compared to the other areas of the spinal cord. This region of the spinal cord is mostly supplied by the artery of Adamkiewicz, a single unilateral medullary artery, which usually enters the spinal cord on the left side from T8 to L4 (26). It is considered the “watershed zone.” Any compressive lesion causing pressure on the spinal cord in this region can lead to ischemic damage to the spinal cord with clinical manifestations much worse than what would be expected from the radiographic abnormality.
The intervertebral discs constitute approximately one third to one fifth of the vertebral column height. Four distinct regions of the intervertebral disc are recognized. The outer layer consists of alternating layers of collagenous fibers that attach to the vertebral endplates. The fibrocartilaginous material makes up the major portion of the annulus fibrosus. The third layer is the transition zone between the fibrocartilaginous area and the central nucleus pulposus. The nucleus pulposus is made of a soft mucoprotein gel containing various mucopolysaccharides, a minor component of collagenous fibers, and a large content of water. The water content of nucleus pulposus at birth is 88% and decreases throughout life (37). With age, the annulus fibrosus thickens and gradually ossifies.
Functionally, intervertebral discs support bending and compressive loads during physiologic movement of the spine. Intervertebral discs, to a lesser extent, also absorb tension and shearing loads. It is extremely unlikely for a disc to fail under axial compressive loads because the nucleus pulposus uniformly distributes the pressure under axial compressive loads (37). Degenerative changes to the disc, as a result of repeated use and trauma to the disc, ultimately result in disc prolapse. The exact etiology of the microfailures that occur secondary to repeated use is unknown, but it is postulated that repeated torsion and bending loads cause micro disruption to the annulus fibrosus, leading to eventual disc degeneration (95). The torque required to cause a tear in the annulus fibrosus of a degenerated disc space and lead to a ruptured disc is 25% less than the torque required to cause a tear in a normal disc space (56).
Epidemiology
Autopsy studies and MRI and CT myelography have reported the frequency of incidentally found thoracic disc disease to be in the range of 15% to 20% in the general population (01; 06; 80; 96). It is estimated that 1 in 1 million patients per year has clinically significant thoracic disc disease, making the incidence of thoracic disc disease less than 1% in the general population (54; 16; 11; 55; 03; 04). Only 4% of all disc operations involve herniated thoracic discs (87; 86; 85).
A large 2018 study coming out of South Korea looked at 2212 patients undergoing thoracolumbar MRI for evaluation of back and leg pain and found that 145 patients (6.5%) had thoracic disc ruptures, predominantly in the lower thoracic spine (32). Most were incidental and just associated with symptomatic lumbar disc herniations. Only six of the 145 thoracic disc herniation patients underwent surgery for their rupture, or 0.27% of the whole studied group.
Symptomatic thoracic disc disease usually occurs between the second and eighth decades of life, with the mean age in the fifth decade. This condition affects both sexes. In a series, Stillerman reports the female-to-male ratio of patients treated for symptomatic thoracic disc to be 37 to 34 patients (85). A history of trauma is reported in approximately one third of patients as the cause of the condition. Interestingly, the most common area of thoracic disc prolapse is reported in the lower segment of the thoracic spine with disc prolapse occurring in approximately 75% of reviewed series. The upper segment of the thoracic spine appears to be relatively immune to disc prolapse, with only 4% of patients with thoracic prolapse in T1 to T3 levels. In about 80% of the patients, the location of the disc is central to centrolateral; approximately 30% are calcified and 6% are intradural (85). About 26% of symptomatic patients are reported to have multiple thoracic discs, and 12% of patients have nonadjacent multiple discs (51). Thoracic discs are usually found to be hard and calcific in contradistinction to lumbar or cervical discs (85). Endplate marrow signal changes were uncommon in thoracic disc disease in a study analyzing MRI changes in patients with thoracic disc-related disorders (30). Acute disc rupture with rapidly progressive myelopathy has also been reported following instrumented thoracic fusion due to acute changes in stress on a degenerated disc above or below the fusion segment (09).
