The central segment of the spine that is attached to the ribcage is termed the thoracic spine, and it is made of vertebral levels T1-T12. If insult occurs to one or more of the T1-T12 spinal nerves, it is called thoracic radiculopathy. If the neural insult involves the spinal cord in the thoracic region with the corresponding upper motor neuron signs, it is termed thoracic myelopathy.
Thoracic radiculopathy is due to spinal nerve insult, usually secondary to intervertebral disc pathology (herniation, discitis).
Other less common etiologies of thoracic radiculopathy include metabolic disturbances such as diabetic thoracic radiculopathy, post herpetic neuralgia, and mechanical compression from infections or tumors.1,2,3
Thoracic myelopathy can result from any pathologic process disrupting the spinal cord from T1-T12. Myelopathy has been associated with thoracic disc herniation (TDH), vertebral body compression fracture, disc calcification, posterior longitudinal ligament and/or ligamentum flavum ossification, spinal stenosis, and anterior spinal cord herniation with prolapse through the dura mater. Infection, including osteomyelitis and epidural abscess are potential sources of spinal compression. Neoplasm is also a consideration, as the thoracic spine is the most common location for spinal mets.Demyelinating processes including multiple sclerosis must also be considered.1,2,3
Iatrogenic causes of thoracic myelopathy have been associated with a variety of spinal interventions, including epidural corticosteroid injections,spinal anesthesia, and neurolysis procedures using alcohol and phenol. These iatrogenic causes can be secondary to particulate steroid microembolism, vascular injury, vasospasm and direct toxicity of medication to neural structures.4 Thoracic myelopathy may result from ligature during lumbar sympathectomy, prolonged clamping during aortic aneurysm surgery, or transoperative microembolization of the anterior spinal cord artery. Dissecting aneurysms can interrupt blood supply to the thoracic cord. The thoracic spinal cord is considered a watershed area, and therefore ischemia is a greater threat compared with the cervical or lumbar cord.2 Intrathecal catheters can develop granulomas at the tip causing devastating compressive myelopathy. Radiation therapy can cause demyelination, focal necrosis and vasculitic changes of the thoracic spinal cord.1,3
Epidemiology including risk factors and primary prevention
Disc herniation is significantly less common in the thoracic spine compared with the cervical and lumbar spine, representing less than 5% of disc herniations.5 The most common location for disc herniation in the thoracic spine is at T11-T123A patient with Scheuermann’s disease has increased risk for TDH. Symptomatic TDH have an incidence of approximately 1 per one million persons. Asymptomatic TDH have an incidence as high as 37%; these may or may not increase in size and usually continue to be asymptomatic, not requiring any active treatment. Most patients present in the fourth to sixth decade, but TDH can affect all age groups with a 3:2 male-to-female ratio.5,6,7
In most cases, thoracic myelopathy is felt to be caused by degenerative changes with subsequent stenosis and cord compression. However, thoracic myelopathy caused by spondylosis is less common compared to myelopathy caused by spondylosis in the lumbar and cervical spine.8 Traumatic spinal cord injury is another cause of thoracic myelopathy, with injuries to the thoracic cord being less common than either cervical or lumbar. Risk factors for traumatic spinal cord injury include male gender and age between 20-40.
Skeletal: The thoracic vertebral canal has a smaller clearance (9.2 mm) between the spinal cord and the osseous wall than the cervical canal (11.3 mm). The cord/canal ratio in the thoracic spine is 40% compared to 25% in the cervical. Therefore, the thoracic spinal cord and nerve roots are at higher risk of injury from space-occupying lesions.3 The thoracic spine is naturally a stable portion of the spine, given its articulation with the ribs. A robust posterior longitudinal ligament is also protective in the thoracic spine against disc herniation.
