Author(s): Keith F. Polston, MD, MS, Carly Berrios, BSN, Ameet Nagpal, MD, MS, MEd
Originally published: October 30, 2012 Last updated: January 23, 2025
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Disease/Disorder

Definition

Radiculopathy is produced by compression or irritation of a spinal nerve root. With regards to “thoracic radiculopathy,” the symptoms are generated from a disease process occurring within the thoracic spine. Myelopathy in contrast occurs when upper motor neurons of the spinal cord itself are affected, rather than lower motor neurons of an individual spinal nerve root. Although they are different, their incidence is not mutually exclusive, and a patient may present with both conditions.

Etiology

Thoracic myelopathy and radiculopathy may occur secondary to degenerative, congenital, infectious, traumatic, vascular, endocrine, neoplastic, or iatrogenic causes. The symptoms of thoracic radiculopathy are multiple and overlap with other conditions affecting the thoracic spine and as such delineating between conditions based on initial patient presentation can be difficult. Thoracic radiculopathy secondary to intervertebral disc herniation is estimated to occur in roughly 1 million people per year.1 Although the incidence is significant, a classic presentation of painful unilateral radiation in a dermatomal pattern is not always seen. A significant number of patients with thoracic disc herniation remain asymptomatic, and discovery is often found incidentally.1,2

In addition to thoracic disc disease, diabetes mellitus (DM) has been associated with the development of thoracic radiculopathy.3 Thought to occur secondary to peripheral neuropathy from persistently poorly controlled diabetes, the etiology is often a downstream diagnosis given multifactorial pathologies affecting the patient.4 Both thoracic disc disease and radiculopathy secondary to DM present with non-specific symptoms such as chest wall pain, pain in the epigastric territory, or upper extremity pain, amongst other symptoms. Given the similarity among presenting symptoms, a broad differential is necessary when evaluating patients.

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 additional potential sources of spinal compression. Neoplasm is also a potential source, as the thoracic spine is the most common location for spinal metastases. Demyelinating processes including multiple sclerosis must also be considered.3

Iatrogenic causes of thoracic myelopathy have also 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, or direct toxicity of medication to neural structures.3Thoracic myelopathy may result from ligature during lumbar sympathectomy, prolonged clamping during aortic aneurysm surgery, or trans-operative micro embolization 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.5 Intrathecal catheters can develop granulomas at the tip causing compressive myelopathy. Radiation therapy can cause demyelination, focal necrosis and vasculitic changes of the thoracic spinal cord.

Epidemiology including risk factors and primary prevention

Disc herniation is significantly less common in the thoracic spine compared with the cervical and lumbar spine, and represents less than 5% of disc herniations.6 The most common location for disc herniation in the thoracic spine is at T11-T12.1Although many of the patients who develop herniation do so secondary to an inciting event or injury, hereditary predilection has been suggested to potentially play a contributing role. Further research is required to elucidate the role that genetics play in thoracic disc disease. Scheuermann’s disease, also known as juvenile discogenic disease, is a condition characterized by thoracic hyperkyphosis with involvement of the vertebral bodies and the discs themselves. As such, it has been proposed that patients with Scheuermann’s disease may be at increased risk for TDH.7TDH is relatively rare and affects up to 1 in 1,000 people in the general population.1 Asymptomatic TDH has 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.2 Most patients present in the fourth to sixth decade, but TDH can affect all age groups with a 3:2 male-to-female ratio.1,2,6In most cases, thoracic myelopathy is caused by degenerative changes with subsequent stenosis and cord compression. However, thoracic myelopathy caused by degenerative spondylosis is less common compared to myelopathy caused by degenerative spondylosis in the lumbar and cervical spine.8

Patho-anatomy/physiology

Skeletal: The thoracic vertebral canal, on average, has a smaller clearance (~15 mm) between the spinal cord and the osseous wall than the cervical canal (17 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.5 The thoracic spine is naturally the most relatively stable segment 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 L5.5 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. The thoracic cord is considered a watershed area with a tenuous blood supply compared to the cervical and lumbar spinal cord.

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.1

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.2Retrospective studies suggest that patients with symptomatic TDH can usually be managed non-surgically and return to their prior level of activity.6 Some patients with radiculopathy will have progression of disease to include sensory deficits and motor weakness which may or may not be reversible. Potential deficits include loss of sensation typically in a dermatomal pattern on the abdomen or chest, weakness of the intercostal muscles, and potentially weakness of the abdominal muscles. Furthermore, direct cord compression is associated with paraplegia and neurogenic bladder in some instances. If the T1 nerve is involved, deficits can be seen with intrinsic hand attributes leading to weakness and muscle atrophy as a secondary effect as well.