Prevention
Due to the rarity of symptomatic thoracic disc prolapse presenting for medical management, no data are available in preventing this condition.
Differential diagnosis
The most common presentation of thoracic disc disease is pain that cannot be distinguished from symptoms of various pathologies of the thoracic and abdominal organs. Moreover, radicular symptoms and myelopathic symptoms can be due to many causes other than disc problems. All of the following are pathologies that may be considered in the differential diagnosis of thoracic disc disease:
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Degeneration of spine supporting elements | ||
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• Disc prolapse or spondylosis | ||
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Degenerative disease of spinal neural elements | ||
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• Amyotrophic lateral sclerosis | ||
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Abnormal growth | ||
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• Metastatic tumor, most commonly extradural or involves the bone | ||
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- Glioma, hemangioblastoma | ||
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• Cystic lesions | ||
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- Syringomyelia, hydromyelia | ||
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Traumatic | ||
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• Vertebral compression fracture or pathologic fracture | ||
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Infectious | ||
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• Vertebral osteomyelitis | ||
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Inflammatory | ||
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• Arachnoiditis | ||
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Metabolic | ||
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• Diabetic neuropathy | ||
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Vascular | ||
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• Hemangioma | ||
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Visceral | ||
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• Myocardial infarction | ||
Diagnostic workup
In most instances, the history and physical exam should guide the physician in obtaining appropriate laboratory testing necessary to make the diagnosis. If there is a strong suspicion that a lesion in the thoracic spine is causing an array of symptoms manifested by the patient, the initial exam should include plain anteroposterior and lateral view roentgenogram of the thoracic spine. This test is used to detect any variation in alignment of the spine and any destructive process of the bony spine (ie, fractures, tumor, or instability). Loss of disc space height or calcification in the spinal canal adjacent to the disc space is highly suggestive of thoracic disc disease. Intraspinal calcification may suggest an intradural herniation.
If any type of thoracic spine lesion is suspected as a cause of the patient’s symptoms, then MRI or CT myelogram is indicated.
CT myelogram has been the imaging modality of choice in the past. Myelogram will show defects in the contrast flow through the subarachnoid space at the level of the disc. For visualization of calcified posterior longitudinal ligament, CT myelogram is superior to MRI. Significant spinal stenoses can also be detected by a complete block of the contrast across the stenotic area. Postmyelographic CT shows soft tissue of the spinal cord and the disc tissue at the same time, detailing the bony spine and the subarachnoid space.
MRI is presently the imaging modality of choice in detecting lesions in the thoracic spine, including disc abnormalities. Not only does MRI reveal compressive lesions of the cord, it also reveals intrinsic lesions of the cord. A sagittal T2-weighted image of the thoracic spine reveals details of the thoracic vertebra body, the subarachnoid space, and the spinal cord. Disc prolapse can be easily visualized, any cord abnormality can be detected, and the level can be localized using this modality. The drawback, as in any MRI imaging, is that bone and calcifications are poorly visualized. Axial scans are used to determine the degree of spinal compression caused by the disc. Not only does MRI detect discs, but in conjunction with gadolinium contrast, it is useful in revealing various lesions, such as ligamentous injury or neoplastic, inflammatory, or infectious processes of the spinal cord and surrounding bony spine.
Noncontrast CT of the thoracic spine will often give better detail of the calcified component of the disc rupture and helps to dictate the surgical approach, so it is used as a preoperative study once the diagnosis is established by thoracic MRI.
Spinal angiography is not indicated in a workup of thoracic spine disc prolapse. It may be useful if a serpiginous pattern of contrast defect on anteroposterior myelogram is apparent or if serpiginous flow void or contrast enhancement in the spinal canal on MRI is seen. In this case, spinal arteriovenous malformation should be suspected, and an appropriate angiogram should be performed.
