Thoracic Discogenic Syndrome

Etiology

Degenerative changes constitute the primary factor behind thoracic discogenic syndrome. As individuals age, the intervertebral disk undergoes a reduction in water content, leading to a gradual loss of its ability to absorb axial loads.[4] This process contributes to the occurrence of disk herniations, annular tears, and the degeneration of endplates. The resulting herniated disks have the potential to exert pressure on nerve roots and the spinal cord. Trauma to the thoracic spine serves as the cause of thoracic discogenic syndrome in approximately 10% to 20% of patients. Engaging in sports such as golf, softball, and baseball, which involve axial spine rotation, elevates the risk of thoracic disk herniation for individuals participating in these activities.[4]

Epidemiology

Thoracic disk herniations are uncommon and typically asymptomatic, often detected incidentally during MRI scans. Autopsy studies in the United States reveal an incidence of 7% to 15%. The incidence based on imaging studies varies between 11% and 37%, depending on the imaging modality used. 

Symptomatic thoracic disk disease comprises 0.3% to 0.8% of all symptomatic disk diseases.[5][6][7] Nearly 80% of affected individuals manifest symptoms in their thirties or forties, with 75% of the affected disks located below the level of the T8-T9 disk. The most commonly affected level is the T11-T12 disk.[5][7] Annually, the occurrence of patients with detectable objective examination findings stands at 1 in 1 million.[4] Surgical intervention for thoracic disk disease is uncommon, with hospital admissions for disk disease related to the thoracic region ranging from 0.13% to 0.15% and constituting 0.2% to 4% of all diskectomies.

Pathophysiology

The thoracic spine is relatively rigid. Articulation with the ribs provides stability in the midsagittal plane but leaves the thoracic spine vulnerable in the lateral and rotational planes. The following features of the thoracic spine increase the risk of spinal cord compression at this level.

• The physiological kyphosis places the spinal cord closer to the posterior aspects of the vertebral bodies.

• A smaller ratio of the spinal canal to the spinal cord.

• Watershed area at the thoracic cord.

• Ossified or calcified discs in 42% of cases.

• Intradural extension of the disk in 70% of cases.

• Reduced mobility of the spinal cord due to denticulate ligaments.[8][9]

The mid-lower region has higher axial loading and is also the turning point of the kyphotic curvature of the thoracic spine.[10] The compressive load stress is maximum at the T8-T9 disk space.[11] Only 4% of cases are above the level of the T2-T3 disk.[12] Approximately 70% of thoracic disk herniations are central or centrolateral. A thoracic herniation comprising more than 40% of the spinal canal is considered a giant herniation. In addition to herniating into the spinal canal, disks can herniate through the vertebral endplates directly into the adjacent vertebral bodies, referred to as Schmorl nodes or cartilaginous nodes.

Approximately 40% of thoracic herniated disks undergo calcification. Rarely, the attachment of this calcified disk to the dura may result in erosion, leading to a cerebrospinal fluid leak. This condition can cause atypical symptoms such as orthostatic hypotension, headaches, and intracranial hypotension, warranting immediate medical intervention.[13]

The mechanical compression of the spinal nerve root or spinal cord within the canal does not solely account for the pain resulting from a herniated or degenerated intervertebral disk. Isolated tears in the annulus fibrosis can transmit painful information to the dorsal root ganglion through the sinuvertebral nerve. Pain may also be a consequence of inflammation affecting the nociceptive neurovascular supply of the outer annulus of the intervertebral disk. In addition, nerve growth factor–dependent neurons contribute to pain modulation in response to intervertebral disk inflammation by transmitting sensory information to dorsal root ganglions, the spinal cord, the brainstem, the thalamus, and cortical areas, resulting in the perception of pain. New nerve fibers extend into the matrix of the inner annulus fibrosus and cartilaginous endplate toward the nucleus pulposus, expanding the distribution of nociceptive nerve endings in the degenerated intervertebral disk. In addition, mechanical and chemical stimuli modify the function of sensory nerves, rendering them hypersensitive and inflammatory. 