Vascular: The ventral 2/3 of the thoracic spine receives its blood supply from the anterior spinal artery and the dorsal 1/3 from two posterior spinal arteries. The anterior spinal artery is fed by 4-5 radicular arteries, the largest of which is the artery of Adamkiewicz, which mainly supplies the lumbosacral spinal cord segments and can enter the cord anywhere from T10 to L5.9,10 It is here where particulate, insoluble steroids can occlude the blood supply to the cord. The venous plexus of the thoracic spine can serve as a conduit for neoplastic metastasis or the seeding of infections to the spine. As mentioned above the thoracic cord is considered a watershed area with a tenuous blood supply compared to the cervical and lumbar spinal cord.2
Neurologic: The spinal nerve is formed by the sensory fibers from the dorsal root and the motor fibers of the ventral root, and it exits the spine via the intervertebral foramen. Compression of the spinal nerve can thus present with sensory and/or motor symptoms.
Most symptoms/signs are due to direct compression of the nerve root or spinal cord by a degenerative disc or zygapophyseal joint. The high spinal cord-to-canal ratio and vulnerable blood supply makes the thoracic spinal cord more susceptible to injury from a TDH.3,9
Disease progression including natural history, disease phases or stages, disease trajectory (clinical features and presentation over time)
Thoracic radiculopathy is generally a reversible disease well managed by conservative treatment. Asymptomatic thoracic disc herniations usually resolve without intervention and overtreatment must be avoided.7 Retrospective studies suggest that 77% of patients with symptomatic TDH managed non-surgically to return to their prior level of activity.11 Some patients with radiculopathy will have progression of disease to include sensory deficits, and motor weakness, which may or may not be reversible. The potential deficits include loss of sensation in a band of skin on the abdomen or chest, weakness of the intercostal muscles and potentially weakness of the abdominal muscles. If the T1 nerve is involved deficits can be seen with intrinsic hand function, but aside from this, thoracic radiculopathy tends to less functionally debilitating than either cervical or lumbar radiculopathy.
Thoracic myelopathy can progress from subtle gait complaints to complete spinal cord injury. As the majority of patients with thoracic radiculopathy can be treated conservatively, signs of myelopathy such as bowel or bladder incontinence, profound motor weakness or hyperreflexia prompt evaluation by surgical colleagues.
Specific secondary or associated conditions and complications
There is evidence to support a link between chronic pain and worsening of depression.12 Thoracic myelopathy, if not properly evaluated and treated, may lead to irreversible spinal cord injury.13
2. ESSENTIALS OF ASSESSMENT
Thoracic radiculopathy most commonly presents with a burning or shooting pain, which can present as back, scapular, chest or abdominal wall pain depending on the level affected. The most common presenting complaint is “band-like” chest pain, present in 67% of patients.14 The pain of radiculopathy tends to follow a dermatomal distribution and is worsened by coughing or straining. The figure below demonstrates the various dermatomes, with the T1-T12 distributions having the potential to be affected by thoracic radiculopathy.
Myelopathy may manifest only by gait abnormalities and increased tendency to fall. It may run in course with orthostasis or autonomic dysreflexia (lesions over T6), bowel/bladder dysfunction, sexuality issues, sensory impairment (dysesthesia or anesthesia) and/or motor deficits.1,3,15
An asymmetric band-like dermatome sensory anomaly in the chest or abdominal wall is suggestive of thoracic radiculopathy, usually associated with neuropathic pain symptoms exacerbated by trunk movements.
The neurologic involvement of myelopathy can be classified and followed according to the American Spinal Injury Association (ASIA) Impairment Scale which can be found on its web site.16 Gait abnormalities, sensory deficits, weakness, hyperreflexia, increased muscle tone, bowel and bladder incontinence and up-going toes are generally seen in myelopathy, although subtle myelopathy may not provide definitive findings. In complete spinal cord injury, there will be no rectum sensation, and increased rectal tone with no volitional sphincter contraction.1,3
Myelopathy can present in a variety of unique syndromes, although clinically the symptoms may not fit perfectly into these categories.
Injury to the artery of Adamkiewicz leads to anterior cord syndrome, which is damage to the corticospinal tract, anterior horn cells and spinothalamic tracts presenting with hyporeflexia, atrophy, variable motor loss, decreased sensation, with preservation of proprioception and vibration sense due to sparing of the dorsal column.
The central cord syndrome presents with weakness, hyperreflexia and preserved sacral sensation with bowel and bladder function minimally affected. This syndrome generally causes weakness in spinal levels most proximal to the lesion as the neurons exiting the corticospinal tract for the anterior horn lie centrally in the spinal cord.
