Thoracic radiculopathy/myelopathy

  1. Disease/Disorder:

    An insult occurring to the neural elements between the T1-T12 vertebral levels is considered thoracic. If it it affects the function of a nerve root, it is called thoracic radiculopathy. If the long tracts of the spinal cord are affected, then it is called thoracic myelopathy.


    Thoracic radiculopathy is due to spinal nerve insult, usually secondary to intervertebral disc pathology (herniation, discitis). Special situations present in diabetic truncal or thoracoabdominal radiculopathy and postherpetic neuralgia.

    Myelopathy has been associated with thoracic disc herniation (TDH), disc calcification, posterior longitudinal ligament and/or ligamentum flavum ossification, spinal stenosis, and anterior spinal cord herniation with prolapse through the dura mater. Hereditary and congenital anomalies include: alkaponuria, syringomyelia, diastematomyelia, tethered cord, X-linked hypophosphatemic rickets, epidural or vertebral vascular malformations, and neurofibromatosis.

    Infectious diseases include: vertebral osteomyelitis, vertebral tuberculosis (Pott's disease), discitis, epidural abscess, human T-lymphotropic virus 1 (HTLV-1), syphilis; schistosomiasis. Compression from intradural or extradural neoplasias can cause myelopathy.

    Iatrogenic ischemic thoracic myelopathy can follow inadvertent intravascular injection of particulate steroids during transforaminal epidural injections, causing embolization and paraplegia. 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.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.1,2

    Epidemiology including risk factors and primary prevention

    Thoracic disc herniations (TDH) account for 0.25% to 0.75% of all disc herniations. 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 can affect all age groups with a 3:2 male-to-female ratio.3,4,5 In most cases, the condition is felt to be caused by degenerative processes. Seventy percent of these herniations occur in a posterolateral direction and 90% of patients have signs of spinal cord compression at the time of diagnosis. TDH can develop at any level, but 75% occur below T7, and approximately 28% occur at T11-12.5,6


    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 with 25% in the cervical. Therefore the thoracic spinal cord and nerve roots are at higher risk of injury from space-occupying lesions.1

    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 Adamkiewicz artery, which mainly supplies the lumbosacral spinal cord segments and enters the cord between T10 and L3.7 It is here where particular steroids can occlude the blood supply to the cord. The venous plexus of the thoracic spine plays a major role in metastatic neoplasias and vertebral seeding of infections.

    Neurologic: Twelve spinal nerves exit from the thoracic spine via the intervertebral foramen, enter the thoracic paravertebral space and divide into anterior and posterior rami.

    The low incidence of thoracic disc herniations is explained by the stabilization of the thoracic spine by ribs and sternum, and the coronal orientation of facet joints. 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.1,7

    Disease progression including natural history, disease phases or stages, disease trajectory (clinical features and presentation over time)

    Thoracic myelopathy can progress from subtle gait complaints to complete spinal cord injury. Asymptomatic thoracic disc herniations usually remain asymptomatic and overtreatment must be avoided.3 Retrospective studies suggest that 77% of patients with symptomatic TDH managed non-surgically to return to their prior level of activity.6

    Specific secondary or associated conditions and complications

    ​​Thoracic radicular pain chronicity can lead to development or aggravation of mental health issues. Progressive thoracic myelopathy will lead to irreversible spinal cord injury.

  2. Essentials of Assessment

    ​​Pain is the most common presenting symptom in 76% of patients; the second most common is myelopathy.8 Most patients present with pain (burning, shooting, prickling) along the dermatomal distribution of the affected root, worsened by coughing or straining. 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 motor deficits.1,2,8 Lower extremity edema may raise suspicion of deep vein thrombosis (DVT).

    Physical examination

    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 in its web site.9 Gait abnormalities, sensory deficits, weakness, hyperreflexia, increased muscle tone, 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, increased rectal tone with no volitional sphyncter contraction.1,2

    Injury to the Adamkiewicz artery leads to anterior cord syndrome, with hyporeflexia, atrophy, variable motor loss, and decreased sensation with preservation of proprioception.

    Expanding intramedullary mass, hematoma, viral infection, hydromyelia or syringomyelia result in central cord syndrome, with weakness, hypereflexia and preserved sacral sensation with bowel and bladder function minimally affected.