Some researchers suggest the concept of disk dysgeneration as opposed to degeneration in patients with isolated thoracic degenerative disk disease.[11] A study reveals that in patients with isolated thoracic disk disease, the location of Schmorl nodes in the thoracic spine is independent of age in adulthood, suggesting a potential developmental etiology.[11] The prevailing thought is that some disks, which appear hypointense earlier on MRI, are never hydrated, as opposed to degeneration, due to water loss in the intervertebral disks. Previous research evaluating the linkage between Schmorl nodes and low back pain reveals that only the combination of a hypointense disk and endplate signal change, with or without Schmorl nodes, is significantly associated with low back pain.

History and Physical

History

As mentioned earlier, most thoracic disk herniations are asymptomatic and are discovered incidentally during MRI scans. Unlike lumbar and cervical disk herniations, thoracic disk herniations have atypical symptoms and are often a diagnosis of exclusion. To diagnose thoracic discogenic pain syndrome accurately, obtaining a detailed history and performing a thorough physical examination are crucial. Assessment of the quality, intensity, and distribution of the pain and alleviating and aggravating factors is essential for a comprehensive patient evaluation.[14]

Pain is the most common symptom associated with thoracic discogenic syndrome. Initially, the pain may be dull and localized to the thoracic region. Lesions in the upper thoracic region may manifest as lower cervical pain, while those in the lower thoracic region may manifest as upper lumbar pain. Pain from thoracic disk herniations may further complicate matters by referring to the epigastric, retrosternal, or inguinal areas, expanding the differential diagnoses to include cholecystitis, myocardial infarction, hernia, or nephrolithiasis. The pain typically progresses to develop radicular, myelopathic qualities, or both, depending on whether the herniated disk compresses the nerve roots or the spinal cord itself.

Isolated annular tears may have different referral patterns based on the location of the tear. Anterior tears may cause pain in the ribs, chest wall, sternum, or visceral structures. Lateral tears can cause radicular pain in both visceral or musculoskeletal sites, and posterior tears generally cause local or diffuse back pain. 

Thoracic disk herniations occur in 4 places as follows: 

• Central thoracic disk herniations are most likely to cause spinal cord compression and myelopathic symptoms. Expected findings may include increased muscle tone, hyperreflexia, abnormal gait, and urinary or bowel incontinence.

• Centrolateral thoracic disk herniations can present with ipsilateral weakness and contralateral pain or sensory disturbances, causing a syndrome that mimics Brown-Sequard syndrome.

• Lateral thoracic disk herniations most likely cause radicular pain due to compression of the spinal nerves as they exit the intervertebral foramen. Radicular pain usually radiates towards the dermatome of the nerve roots innervated by the exiting nerve.

• Intradural thoracic disk herniations are rare and occur in less than 10% of cases.

Nerve root compression: Patients with spinal cord compression present with pain following a dermatomal distribution. Burning, electrical, or shooting are common terms used to describe the pain. Helpful dermatomal landmarks for thoracic disk herniations are as follows:

• T1 nerve root compression causes pain that radiates to the medial forearm.

• T2 nerve root compression causes pain that radiates to the axilla.

• T4 nerve root compression causes pain that radiates to the nipple area.

• T10 nerve root compression causes pain that radiates to the umbilicus.

• T12 nerve root compression causes pain just superior to the inguinal ligaments.

The T10 dermatome is often the focus of pain regardless of the involved dermatome. Sensory symptoms such as numbness and paresthesias occur in 25% of patients. Patients with nerve root compression also experience sensory symptoms in a dermatomal distribution.

Spinal cord compression: Patients affected by spinal cord compression experience myelopathy. The pain and sensory disturbance can be experienced anywhere below the affected spinal cord level. Additional symptoms include lower extremity numbness and weakness, gait abnormalities, hyperreflexia, and, in rare cases, paraplegia. Approximately 25% of patients with myelopathy due to thoracic disk herniation present with isolated sensory symptoms. The combination of intracranial hypotension, postural hypotension, and headache signifies a potential cerebral spinal fluid leak due to a tear in the dura from an adherent calcified disk. 