Tertiary syphilis (tabes dorsalis) and Vitamin B-12 deficiency can result in posterior cord syndrome, which is an insult to the dorsal column pathway. This syndrome displays deficits in gait due to proprioceptive loss with relative sparing of motor and sensory tracts.1,2,3
Disability caused by thoracic radiculopathy is usually secondary to pain. Activities of daily living (ADL) and simple work-related tasks may be affected, especially if intrinsic hand function is impaired due to lesions at T1.
Thoracic myelopathy results in functional disability relative to the spinal cord level affected. High thoracic myelopathy affects trunk control and mobilization of pulmonary secretions. The Spinal Cord Independence Measure (SCIM) is used for traumatic and non-traumatic, acute and chronic spinal cord injury. The walking index for spinal cord injury (WISCI) measures the ability to walk and need for assistance. The American Spinal Industry Association (ASIA) Impairment Scale helps predict functional expectations.16
When discitis is suspected, complete blood count (CBC), C-reactive protein test (CRP) and blood cultures should be performed. They should include checking for acid-fast bacillus in immunocompromised patients or travelers from endemic TB areas. Urologic evaluation may be indicated in myelopathy.
If pursuing conservative management of thoracic radiculopathy it is reasonable to start with plain films and to delay magnetic resonance imaging (MRI). If there is concern for myelopathy, imaging should not be delayed. MRI is the study of choice for evaluation of TDH or intrinsic spinal cord lesions. Neoplasias may need further studies to check for other focci of metastasis (e.g., positron emission tomography [PET] or isotope scanning). CT-myelography has equal sensitivity to MRI to diagnose TDH. On the other hand, MRI is noninvasive and has high soft tissue resolution to evaluate the spinal cord, but it is a more expensive test. Gadolinium is useful in delineating neoplasm and scar formation.7,17
Supplemental assessment tools
Electromyography of thoracic radiculopathy is challenging and rarely performed. Although they have been studied, there are no definite recommendations regarding motor-evoked potentials and transcranial magnetic stimulation.
Early predictions of outcomes
Fifty percent of patients with ASIA-B classification spinal cord injuries (Incomplete = sensory but no motor function is preserved below the level of injury, including the sacral segments) will become ambulatory. The ASIA Lower Extremity Muscle Score (LEMS) results from adding the bilateral lower extremity muscle strength (normal is 50); values above 30 are associated with community ambulation.16 Abnormally high levels of cytokines, especially IL-6, may suggest poor prognosis and recurrence.18
Environmental and vehicular modifications allow adequate access with wheelchairs or other assistive devices. Home evaluations by Occupational Therapy can identify possible safety issues and provide recommendation for adaptive equipment.
Social role and social support system
Thoracic myelopathy treatment should address skin integrity, pain, bowel and bladder management, mental health, sexual and reproductive issues, DVT, spasticity, heterotopic ossification, osteoporosis and the potential for development of autonomic dysreflexia. The participation of the entire rehabilitation team is instrumental in helping to reintegrate the individual to society. Physical therapy and occupational therapy assist in strength training and range of motion, assess for adaptive equipment, position and splint to decrease spasticity and avoid contractures. Social work assists in transitioning to the home. Vocational and avocational rehabilitation help to maintain a productive life within the patient’s limitations.
The rehabilitation team should actively engage the patient’s family members and social circle in the rehabilitation treatment program.
A thoracic radiculopathy work-up should be oriented towards ruling out progressive disease that can lead to myelopathy. However, myelopathy can present without classic signs or symptoms and should be suspected with mild neurological symptoms, such as mild gait abnormalities.
3. REHABILITATION MANAGEMENT AND TREATMENTS
Available or current treatment guidelines
Rehabilitation treatment of thoracic radiculopathy will depend on the symptoms presentNonsteroidal anti-inflammatories, a short course of glucocorticoids and/or physical therapy are commonly utilized treatment options but lack evidence in terms of outcomes. There is evidence to support transcutaneous electrical nerve stimulation being a useful modality for pain control, and it is relatively inexpensive and low risk.19 For long standing neuropathic pain, agents such as gabapentin, pregabalin, amitriptyline and other anticonvulsants may be considered because they have shown efficacy for neuropathic pain.20,21 Opioid pain medications may be used in refractory cases but given their significant addictive potential and side effect profile, discretion must be used.