Thoracic myelopathy symptoms and signs are varied and depend on the magnitude of cord involvement. Complaints range from subtle weakness to paraplegia and incontinence in severe instances. In contrast to patients suffering from thoracic radiculopathy, who can usually be treated conservatively, signs of myelopathy such as bowel or bladder incontinence, profound motor weakness, or hyperreflexia warrant prompt surgical evaluation.

Specific secondary or associated conditions and complications

There is evidence to support a link between chronic pain and worsening of depression.9Chronic back pain can result in significant physical and emotional distress and as such the risk for psychological conditions such as depression is significant. Although not singular to patients with thoracic pathology, roughly 50% of patients with enduring chronic pain suffer from depression.10 This sequela has significant implications for the medical system and goal directed therapy during patient evaluation.

Chronic herpes zoster radiculitis is a condition which should be included in the differential for thoracic radiculopathy and has significant implications for patient quality of life. The varicella zoster virus lies dormant in the dorsal root ganglion of the affected nerve. Common clinical features include dermatomal pain, dysesthesias, and pruritus, amongst other features. The condition is associated with paresis in 1-5% of patients.11

Essentials of Assessment

History

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 wall pain. The pain of radiculopathy tends to follow a dermatomal distribution and is typically worsened by coughing or straining.

Myelopathy may manifest only by reflex or gait abnormalities. It may, however, be associated with orthostasis or autonomic dysreflexia (in lesions over T6), bowel/bladder dysfunction, sexuality issues, sensory impairment (dysesthesia or anesthesia) and/or motor deficits.1,3,12

Physical examination

An asymmetric, band-like, sensory anomaly in the chest or abdominal wall usually along a single dermatome is suggestive of thoracic radiculopathy. Neuropathic pain may be exacerbated by trunk movements.

Spinal cord injury is classified according to the American Spinal Injury Association (ASIA) Impairment Scale (AIS) which can be found on its website.13 Gait abnormalities, sensory deficits, weakness, hyperreflexia, increased muscle tone, bowel and bladder incontinence, and up-going toes on Babinski testing are generally seen in myelopathy, although subtle myelopathy may not provide definitive findings. In complete spinal cord injury, there will be no rectal sensation and increased rectal tone with no volitional sphincter contraction.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 includes damage to the corticospinal tract, anterior horn cells and spinothalamic tracts presenting with hyporeflexia, atrophy, variable motor loss, and decreased sensation with preservation of proprioception and vibration sense due to sparing of the dorsal columns.12

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.12

Tertiary syphilis (tabes dorsalis) and Vitamin B-12 deficiency can result in a posterior cord syndrome with an insult to the dorsal columns. This syndrome causes deficits in gait and balance due to proprioceptive loss with relative sparing of motor and sensory tracts.3

Functional assessment

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 involving the T1 nerve root.

Thoracic myelopathy results in functional disability relative to the spinal cord level affected. High thoracic cord lesion may affect trunk control and mobilization of pulmonary secretions. The Spinal Cord Independence Measure (SCIM) is used to further document traumatic and non-traumatic, acute and chronic, spinal cord injuries.14The Walking Index for Spinal Cord Injury (WISCI) measures SCI patients’ ability to walk and need for assistance.14 The AIS may further help predict functional outcomes.13

Laboratory studies

When thoracic discitis is suspected, a complete blood count (CBC), C-reactive protein (CRP) and blood cultures should be performed. Checking for acid-fast bacillus in immunocompromised patients or travelers from areas with endemic tuberculosis may be needed. Urodynamic studies may be warranted for patients with myelopathy to determine whether urologic dysfunction is secondary to a neurogenic etiology.15

Imaging

In pursuing conservative management of thoracic radiculopathy, it is reasonable to start with plain radiographs and to delay magnetic resonance imaging (MRI). If there is concern for myelopathy, advanced imaging should not be delayed. MRI is the study of choice for evaluation of TDH or intrinsic spinal cord lesions due to superior soft tissue visualization. Neoplasms may need further studies to check for other foci of metastasis (e.g., positron emission tomography [PET] or isotope scanning). 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.2