Approximately 17% of patients with thoracic discogenic syndrome can present with weakness as their only symptom. The thoracic nerves innervate the muscles of the intracostal and abdominal walls. Weakness in the abdominal wall and intercostal muscles is usually a late finding, and lower extremity weakness due to myelopathy is more likely. Bowel or bladder incontinence suggests myelopathy and is the presenting feature in 2% of affected patients.

Physical Examination

The physical examination begins with a thorough evaluation of the cervical, thoracic, and lumbar spine, and the hips and abdomen. Findings may include myofascial pain, inflexibility, and weakness, predisposing the patient to thoracic discogenic syndrome. A sensory examination should include an assessment of sensation with pinprick and touch in the upper extremities, thorax, abdomen, and lower extremities. Consistent sensory loss below 1 dermatome suggests myelopathy. Evaluation of muscle strength in the lower extremities and abdominal muscles is necessary. A lesion at the T9 and T10 nerve roots may result in paralysis of the lower abdominal muscles but spare the upper abdominal muscles. The result is an upward movement of the umbilicus when the abdominal wall contracts, known as the Beevor sign. Testing of the lower extremity strength and deep tendon reflexes is also necessary. Lower extremity weakness associated with spasticity or hyperactive reflexes indicates myelopathy. 

Evaluation

Radiology Studies

The diagnosis of thoracic discogenic syndrome involves a thorough musculoskeletal and neurological examination. Initial imaging may begin with plain radiographs. Although plain radiographs are not specifically designed to diagnose disk herniations, they provide information regarding fractures, neoplasms, dislocations, and infection. Osteophytes and disk-space narrowing suggest degenerative disk disease. Approximately 70% of individuals experiencing thoracic disk herniation exhibit calcification in their thoracic disks, highlighting this discovery as a reliable indicator of thoracic disk herniation. Calcification of the disk is only present in 4% to 6% of patients with cervical or lumbar herniations.

The advent of MRI has led to the less frequent usage of computed tomography (CT) myelography. CT myelography helps diagnose lateral disk herniations and visualize calcifications and is most useful in preoperative planning. MRI is the preferred screening imaging modality due to its high sensitivity and specificity, allowing for the visualization of the surrounding soft tissue.[14] 

In addition to a thorough neurological examination, an MRI of the thoracic spine is highly sensitive and specific for diagnosing thoracic disk herniations. In some situations, thoracic diskography can confirm that the pain is of discogenic origin, as most thoracic discogenic syndrome can be asymptomatic.[14] Advancements in technology have enhanced the ability to detect thoracic disk herniations. Magnetic resonance images cannot predict the prognosis or clinical significance of identified lesions. MRI is also less sensitive in detecting annular tears, especially in the thoracic region. Therefore, emphasizing the importance of the patient's history and physical examination is crucial for accurate diagnosis and treatment planning.

Researchers have proposed a classification system for thoracic disk herniations, with a recent study indicating that this system has a high interrater and intrarater reliability.[14] This system categorizes herniations into following 5 types:

• Type 0: small herniation involving ≤40% of the spinal canal without significant spinal cord or nerve root effacement.
• Type 1: small herniation with a paracentral location.
• Type 2: small herniation with a central location.
• Type 3: giant herniation involving >40% of the spinal canal with a paracentral location.
• Type 4: giant herniation with a central location.

Types 1 to 4 have both clinically and radiologically evident spinal cord compression.[14]

Electrodiagnostic Studies

Nerve conduction studies, needle electromyography, and somatosensory evoked potentials can provide helpful additional diagnostic information. Due to their inability to localize the level of involvement and the risk of pneumothorax and penetration of the abdominal cavity, they are particularly useful for ruling out other possible diagnoses, such as cervical radiculopathy, lumbosacral radiculopathy, and peripheral neuropathy. Somatosensory evoked potentials distinguish between upper motor neuron and lower motor neuron processes. 

Diskography 

During a diskogram, the medical professional injects contrast material into the disk and observes the patient's response. The reproduction of pain similar to the patient's complaints suggests that the disk is the source of the pain. Diskograms are most valuable when they demonstrate single-level concordant pain associated with endplate irregularities or annular tears, and the adjacent disks are normal.

