14 Midline Disc Herniations of the Thoracic Spine Abstract Symptomatic midline thoracic disc herniations (TDHs) are uncommon. Typically, TDHs are degenerative in nature, presenting with back pain progressing to myelopathy. Thorough physical examination and proper diagnostic imaging are vital as symptomatology can initially be difficult to isolate to the thoracic spine. The majority of cases can be treated conservatively; however, early surgery is key in the presence of neurological compromise or unremitting pain. Calcification and location must be evaluated, as preoperative planning is dependent on these characteristics. Posterior decompressive laminectomies are not recommended due to a high risk of neurological deterioration. Ideal surgical approaches to thoracic spine for midline disc herniations allow direct exposure of the herniation with minimal to no spinal cord manipulation. The majority of patients improve with timely and appropriate surgical intervention; however, there is a real risk of neurological deficits with surgery. Keywords: midline, thoracic, disc herniation, calcified, transpedicular, costotransversectomy, lateral extracavitary, myelopathy Clinical Pearls • The majority of midline thoracic disc herniations (TDHs) are asymptomatic. Of the symptomatic cases, approximately 63% may be treated with conservative management. • Midline TDHs are more likely to cause myelopathy than lateral TDHs. • Early surgical management in patients with myelopathy is recommended to avoid rapid deterioration. • About 70% of TDHs are calcified, requiring appropriate preoperative planning to gain optimal midline and ventral exposure. • Confirmation of spinal level with intraoperative fluoroscopy or preoperative radiographic tagging/marking and correlation to preoperative imaging is vital. • Laminectomy for access to midline disc is not recommended due to high risk of neurological deterioration. • Minimally invasive lateral and anterior transthoracic approaches have lower risk of new postoperative neurological deficits and are best for calcified midline TDH. • Instrumented fusion should be considered when extensive bone resection is conducted and instability is suspected. The true incidence of thoracic disc herniations (TDHs) is difficult to ascertain as many tend to be asymptomatic; however, it is estimated that 1 in 1 million people per year develop symptoms at some point.1 In stark contrast to the cervical and lumbar regions, the thoracic spine accounts for 0.25 to 0.75% of all symptomatic disc herniations, representing 0.15 to 4% of all disc surgeries.1,2,3 The lower incidence of TDH is likely due to the rigidity of the thoracic spine afforded by the stabilizing ribs. For this reason, 75% occur below T8, mostly at T11–T12—the more mobile region of the thoracic spine. The majority of TDHs occur in the midline (94%).3,4,5,6 Most (80%) TDHs occur in the third to fifth decades and tend to be a result of degenerative disc disease in the thoracolumbar spine.2,4 These disc herniations are more likely to be calcified, which occur in up to 70% of all TDHs.7 Calcified disc herniations can become adherent to the ventral dura (44%) and may be associated with an intradural component in up to 17% of cases.8 Younger patients typically have soft disc herniations and often have a history of trauma.9 These patients have acute onset of symptoms. There are two beliefs on the pathogenesis of neurological symptoms from thoracic disc herniations: direct spinal cord compression and vascular compromise. The thoracic spinal cord anatomy lends itself to be more vulnerable to direct compression than the cervical and lumbar spine. The central canal diameter is smaller with shorter pedicles, accounting for 40% of the canal being occupied by the spinal cord, whereas the cervical cord occupies 25% of the central canal.10 The thoracic kyphosis places the spinal cord more anteriorly in the canal, in near proximity to the posterior longitudinal ligament and intervertebral disc. When a central TDH occurs, posterior migration of the spinal cord is limited by the dentate ligaments, which anchor the cord to the dura increasing the effects of spinal cord compression. The spinal cord is fed by a single midline anterior spinal artery and paired posterior spinal arteries. The anterior spinal artery supplies the majority of the spinal cord, except the dorsal columns. Midline thoracic disc herniations may cause compression of the anterior spinal artery, leading to vascular insufficiency and even thrombosis. Vascular insufficiency may explain instances where symptomatology is localized to higher spinal levels than that of the thoracic disc herniation. Abrupt neurological decline may also be explained by vascular compromise, especially in the setting of chronic disc herniations. Thoracic disc herniations can present in various ways. Initially, most patients have axial thoracic back pain (57%) which later progresses to a combination of both motor and sensory symptoms (61%). Pain is typically in a band-like distribution radiating ventrally along thoracic dermatomes.4 The sensory and radicular pain pattern on physical examination can provide vital detail into localization of the herniated thoracic disc to a specific level. Because of pain anteriorly on the chest and abdomen, the clinical presentation may be confused with cardiac, pulmonary, or abdominal etiologies. Bladder dysfunction occurs in 30% of cases.4 Signs of myelopathy, including increased deep tendon reflexes of the lower extremities, clonus, and positive Babinski sign, are worrisome. Midline herniations are more likely to be associated with cord compression and myelopathy than lateral disc herniations, which cause radicular symptoms. As with all spinal pathologies complete and thorough physical examination is required. Diagnostic imaging has now become the mainstay in evaluation for spinal pathology with the use of magnetic resonance imaging (MRI), computed tomography (CT), and myelography. Imaging findings should be correlated with symptoms and physical examination