At different disease stages
Treatment depends on the etiology. The natural history of TDH favors non-surgical treatments. Surgical procedures are relegated to progressive compressive myelopathy or unrelenting compressive radiculopathy. Interventional spine procedures including epidural steroid injections and selective nerve blocks, can provide significant pain relief, and also have the potential to provide diagnostic information. There is fair evidence supporting the use of thoracic interlaminar steroid injections for relieving radiating pain 22Progressive disease with no response to conservative treatment should be referred for surgical consultation. Newer thoracoscopic microsurgical techniques show less complications with almost 80% of patients reporting good or excellent pain outcomes.23 If chronic pain significantly interferes with daily activities, the recommended treatment consists of a comprehensive integrated interdisciplinary approach. Chronic spasticity management in spinal cord injured patients may require the use of oral baclofen or the implantation of a catheter-pump system for the delivery of intrathecal baclofen.
Coordination of care
Spine surgery, infectious disease, oncology, plastic surgery, urology, psychology, psychiatry, support group, physical and occupational therapies may all play a role, depending on the nature of the clinical symptoms, as indicated throughout this article.
Patient & family education
Patient and family teaching is of paramount importance to foster the understanding of myelopathy, its ramifications and treatment options. The rehabilitation teams should develop specific short-, mid- and long-term goals based on the individual’s functional abilities. Bowel and bladder training, safe transfer education and skin precautions can empower the patient and family, and will hopefully limit hospitalization.
Translation into practice: practice “pearls”/performance improvement in practice (PIPs)/changes in clinical practice behaviors and skills
Thoracic myelopathy and radiculopathy may occur secondary to degenerative, congenital, infectious, traumatic, vascular, endocrine, neoplastic or iatrogenic causes. The physical exam can provide clues to the diagnosis, but oftentimes MRI is required to make a definitive diagnosis. If radiculopathy is expected, it is reasonable to delay MRI, thus reducing unnecessary costs while a trial of conservative treatment is tried for 4-6 weeks.
4. CUTTING EDGE/EMERGING AND UNIQUE CONCEPTS AND PRACTICE
Cutting edge concepts and practice
Regenerative Medicine techniques including injections with stem cells and platelet rich plasma may provide relief to patients 24, but these techniques are still being investigated to demonstrate safety and efficacy. Neural stem cell transplantation is currently being investigated in murine embryonic stem cells.25
The use of functional electrical stimulation (FES) and other related devices, including FES bikes, are being promoted in aiding gait, mobility and improving cardiovascular status.
5. GAPS IN THE EVIDENCE-BASED KNOWLEDGE
Gaps in the evidence-based knowledge
Not available at this time.
- Schmalstieg WF, Weinshenker BG. Approach to acute or subacute myelopathy. Neurol Clin Prac. 2010;75(Suppl 1):S2-S8.
- Yashon D. Spinal injury. New York: Appleton-Century-Crofts;1978, 98.
- O’Connor RC, Andary MT, Russo RB, DeLano M. Thoracic radiculopathy. Phys Med Rehabil Clin N Am. 2002;(13):623-644.
- Kim BH, No MY, Han SJ, Park CH, Kim JH. Paraplegia Following Intercostal Nerve Neurolysis with Alcohol and Thoracic Epidural Injection in Lung Cancer Patient. The Korean Journal of Pain. 2015;28(2):148. doi:10.3344/kjp.2015.28.2.148.
- Arce CA, Dorhmann GJ. Thoracic disc herniation: improved diagnosis with computed tomographic scanning and a review of the literature. Surg Neurol. 1985;23:356-361.
- Deitch K, Chudnofsky C, Young M. T2-3 thoracic disc herniation with myelopathy. J Emer Med. 2009;36(2):138-140.
- Wood KB, Blair JM, Aepple DM, et al. The natural history of asymptomatic thoracic disc herniations. Spine. 1997;22(5):525-529.