Treatment / Management

The initial treatment of thoracic discogenic syndrome is typically conservative, including rest, anti-inflammatory medications, and physical therapy.[6] The initial goal is pain reduction, with a rehabilitation program involving adjustments to daily activities with a focus on proper posture and body mechanics. This helps prevent further injury and reduce intradiskal pressure from activities such as sitting, bending, or heavy lifting. Electrical stimulation should be limited to the early stages so affected patients can focus on treatment modalities that encourage strengthening and increased flexibility. Bed rest should be limited to 2 days or less.

During the recovery phase, rehabilitation programs focus on extension-based strength exercises and continued focus on proper posture and body mechanics. Effective pain management, often utilizing nonsteroidal anti-inflammatory medications, acetaminophen, or other agents, may be necessary to allow participation in therapy sessions. As pain decreases, the focus switches to a stabilization and maintenance program, including strengthening the abdominal and gluteal muscles.

Epidural Steroids

Thoracic epidural steroid injections are a viable option for patients experiencing persistent significant pain despite conservative treatment, particularly for those who are not suitable candidates for surgery or prefer nonsurgical interventions. Injections can be in a series of 1 to 3 at least 1 month apart. However, a repeat injection is not recommended if the first injection does not provide relief. 

Medications

Nonopioid analgesics: Initial therapies involve nonsteroidal anti-inflammatories such as ibuprofen 400 to 800 mg every 6 to 8 hours or acetaminophen 650 mg every 6 hours for 1 to 2 weeks. However, recent evidence reveals that acetaminophen is ineffective for radicular pain.[15] Nonsteroidal medications should be avoided in patients with renal disease, gastritis or peptic ulcer disease, and cardiovascular comorbidities. Patients with hepatic disease should avoid acetaminophen. Studies have demonstrated that nonsteroidal anti-inflammatories may not have a statistically significant effect on radicular pain, but they contribute to overall improvement compared to placebo.[16][17] (A1)

Opioid analgesics: For patients who have failed alternative medications, prescribing opioid medications such as oxycodone on a scheduled basis instead of as needed is recommended. This approach establishes a baseline dose to achieve adequate analgesia and enables active participation in a rehabilitation program. Tramadol, a nonopioid, is also a potential alternative.

Muscle relaxants: Studies reveal that skeletal muscle relaxants such as cyclobenzaprine and tizanidine are effective for short-term pain relief in acute lower back pain but may cause sedation.[15](A1)

Corticosteroids: Oral glucocorticoids may provide limited pain relief in patients with thoracic disk herniations. Although dose-dependent and more likely associated with long-term courses of corticosteroids, the significant adverse effects associated with corticosteroids are elevated blood pressure, mood disorders, psychosis, insomnia, gastritis, ulcer formation, gastrointestinal bleeding, hyperglycemia, bone loss, and heightened risk of infections.[15](A1)

Other: The antidepressant duloxetine, a selective serotonin-norepinephrine reuptake inhibitor, has demonstrated moderate efficacy in treating chronic low back pain. Patients initiate treatment at a dosage of 30 mg/d for 1 week, followed by a subsequent increase to 60 mg/d thereafter.

Surgery

No strict guidelines exist for the indications for thoracic disk surgery. Myelopathy, persistent axial back pain, refractory intercostal neuralgia, and intractable radiculopathy are all indications for surgical interventions.[10][4]

Surgery involves the removal of the ossified disk and the decompression of the nerve or spinal cord. Despite advancements in thoracic disk herniation surgery, 20% to 30% of patients experience complications.[9] The limited space within the thoracic spinal canal and the tenuous blood supply in the area puts the spinal cord at an increased risk of compromise.[14] The presence of the ribs, sternum, heart, and lungs also makes thoracic disk decompression more challenging. A posterior laminectomy was the initial surgical treatment and eventually stopped due to the high complication rate. Nearly 35% of patients following laminectomies experienced neurological deterioration due to the inevitable manipulation of the spinal cord, causing cord ischemia.[18][14] Consequently, newer approaches have been developed, including anterior, lateral, and posterolateral techniques.[9] Among these approaches, the anterior transthoracic approach offers an optimal corridor but causes increased in-hospital morbidity and mortality rates compared to nonanterior approaches.[9] Calcified and adherent herniations pose a risk of dural tears during surgery, leading to cerebrospinal fluid leaks and complications such as intracranial and orthostatic hypotension and headaches.[9](B2)