findings, especially in cases with multiple thoracic disc herniations. MRI can provide information on soft tissue, particularly the intervertebral disc and spinal cord. The degree of ventral compression can be assessed by evaluating surrounding cerebrospinal fluid (CSF) and deformation of the spinal cord, however, disc herniations may be exaggerated on T2 sequences. Spinal cord edema noted by the T2 signal changes can shed light onto the severity of compression. MRI has the potential to distinguish intradural disc herniations. Although difficult to ascertain, calcifications in a disc are hypointense on T1 and T2. Thoracic CT is vital to assess bony anatomy and evaluate for calcified discs, which impacts surgical planning. CT myelography is an option when an MRI is contraindicated or cannot be obtained. A focal disruption in contrast in the CSF can indicate a herniated disc; however, a complete block is only found in 10 to 15% of cases.11 Nerve roots, bone anatomy, and calcified disc can be characterized with myelography, but information about the spinal cord parenchyma cannot be assessed. Spinal radiographs may aid in identification and localization of calcified discs; however, because of more specific and detailed imaging modalities, it has a limited use in diagnosis of TDH. Spinal radiographs can provide information on global alignment, regional kyphosis or lordosis, and signs of instability on dynamic imaging—all of which can impact surgical planning and indications for possible fusion and instrumentation. Nonsurgical management of thoracic disc herniations is the first course of treatment when pain is the only symptom. Brown et al found that 63% of patients notice an improvement in pain with conservative management, which includes nonsteroidal anti-inflammatory drugs, oral pain medications, oral steroids, epidural steroid injections, physical therapy, and bracing.12 When sensory changes or radiculopathy in dermatomal distribution are the only symptoms, all measures of conservative therapy should be first exhausted before attempting any surgical options. Radiofrequency ablation, facet injections/blocks, nerve root rhizotomies, and transforaminal epidural steroid injections are all preferred methods of treatment in patients who have no neurological compromise. Patients should be referred for pain management for further treatment options. Although few thoracic disc herniations require intervention, indications for surgical treatment of thoracic disc herniations include (1) pain that is refractory to conservative management and (2) signs of myelopathy, including hyperreflexia of patellar and Achilles reflexes, Babinski sign, clonus, ataxic gait, lower extremity weakness, and bowel or bladder dysfunction. Surgical treatment of midline thoracic disc herniations requires detailed preoperative planning tailored to each case. Localization of the correct disc space is vital on intraoperative fluoroscopy by counting up from the sacrum, and must be confirmed with preoperative imaging studies. Simply assuming the most caudal rib as T12 may lead to miscounting and arrival at the incorrect level due to inconsistency of lower ribs from patient to patient. Unique morphological characteristics that are also seen on preoperative imaging studies can be utilized to further confirm correct level. Alternatively, patients can be referred to interventional radiology to mark specific thoracic level prior to surgical intervention. Calcified discs should be identified preoperatively and evaluated for potential intradural components. These discs are more likely to be adherent to the ventral dura, leading to higher risks of durotomy. Calcified discs require a more extensive resection of the surrounding bony structures to safely remove the disc without retraction on the spinal cord. Typically, in order to avoid a durotomy and neurological injury, a thin shell of calcified disc is left if it is severely adherent to the ventral dura ( Historically, a posterior approach with a decompressive laminectomy was the treatment for TDH. However, this has been abandoned due to high risk of neurological compromise, as excessive spinal cord retraction is needed to remove a central disc. As shown in The lateral surgical corridor comprises the costotransversectomy approach, developed by Menard in 1894, and later revised by Larson in 1976 as the lateral extracavitary approach.13,14 Both require resection of the ipsilateral transverse process, rib head, and pedicle to obtain exposure to the disc space. The corridor remains in the retropleural space, reducing pulmonary complications and without the need for a chest tube. Midline exposure is limited with a costotransversectomy—reserving this approach as best for paracentral disc herniations. However, with further lateral resection of the rib the midline can be accessed with a lateral extracavitary approach. A rhizotomy is conducted to further open a corridor toward the midline. However, both approaches have limited exposure of the ventral dura, making resection of a calcified midline TDH difficult. If a durotomy is encountered, repair of a ventral tear is usually not possible. The segmental artery is typically ligated when exposing the lateral vertebral body. There is a risk of vascular compromise to the spinal cord if the artery of Adamkiewicz, a major medullary feeder, is injured.
14.1 Epidemiology
14.2 Pathogenesis
14.3 Clinical Presentation
14.4 Diagnostic Evaluation
14.5 Nonsurgical Management
14.6 Surgical Management
14.6.1 Indications for Surgery and Preoperative Planning
Fig. 14.1).
14.6.2 Surgical Approaches
Fig. 14.2, an appropriate surgical approach must be utilized to obtain adequate access to the midline of the disc bilaterally and the ventral dura, with minimal to no retraction and manipulation of the spinal cord. A laminectomy or transpedicular approach does not accomplish this goal. 
Table 14.1 summarizes the advantages and disadvantages of each approach for midline TDH.
Costotransversectomy and Lateral Extracavitary
Thoracic Key
Fastest Thoracic Insight Engine