Management
For patients presenting with localized thoracolumbar spinal pain or radiculopathy, conservative treatment is the initial management of choice, including short-term activity restriction and nonsteroidal anti-inflammatory drugs. However, muscle relaxants, a short course of low-dose steroids, and nightly medication with low-dose amitriptyline can be instituted when the patient complains of extreme pain or discomfort. Narcotic analgesics may help with short-term pain control, but in the long term, use is contraindicated because of the risk of drug dependence.
Management of these patients should include consideration of radiographically significant abnormalities versus clinically significant disease processes. Awwad and colleagues reported a retrospective study of radiographic characteristics of symptomatic and asymptomatic thoracic disc patients (07). Symptomatic patients were not distinguishable from asymptomatic patients in a study of postmyelographic CT scans. Given this finding, assessment of symptoms and a physical exam is paramount when evaluating a patient who presents with a diagnosis of thoracic disc prolapse. If the patient is asymptomatic, treatment should be postponed and the patient should be monitored. With the advent of posterolateral approaches with use of the endoscope or operating microscope, avoiding the morbidity of open thoracotomy for disc removal, it is reasonable to offer surgery in select patients who have failed conservative measures of treatment for isolated thoracic root pain due to disc rupture. Symptomatic relief from radiculitis and discogenic pain from lateral disc rupture can be relieved in a significant number of patients without disc removal, but with one or a series of fluoroscope-guided epidural injections; injection of local anesthetic with or without steroids has been shown to reduce pain in as many as 80% of patients reporting 12 months after injection (58).
Patients who present with myelopathic symptoms, motor symptoms, or bowel and bladder abnormalities should be evaluated for surgical interventions. Evaluation for surgical intervention does not imply that the patient should be operated on immediately, but the patient should be followed by a surgeon who specializes in treating pathologies of the spine. The patient should be started on a short course of high-dose steroids, preferably dexamethasone or methylprednisolone.
Myelopathy is generally accepted as an indication for surgical therapy, although this may be delayed if the patient is manifesting improvement in the neurologic deficit (47). There are cases of symptomatic acute disc herniations that presented with myelopathy and underwent resorption with conservative therapy (33). A patient with severe or progressing myelopathy or with motor or bowel and bladder deficits, and who is also medically stable, should be an immediate candidate for surgical intervention. However, patients can present with multiple-level thoracic disc disease with myelopathy. Such a presentation can be confounding for surgeons deciding on the symptomatic level. Decompression may be necessary at multiple levels in such cases (19; 05).
Location of thoracic disc prolapse hinders easy surgical treatment, in contrast to cervical or lumbar disc disease. The first two reports of surgical treatment for thoracic disc prolapse were in 1931 and were independently reported by Antoni and Elsbrug (88). Historically, treatment of thoracic disc herniations consisted of decompressive laminectomy, in which lamina of the thoracic spine are removed to give more space for the spinal cord to traverse the offending level of the spinal canal. Laminectomy alone has been shown to be a suboptimal approach fraught with complications for thoracic discectomy (53; 88; 89; 57; 86). A significant number of patients were made worse by the surgery, presumably due to excessive spinal cord manipulation, or due to impaired blood flow to the cord that has been allowed to shift posteriorly into the laminar defect and away from the anteriorly compressing disc. Given the tenuous blood supply of the thoracic spinal cord, it is postulated that the spinal cord is not able to tolerate any form of manipulation, leading to the poor outcome after this procedure (53; 74; 55; 56; 77). Irregardless of the approach, careful attention must be paid to maintaining spinal cord perfusion pressures with continuously adequate intraoperative fluid volume and blood pressure. Potential neurologic compromise as measured by deterioration of motor and sensory evoked potentials has been shown to occur with a fall in mean arterial pressures during anesthetic induction, prior to any repositioning of the patient or manipulation of the spinal elements (101). Laminectomy may be useful in cases of degenerative thoracic spinal stenosis in which the posterior elements (facets, ligamentum flavum, lamina) contribute more to the canal narrowing than does a prominent disc.