Thoracic disk surgery typically involves a diskectomy but may also require a fusion. Fusion is recommended when there are multilevel herniations, herniations in the context of Scheuermann disease, with resection of more than 50% of the bone from the vertebral body, and in patients with preoperative back pain or herniation at the thoracolumbar junction. The primary objective of thoracic disk surgery is to achieve sufficient neural decompression, establish a solid bony fusion when necessary, and avoid approach-related injuries.[19] Some risks associated with surgery include neurological worsening, dural breach, subarachnoid-pleural fistulas, intercostal neuralgia, cerebral spinal fluid leak, atelectasis, pleural effusion, paraplegia, and monoplegia.(B2)

There is no gold standard approach to thoracic disk surgery.[18] Instead, the surgical approach is tailored to the individual.[4] Single-level microdiskectomy does not hamper kinematics and load-deformation relationships.[18] (B2)

Some surgeons recommend arteriography to locate the Adamkiewicz artery or the dominant thoracolumbar segmental artery that supplies the spinal cord. Locating this artery aids in determining the appropriate side for a transthoracic approach, as it often arises from the left side between the T9 and L1 vertebrae, where thoracic disk herniations commonly occur. Although magnetic resonance angiography is less invasive compared to traditional angiography, it has limited resolution. There is currently no consensus regarding the use of intraoperative neurological monitoring during thoracic diskectomy.

Posterolateral approaches: Soft lateral hernias and multilevel compression due to ossification of the posterior longitudinal ligament warrant a posterolateral approach. 

• The posterior approach and a unilateral or bilateral arthrectomy provide access to the disk space.

• The posterior side of the vertebral body is reamed until curved currettes and angled tamps can gradually collapse the hernia.

• Fusion occurs in all cases. 

• The overall reported complication rate is 12% to 30%.

• After reaming the posterior margin of the vertebral body, some surgeons visualize the anterior side of the sheath with an angled endoscope, allowing access to central hernias without damaging the dural sheath.

• Chi et al propose performing transpedicular microscopic diskectomy through an endoscope tube to reduce morbidity.[10]

 Lateral or retropleural approaches:

• Retropleural costotransversectomy was popular until the 1980s due to its better lateral view compared to the posterior approach, but it resulted in more tissue damage.[20]
(B2)

• Lateral extracavitary approaches offer a more central view compared to posterolateral approaches without the drawbacks of anterior approaches.
  • Associated with a 30% risk of pleural breach and the need for a thoracic drain.[20]
(B2)

Anterior approaches: 

• Provide a direct view of the hernia and the sheath, particularly for central or calcified hernias.

• Associated with a higher morbidity rate of 21% to 39% due to the thoracotomy.[14]

• Higher morbidity led to the development of thoracoscopy techniques.
  • Thoracoscopy is the preferred approach for small lateral and noncalcified thoracic hernias.
  • The prolonged learning curve and limited magnification limit thoracoscopy.
  • Thoracoscopy continues to have a 21% complication rate.

• A retropleural approach reduces morbidity by providing a direct approach to the thoracic spine and preserving the pleura.

• Open mini-thoracotomy, preferably retropleural, appears to be the best compromise for reducing the morbidity of thoracotomy while getting around the challenges associated with thoracoscopy. Despite the reduced morbidity, the risk of destabilizing facet bone and higher odds of requiring a chest tube still exists.[14]

Summary of Surgical Approaches

• The recommended approach for soft lateral herniations is posterolateral.

• Central herniations are difficult but possible to visualize using posterolateral approaches.

• Nearly every case approached through a posterior approach requires an instrumented fusion.

• Minimally invasive transtubular approaches are possible and reduce morbidity.

• Lateral extrapleural approaches provide a more mid-line approach to the dural sheath but are more damaging to the tissues.