- Gay CW, Bishop MD, Beres JL. Clinical presentation of a patient with thoracic myelopathy at a chiropractic clinic. Journal of Chiropractic Medicine. 2012;11(2):115-120. doi:10.1016/j.jcm.2011.10.007.
- Akuthota V, Tobey J. Developmental and functional anatomy of the thoracic spine. In: Slipman CW, Derby R, Simeone FA, Mayer TG, eds. Interventional Spine an Algorithmic Approach. USA: Saunders Elsevier; 2008:767-776.
- Hoehmann CL, Hitscherich K, Cuoco JA. The Artery of Adamkiewicz: Vascular Anatomy, Clinical Significance and Surgical Considerations. International Journal of Cardiovascular Research. 2016;05(06). doi:10.4172/2324-8602.1000284.
- Brown CW, Deffer PA, Akmakjian J, Donaldson DH, Brugman JL. The natural history of thoracic disc herniation. Spine. 1992;S97-S102.
- Bair MJ, et al. “Depression and Pain Comorbidity: A Literature Review,” Archives of Internal Medicine ( Nov. 10, 2003): Vol. 163, No. 20, pp. 2433–45.
- Kaito HFT. Thoracic Disc Herniation Presenting with Predominant Abdominal Pain. Journal of Spine. 2013;02(05). doi:10.4172/2165-7939.1000144.
- Bicknell J, Johnson S. Widespread electromyographic abnormalities in spinal muscles in cancer, disc disease, and diabetes. Univ Mich Med Center J 1976; 42: 124-7.
- Stillerman CB, Weiss MH. Management of thoracic disc disease. Clin Neurosurg. 1992;38:325-352.
- American Spinal Injury Association Website. http://www.asia-spinalinjury.org/publications/59544_sc_Exam_Sheet_r4.pdf. Accessed July 2, 2012.
- Xiong Y, Lachmann E, Marini S, Nagler W. Thoracic disc herniation presenting as abdominal and pelvic pain: a case report. Arch Phys Med Rehabil. 2001;82:1142-1144.
- Wolf VL, Lupo PJ, Lotze TE. Pediatric Acute Transverse Myelitis Overview and Differential Diagnosis. Journal of Child Neurology. 2012;27(11):1426-1436. doi:10.1177/0883073812452916.
- Plastaras CT, Schran S, Kim N, et al. Complementary and alternative treatment for neck pain: chiropractic, acupuncture, TENS, massage, yoga, Tai Chi, and Feldenkrais. Phys Med Rehabil Clin N Am 2011; 22: 521-37
- Kasimcan O, Kaptan H. Efficacy of Gabapentin for Radiculopathy Caused by Lumbar Spinal Stenosis and Lumbar Disk Hernia. Neurologia medico-chirurgica. 2010;50(12):1070-1073. doi:10.2176/nmc.50.1070.
- Selph S, Carson S, Fu R, et al. Drug class review: neuropathic pain: final update 1 report [ Internet]. Drug Class Reviews 2011;.
- Richardson J, Jones J, Atkinson R. The effect of thoracic paravertebral blockade on intercostal somatosensory evoked potentials. Anesth Analg 1998; 87: 373-6
- Quint, Ulrich, Gerd Bordon, Inge Preissl, Christoph Sanner, and Daniel Rosenthal. “Thoracoscopic treatment for single level symptomatic thoracic disc herniation: a prospective followed cohort study in a group of 167 consecutive cases.” European Spine Journal4 (2011): 637-45. Web.
- Zeckser J, Wolff M, Tucker J, Goodwin J. Multipotent Mesenchymal Stem Cell Treatment for Discogenic Low Back Pain and Disc Degeneration. Stem Cells International. 2016;2016:1-13. doi:10.1155/2016/3908389.
- Otsu M. Pluripotent stem cell-derived neural stem cells: From basic research to applications. World Journal of Stem Cells. 2014;6(5):651. doi:10.4252/wjsc.v6.i5.651.
Original Version of the Topic
Ameet Nagpal. Thoracic Radiculopathy / Myelopathy. 10/30/2012
Ameet Nagpal, MD
Nothing to Disclose
Daniel Johnson, DO
Nothing to Disclose