Anterior, anterolateral, lateral, and posterolateral approaches have been developed to treat thoracic disc disease. The transpedicular approach was first described by Patterson and Arbit in 1978. In this approach, a wide unilateral facetectomy and pedicle removal is performed to expose the posterior-lateral surface of the disc. Exposure of ventral pathology is limited (69). The similarity of this approach to posterior lumbar discectomy ensures that most surgeons will be comfortable with the exposure. Anterior approach to an upper thoracic disc herniation presents a particular challenge because of the anatomic relationship between the disc and the obstructing sternum and location of great vessels. Radiological landmarks have been proposed to help determine the safest and most appropriate anterior approach for upper thoracic discs, including planning for sternotomy, if needed (28).
Lateral approaches to the thoracic spine involve exposing and removing various amounts of the transverse process of the vertebral body and the corresponding rib. As more bone is removed, the operative exposure is expanded, although there is risk of damage to the pleura; ventral exposure is still not optimal without a large-scale bone removal (the lateral extracavitary approach).
The transthoracic or anterior-lateral approach was first described by Perot and Munro (71). Briefly, the level of the incision and the side of exposure is dictated by the pathology. Some surgeons will always perform angiography and incise on the opposite side from the artery of Adamkiewicz. In the thoracic spine, the rib articulates at the level of the disc space above its corresponding body-transverse process. Removal of the distal rib and pedicle allows wide exposure to the posterior disc space. Autologous rib can then serve as a buttress much like anterior cervical discectomy and fusion. This approach is indicated for midline pathology. Spinal cord manipulation is minimized, although the morbidity of the operation is significant, and many patients will require a postoperative chest tube.
McCormick describes his group’s experiences with retropleural approaches to the thoracic spine and thoracolumbar junction (59). In their study, they recommend different incisions and locations to start one’s approach to a thoracic disc based on the level of pathology. For example, for lesions between T5 and T12, the surgical approach should be over the affected rib and from the posterior axillary line to 4 cm off of midline. On the contrary, however, if a patient has a thoracic disc at higher cervical levels, a hockey stick incision should be used. Upper thoracic disc herniations present an even higher surgical challenge. Cornips and colleagues describe a transaxillary approach to the spinal canal for T3 and T4 disc herniation and satisfactory outcome in a series of eight patients (22).
Calcified centrally located discs are difficult to resect via a posterior approach. In one study by Dickman and colleagues, patients with past history of thoracic discectomy and recurrent symptoms were reviewed (25). Of the 15 patients, with predominantly calcified centrally located discs, 11 patients had undergone a previously failed posterolateral approach. The authors stress that a ventral approach leads to a safer and more complete decompression when dura is clearly visualized.
The spine group at Johns Hopkins published their experience over the last five years with transthoracic approaches to centrally located discs (08). Although they were able to achieve very good resections of the offending disc fragment, their study was tainted by almost one fifth of the patients developing a major complication. In general, if the offending soft or hard disc can be safely and adequately removed and decompression of the spinal cord achieved from either an anterior or posterior (or posterolateral) approach, the anterior surgery is avoided because of its higher morbidity and mortality (99; 42).
Another technique that allows the posterior approach is the transpedicular route. When this approach is planned, the incision can be the standard midline or para median on the side of pathology. The high-speed drill is used to remove the facet and pedicle immediately inferior to the involved disc space. This provides a posterior, lateral visualization to the disc space without retraction of the spinal cord. This approach can even be performed bilaterally to facilitate removal of midline discs (49). A further consideration of the posterior midline approach favoring fusion without discectomy is raised by a group in Cleveland: in a case presenting with urinary urgency and sensory changes, but without motor deficit, a multisegment laminectomy, pedicle screw thoracic fusion was performed, leading to symptom resolution and regression of large calcified disc herniation by MRI (02). Elimination of micromotion at the cord compression level was proposed as the mechanism of disc resorption.