• Transthoracic approaches are safer for giant, calcified, central hernias but result in more complications.

• Thoracoscopy reduces the morbidity associated with thoracotomy, but the learning process is lengthy. 

Full Endoscopy Versus Conventional Microsurgical Techniques

Benefits: When comparing full endoscopy to conventional microsurgical techniques, the advantages encompass improved visibility, minimized access to trauma, reduced risk of instability, fewer complications, decreased recovery time, early return to activity, and financial benefits.[21]

Foraminoplasty is the pivotal step for ensuring adequate working area throughout the decompression.

• Using the superior articular process as a landmark guides the working cannula to prevent entry into the spinal canal.

• The superior articular process serves as a fulcrum during bone graft bed preparation.

• The superior articular process can be utilized as an autograft for fusion, offering an alternative to relying on an allograft and recombinant bone morphogenetic protein 2 (rhBMP-2).

Limitations: When comparing full endoscopy to conventional microsurgical techniques, limitations arise, such as cost, a 2-dimensional view, a steep learning curve, challenges in managing intraoperative complications, and hindrances posed by rib heads and scapula in the upper thoracic spine.[14]

A systematic review reveals that a surgeon needs a minimum of 20 to 30 consecutive cases for the most minimally invasive techniques and 22 to 33 cases for full endoscopic diskectomy to achieve proficiency.

Differential Diagnosis

The possible differential diagnoses for thoracic discogenic syndrome include mechanical back pain, discal cyst, synovial cyst, osteophytes, cholecystitis, nephrolithiasis, myocardial infarction, osteoma, metastasis, epidural hematoma, lumbosacral radiculopathy, cervical radiculopathy, cervical disk injury, lumbar disk injury, lumbosacral spondylolysis, lumbosacral spondylolisthesis, lumbosacral discogenic syndrome, osteodiscitis with abscess, and benign intra-axial tumors such as a meningioma or schwannoma.[22][23]

Prognosis

Nearly 80% of patients return to their previous activity level with conservative measures. However, for those who persist with intractable pain, bilateral symptoms, or neurologic deficits, surgical intervention is often necessary. Surgical treatment of thoracic disk herniation results in the following outcomes:

• Neurological improvement in 50% of patients.
• Preservation of spinal stability in 40% of patients.
• Neurological worsening in 5% of patients.[24]

Complications

The surgical complication rate is 20% to 30%.[9] The following list contains potential surgical complications.

• Increased incidence of pneumonia and other pulmonary and mediastinal complications is higher in anterior approaches.[18][10]
  • The rate of pneumonia in patients undergoing an anterior approach is 6% compared to 1%, 3%, and 0% in the lateral, transpedicular, and laminectomy approaches, respectively.

• Spinal cord compromise.[10]

• Worsening neurologic symptoms.

• Segmental instability.[25]

• Radiation hazards following intraoperative fluoroscopy usage.
  • In a study investigating orthopedic, urology, and plastic surgeons, orthopedic surgeons have twice the expected rate of total cancers and 2.9 times the rate of expected breast cancers.[26]

• Symptom recurrence rate of 0.5% to 25%.[4]

• Increased intracranial pressure and seizures following saline perfusion in endoscopic surgeries.

• Dural tear causing cerebrospinal fluid leakage and pseudomeningocele.[10][19]

• Intercostal neuralgia.[14]

• Delayed progressive neurological deficits.
  • Occur in 23%.
  • Primarily due to hypotension, instrumentation-related compression, or an epidural hematoma.[9]

• Abdominal pseudo-hernia.[27]

• Horner syndrome.[12]

Endoscopic procedures are increasingly popular due to the high complication rate associated with open techniques. The complication rate of endoscopic techniques is 20%.[14] A meta-analysis of endoscopic techniques, 90% using a transforaminal approach, reveals no cases of infection or death.[28] The remaining complication rates in this study reveal dural tears at 1.3%, dysesthesia at 4.7%, recurrent disk herniation at 2.9%, myelopathy at 2.1%, epidural hematoma at 1.1%, and reoperation at 1.7%.[28]