Supplemental assessment tools

Electromyography of thoracic radiculopathy is challenging and rarely performed. This is likely secondary to the potential invasive nature of the study coupled with the low sensitivity attributed to the results.1Furthermore, EMG and nerve conduction studies have a low combined sensitivity and specificity for thoracic radiculopathy, and do not reveal the biological etiology of the lesion. As such, the invasive and costly procedure is often avoided in the clinical setting.16 There is also a risk of pneumothorax from the needle electromyography, and there is no reliable nerve conduction study protocol described. Although they have been studied, there are no definitive recommendations for performance of motor-evoked potentials and transcranial magnetic stimulation.  The use of monitoring of motor evoked potentials and somatosensory evoked potentials is an incredibly useful intra-operative tool that provides additional data for surgeons and anesthesiologists operating on or near the spinal cord. Real time intraoperative monitoring of SSEP and MEP help surgeons navigate around the spinal cord without causing long term damage.

Early predictions of outcomes

Fifty percent of patients with AIS-B classification spinal cord injuries [(i.e., 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.13 Abnormally high levels of cytokines, especially IL-6, may suggest poor prognosis and recurrence.1

Environmental

Environmental and vehicular modifications allow access for patients with SCI who use wheelchairs or other assistive devices. Home evaluations by Occupational Therapy can identify possible safety issues and provide recommendations for adaptive equipment.

Social role and social support system

Treatment of thoracic myelopathy should address patients’ 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 workers can assist transitioning patients back home and with community reintegration. Vocational rehabilitation therapists help patients maintain a productive life adapting to patients’ new limitations.  The rehabilitation team should also actively engage the patient’s family members and social circle in the rehabilitation treatment program.

Professional issues

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.

Rehabilitation Management and Treatments

Available or current treatment guidelines

Rehabilitation treatment of thoracic radiculopathy will depend on the symptoms present. Nonsteroidal anti-inflammatories, a short course of glucocorticoids and/or physical therapy are commonly utilized treatments but lack evidence in terms of outcomes. There is evidence to support transcutaneous electrical nerve stimulation as being a useful modality for pain control, as it is relatively inexpensive and low risk.17 For long standing thoracic neuropathic pain, gabapentin, pregabalin, amitriptyline, or other anticonvulsant agents may be considered given their efficacy in other neuropathic pain conditions.17 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. Surgery may be considered for progressive myelopathy or unrelenting radiculopathy. Interventional spine procedures including epidural steroid injections and selective nerve root blocks can provide significant pain relief and have the potential to provide diagnostic information.1Newer thoracoscopic microsurgical techniques show less complications with almost 80% of patients reporting good or excellent pain outcomes.18 If chronic pain significantly interferes with daily activities, the recommended treatment consists of a comprehensive integrated interdisciplinary approach. This includes contributions from a chronic pain specialist, physical therapy, family medicine physician, surgical service, and others.

Coordination of care

Spine surgery, infectious disease, oncology, plastic surgery, urology, psychology, psychiatry, support group, physical therapy, 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 may limit hospitalization.

Translation into practice: practice “pearls”/performance improvement in practice (PIPs)/changes in clinical practice behaviors and skills

The physical exam can provide clues to the diagnosis, but often MRI is required to make a definitive diagnosis. If radiculopathy without myelopathy is expected, it is reasonable to delay MRI, thus reducing unnecessary costs while a trial of conservative treatment is tried for 4-6 weeks. If myelopathy is suspected, immediate advanced imaging is necessary.

Cutting Edge/Emerging and Unique Concepts and Practice

Regenerative medicine injections of stem cells or platelet rich plasma may provide relief to patients, but these treatments remain investigational as safety and efficacy have not been adequately established. Neural stem cell transplantation is currently being investigated in murine embryonic stem cells for the regeneration of disc material in patients suffering from chronic back pain.19 These studies are in their early phase and have primarily been done in-vitro, although some in-vivo work is currently underway. Elucidating different etiologies of back pain and their potential responses to specific therapy has not yet been established in the research community. Moreover, preliminary studies evaluating the efficacy of platelet-rich plasma (PRP) epidural injections in the setting of lumbar radiculopathy and degenerative disk disease are underway, although more research is necessary to elucidate its effectiveness in thoracic radiculopathy/myelopathy.20