    Syphylis (tabes dorsalis) and Vitamin B-12 deficiency results in posterior cord syndrome, causing proprioception and gait alterations.

    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.

    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.9

    Laboratory studies

    When discitis is suspected, complete blood count (CBC), C-reactive protein test (CRP) and hemocultures 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.


    Magnetic resonance imaging (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, however MRI is noninvasive and has high soft tissue resolution to evaluate the spinal cord. Gadolinium is useful in delineating neoplasm and scar formation.3,10

    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 (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.9 In the pediatric population, transverse myelitis has been associated with a better functional outcome in patients older than 3 years of age at time of diagnosis, shorter time to diagnosis, lower sensory and anatomic levels of spinal injury, absence of T1 hypointensity on spinal MRI obtained during the acute period, lack of white blood cells in the CSF, and fewer affected spinal cord segments. Abnormally high levels of cytokines, especially IL-6, may suggest poor prognosis and recurrence.


    Environmental and vehicular modifications allow adequate access with wheelchairs or other assistive devices.

    Social role and social support system

    Spinal cord injury patients are at risk for dependency, depression, drug addiction and divorce. The rehabilitation team should actively engage family members and the patient's 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.

  3. Rehabilitation Management and Treatments
    Available or current treatment guidelines

    Rehabilitation treatment of thoracic radiculopathy will depend on the symptoms present. Allodynia should be addressed with desensitization, transcutaneous electrical nerve stimulation (TENS), and reassurance to decrease fear-avoidance reactions.

    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 intrumental 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.

    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.6 Selective nerve root blocks, paravertebral blocks, epidural steroid injections and intercostal blocks have been used as adjuvants during the acute or subacute stage of thoracic radiculopathy, however evidence-based literature is scant. Chronic pain management includes NSAIDS, gabapentoids, tricyclic antidepressants and anxiolytics, as well as cautious use of opioid analgesics. If chronic pain significantly interferes with daily activities, the recommended treatment consists of a comprehensive integrated interdisciplinary approach. Chronic spasticity management 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.

    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.

    Emerging/unique Interventions

    The Functional Independence Measure (FIM) helps to measure independence and function. The Spinal Cord Independence Measure (SCIM) assesses self-care, respiration and sphincter management, and mobility. The Walking Index for Spinal Cord Injury (WISCI) is designed to be a more precise measure of improvement in functional limits; it assesses the amount of physical assistance needed and devices required for walking.

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

    Thoracic myelopathy/radiculopathy may result secondary to degenerative, congenital, infectious, traumatic, vascular, endocrine, neoplastic or iatrogenic causes. Physical examination may not provide enough information to make a definitive diagnosis and clinical suspicion will often drive the request for an MRI to help make a definitive diagnosis.

  4. Cutting edge/emerging and unique concepts and practice
    Cutting edge concepts and practice

    Neural stem cell transplantation is currently being investigated in murine embryonic stem cells.

    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.


    1. O'Connor RC, Andary MT, Russo RB, DeLano M. Thoracic radiculopathy. Phys Med Rehabil Clin N Am. 2002;(13):623-644.
    2. Schmalstieg WF, Weinshenker BG. Approach to acute or subacute myelopathy. Neurol Clin Prac. 2010;75(Suppl 1):S2-S8.
    3. Wood KB, Blair JM, Aepple DM, et al. The natural history of asymptomatic thoracic disc herniations. Spine. 1997;22(5):525-529.
    4. Deitch K, Chudnofsky C, Young M. T2-3 thoracic disc herniation with myelopathy. J Emer Med. 2009;36(2):138-140.
    5. 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.
    6. Brown CW, Deffer PA, Akmakjian J, Donaldson DH, Brugman JL. The natural history of thoracic disc herniation. Spine. 1992;S97-S102.
    7. 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.
    8. Stillerman CB, Weiss MH. Management of thoracic disc disease. Clin Neurosurg. 1992;38:325-352.
    9. American Spinal Injury Association Website. http://www.asia-spinalinjury.org/publications/59544_sc_Exam_Sheet_r4.pdf. Accessed July 2, 2012.
    10. 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.
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