Bransford and colleagues advocate a newer transfacet pedicle-sparing approach for disc herniations, followed by interbody fusion with short-segment pedicle screw fixation (13). Although their study was complicated by a high rate of reoperation for infection and hardware malpositioning, their approach did result is good decompression of the spinal cord. A subsequent review of this approach confirms its safety and efficacy (18). Several authors have presented series of patients with thoracic disc herniations, partially or entirely calcified, which have been safely approached and removed by these modified posterior approaches (41; 68).
The most recent surgical approach to herniated thoracic disc disease is the thoracoscopic microsurgical approach. Rosenthal and Dickman described using this technique in 55 individuals with thoracic herniated discs. Radiculopathy resolved completely in 15 of 19 patients, and myelopathy improved completely in 22 of 36 individuals (79). The minimal tissue and rib retraction of the endoscopic procedures has reduced postoperative pain and hospitalization in these patients. Adequate training and the surgical experience needed to obtain and maintain the skills required in these complex operations are essential for surgeons who perform thoracoscopic spine surgery (66). A 10-year prospective study of 167 consecutive single-level thoracic disc herniations treated thorascopically was reported to yield 79% good to excellent pain relief and 80% good to excellent motor recovery by patients at 2-year follow-up; however, this is a technically challenging procedure that yielded a 15.6% complication rate in the hands of this endoscopic specialty group (72). Advances in endoscopes and instrumentation for safely removing soft disc fragments, cartilage, and bony ridges even ventral to the spinal cord have significantly expanded the role of minimally invasive approaches, such as transforaminal endoscopic foraminotomy and discectomy (93; 98; 14). Whether through an open thoracotomy or through a tubular dissection using a thorascope, CSF-pleural fistula can be a challenging surgical complication to manage. Because negative intrapleural pressure during normal breathing creates a suction effect on spinal fluid from a dural surgical tear, these fistulas are difficult to seal without intervention. Prolonged positive pressure mechanical ventilation with lumbar drainage has been advocated, as has lumbar drainage with chest tube and omental graft (90; 82).
The posterolateral approach to the spine allows one to perform the discectomy without entry into the chest cavity. Some centers favor this approach regardless of the location or size of the thoracic disc rupture, or presence of calcification, in order to avoid complications of the transpleural or retropleural approach. A series of 30 consecutive patients seen over five years with various thoracic disc rupture types were surgically managed successfully by the Cleveland group using a transpedicle or transfacet approach with instrumented fusion (68). Perez-Cruet and colleagues (70) have developed a novel posterolateral, minimally invasive thoracic microendoscopic discectomy technique. This technique provides an approach to the thoracic spine that is associated with less morbidity. Under fluoroscopic guidance, a muscle dilation approach is utilized and the procedure is performed with endoscopic visualization through a tubular retractor. In their series of the seven patients undergoing this procedure, there were no complications. There was significantly lower intraoperative blood loss and shorter hospital stays with the thoracic microendoscopic discectomy technique when compared to the open technique. A percutaneous posterolateral thoracic microendoscopic discectomy in a human cadaver model has been reported (40). Using microendoscopic discectomy techniques, the discectomies were performed throughout the mid and lower thoracic spine. The authors found that this technique required much less bone removal than the open technique and yielded adequate canal decompression as determined by computed tomography. A more extensive review of 60 patients operated on in five institutions was reported using a lateral, minimally invasive approach that still allowed use of an operating microscope as well as interbody and pedicle screw instrumented fusion in a majority of patients, with greater than 80% improvement in myelopathy and pain and with low rate of complications (92). A further variation using a microscope, rather than an endoscope, through a more easily tolerated posterolateral approach similar to selective nerve root block—the minimally invasive transforaminal microdiscectomy—has been described in a preliminary report of 12 patients with satisfactory outcomes (75). Larger series are now available that report favorable outcomes following these minimally invasive approaches for simple discectomy, and this technique has also been adapted for discectomy with interbody fusion (50; 83). Transforaminal endoscopic approaches have been described, which expands the minimally invasive options, and a tubular system that allows a minimally invasive retropleural approach is also being used in some centers (38; 60). A majority of patients undergoing thoracic discectomy will not need instrumented fusion, and this decision is best made according to the surgical approach, considerations regarding preexisting abnormalities in spinal alignment, and the surgeon's prediction of delayed instability or kyphotic deformity. The group at Barrow Neurological Institute found that of 226 consecutive patients undergoing thoracic discectomy between 1992 and 2012, using various thoracotomy, thoracoscopy, and posterolateral approaches, only 78 required instrumented fusion; of the remaining 148 that underwent discectomy without fusion, only three (2.1%) underwent a second fusion surgery for delayed instability or deformity (65). Real-time stereotactic navigation using intraoperative CT (O-arm) has also refined the minimally invasive approach to transpedicular thoracic discectomy, particularly for central calcified rupture (63).