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.9

Gaps in the Evidence-Based Knowledge

N/A

References

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  3. O’Connor RC, Andary MT, Russo RB, DeLano M. Thoracic radiculopathy. Phys Med Rehabil Clin N Am. 2002;13(3):623-44, viii. doi: 10.1016/s1047-9651(02)00018-9. PubMed PMID: 12380552.
  4. Brewer R, Bedlack R, Massey E. Diabetic thoracic radiculopathy: an unusual cause of post-thoracotomy pain. Pain. 2003;103(1-2):221-3. doi: 10.1016/s0304-3959(02)00446-3. PubMed PMID: 12749978.
  5. Peabody T, Black AC, Das JM. Anatomy, Back, Vertebral Canal.  StatPearls. Treasure Island (FL)2024.
  6. Deitch K, Chudnofsky C, Young M. T2-3 Thoracic disc herniation with myelopathy. J Emerg Med. 2009;36(2):138-40. Epub 20070731. doi: 10.1016/j.jemermed.2007.03.015. PubMed PMID: 17976778.
  7. Kapetanos GA, Hantzidis PT, Anagnostidis KS, Kirkos JM. Thoracic cord compression caused by disk herniation in Scheuermann’s disease: a case report and review of the literature. Eur Spine J. 2006;15 Suppl 5(Suppl 5):553-8. Epub 20060119. doi: 10.1007/s00586-005-0053-0. PubMed PMID: 16421745; PMCID: PMC1602190.
  8. Gay CW, Bishop MD, Beres JL. Clinical presentation of a patient with thoracic myelopathy at a chiropractic clinic. J Chiropr Med. 2012;11(2):115-20. doi: 10.1016/j.jcm.2011.10.007. PubMed PMID: 23204955; PMCID: PMC3368975.
  9. McDaniel J, Lombardo LM, Foglyano KM, Marasco PD, R JT. Cycle Training Using Implanted Neural Prostheses: Team Cleveland. Eur J Transl Myol. 2017;27(4):7087. Epub 20171206. doi: 10.4081/ejtm.2017.7087. PubMed PMID: 29299221; PMCID: PMC5745386.
  10. Bair MJ, Robinson RL, Katon W, Kroenke K. Depression and pain comorbidity: a literature review. Arch Intern Med. 2003;163(20):2433-45. doi: 10.1001/archinte.163.20.2433. PubMed PMID: 14609780.
  11. Bhushan S, Dominguez L, Shirazi E, Gupta V. Acute Herpes Zoster Radiculopathy of the Lower Extremity With Dermatomal Rash and Lumbar Nerve Enhancement on MRI. Mayo Clin Proc Innov Qual Outcomes. 2020;4(5):608-10. Epub 20200819. doi: 10.1016/j.mayocpiqo.2020.06.001. PubMed PMID: 33083710; PMCID: PMC7557183.
  12. Ganapathy MK, Reddy V, Tadi P. Neuroanatomy, Spinal Cord Morphology.  StatPearls. Treasure Island (FL)2024.
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  16. Charles JA, Souayah N. EMG/NCS in the evaluation of spine trauma with radicular symptoms. Neurol Clin Pract. 2013;3(1):8-14. doi: 10.1212/CPJ.0b013e318283ff78. PubMed PMID: 29406535; PMCID: PMC5765938.
  17. Bielewicz J, Kamieniak M, Szymoniuk M, Litak J, Czyzewski W, Kamieniak P. Diagnosis and Management of Neuropathic Pain in Spine Diseases. J Clin Med. 2023;12(4). Epub 20230209. doi: 10.3390/jcm12041380. PubMed PMID: 36835916; PMCID: PMC9961043.
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  19. Otsu M, Nakayama T, Inoue N. Pluripotent stem cell-derived neural stem cells: From basic research to applications. World J Stem Cells. 2014;6(5):651-7. doi: 10.4252/wjsc.v6.i5.651. PubMed PMID: 25426263; PMCID: PMC4178266.
  20. Mohammed S, Yu J. Platelet-rich plasma injections: an emerging therapy for chronic discogenic low back pain. J Spine Surg. 2018;4(1):115-22. doi: 10.21037/jss.2018.03.04. PubMed PMID: 29732431; PMCID: PMC5911760.

Original Version of the Topic

Ameet Nagpal. Thoracic Radiculopathy/Myelopathy. 10/30/2012

Previous Revision(s) of the Topic

Ameet Nagpal, MD, Daniel Johnson, DO. Thoracic Radiculopathy/Myelopathy. 7/31/2017

Ameet Nagpal, MD, MS, MEd, Kenneth Brooks, MD. Thoracic Radiculopathy/Myelopathy. 12/22/2021

Author Disclosure

Keith F. Polston, MD, MS
Nothing to Disclose

Carly Berrios, BSN
Nothing to Disclose

Ameet Nagpal, MD, MS, MEd
Nothing to Disclose