Negwer and colleagues have presented a series of 12 patients with large central calcified disc presenting with compressive myelopathy that were approached through a posterior, transdural route (64). This allowed direct manipulation of the calcified disc material while visualizing the spinal cord directly, thus, avoiding the occult spinal cord injury and deficit that can occur with instrument impact or trauma to the closed dura. All 12 patients had neurologic recovery with surgery, with four sustaining transient deficits that cleared by discharge. LeRoy and colleagues describe a similar posterior transdural approach for both soft and calcified thoracic disc herniations by creating a ventral dural “sling” that permits safe rotation of the spinal cord away from the operative trajectory (48).
Complications from thoracic disc surgery continue to be significant—29% overall by meta-analysis of the literature—despite the various tailored approaches, including neurologic injury (5%), spinal fluid leakage (8%), wound healing issues (11%), and medical complications (21%) (15). A large series of 257 thoracic disc surgeries presented by a Chinese group from Peking University was studied for postoperative neurologic deficits, noting 16 patients with significant postoperative decline (6.23%) (100). Ten of these patients had excellent neurologic recovery within 6 months of surgery, and an additional four of the 16 had partial recovery by 9 months. Deficits were associated with higher spinal canal occupancy ratio, U-shaped compressed spinal cord, calcified herniated disc, anterior approach, and massive intra-operative blood loss (greater than 1500 ml). The authors encouraged full disclosure of the high risk of these surgeries so that patients and family were aware of the significant chance of transient or permanent postoperative deficits, and the possible need for months of recovery (100).
Special considerations
Pregnancy
Not enough data exist concerning the relationship between pregnancy and thoracic disc disease.
Anesthesia
General anesthesia is required for surgically decompressing the thoracic spine. The anterior approaches require a thoracotomy for accessibility, requiring special intubation of the ipsilateral main stem bronchus.
Media
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Contributors
All contributors' financial relationships have been reviewed and mitigated to ensure that this and every other article is free from commercial bias.
Author
-
Saul S Schwarz MD
Dr. Schwarz of the University of Colorado Health Sciences has no relevant financial relationships to disclose.
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Editor
-
Randolph W Evans MD
Dr. Evans of Baylor College of Medicine received honorariums from Abbvie, Amgen, Biohaven, Impel, Lilly, and Teva for speaking engagements.
See Profile
Former Authors
- Peter C Shin MD (original author), Aftab Karim MD, Anil Nanda MD, Donald Smith MD, Rajesh Acharya MD, Richard Polin MD, Ibrahim Ali Omeis MD, and Vikas Rao MD
Patient Profile
- Age range of presentation
-
- 19 to 65+ years
- Sex preponderance
-
- male=female
- Heredity
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- none
- Population groups selectively affected
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- none selectively affected
- Occupation groups selectively affected
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- none selectively affected
ICD & OMIM codes
- ICD-9
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- Degeneration of thoracic or thoracolumbar intervertebral disc: 722.51
- ICD-10
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- Other specified intervertebral disc degeneration: M51.3
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