Thoracic Disc Injuries 

Updated: May 30, 2017
Author: Kambiz Hannani, MD; Chief Editor: Sherwin SW Ho, MD 

Overview

Background

Thoracic disc injury, first described in 1838, is an uncommon site of injury owing to the stabilizing effect of the rib cage.[1] The similarity of symptoms to lumbar disc herniation makes the diagnosis of a thoracic disc injury difficult,[2, 3, 4, 5, 6] but the process tends to be self-limiting and rarely requires surgical intervention.[4]

(See also the articles Disk Herniation and Thoracic Spine, Trauma [in the Radiology section], Thoracic Discogenic Pain Syndrome [in the Sports Medicine section], Lumbar Disc Disease [in the Neurosurgery section], and Herniated Nucleus Pulposus [in the Orthopedic Surgery section], as well as Return to Contact Sports After Spinal Surgery and Thoracoscopic Spine Surgery for Decompression and Stabilization of the Anterolateral Thoracic and Lumbar Spine on Medscape.)

For patient education resources, see the Bone Health Center, Back, Ribs, Neck, and Head Center, Back, Neck, and Head Injury Center, and Muscle Disorders Center, as well as Back Pain and Chronic Pain.

Epidemiology

Frequency

United States

The incidence of thoracic disc injuries is 1 in 1 million persons per year, and these injuries account for 0.25-0.75% of all disc herniations.[7]

Functional Anatomy

The thoracic discs are unusually stable compared with the cervical and lumbar discs. The stability of the thoracic discs is secondary to the surrounding rib cage, with the stabilizing effect of the rib articulations. However, the blood supply of the thoracic spine is more tenuous than the cervical and lumbar spine, especially at the T4-T9 watershed area, which is more prone to ischemic injury.

Sport-Specific Biomechanics

The facet orientation in the thoracic spine is vertical, with a slight medial angulation. This orientation allows for easier lateral bending and rotation versus pure bending. Biomechanical studies have shown that intervertebral discs are at the highest risk of injury when combined with bending and torsional forces. Therefore, the thoracic spine discs are at a decreased risk of injury because of the decreased bending potential in this segment of the spine.

The spinal cord-to-canal ratio (the ratio of the cross-sectional area of the cord to the cross-sectional area of the spinal canal) is 40% in the thoracic spine versus 25% in the cervical spine. The thoracic spine is also naturally kyphotic. These 2 facts make the thoracic spine more sensitive to cord compression from disc herniation.

 

Presentation

History

Determine the location and type of the patient's pain. Is the pain mainly located in the thoracolumbar spine, and is it radicular or mechanical in nature?

  • Thoracic disc disease may emulate the symptoms of lumbar disc disease.

    • Shooting pain down the legs implies nerve root irritation versus cord compression.

    • Pain in the thoracic area signifies mechanical pain that is possibly secondary to fractures, degenerative disc disease, tumors, or infections. (See also the articles Degenerative Disk Disease and Thoracic Spine Fractures and Dislocations [in the Orthopedic Surgery section].)

    • Night pain that wakes the patient is suggestive of infection or an oncologic process.

  • Cord compression is present with myelopathy, which requires immediate attention.[2] (See also the articles Spinal Stenosis [in the Orthopedic Surgery section] and Spinal Cord, Topographical and Functional Anatomy [in the Neurology section].) Myelopathy is seen with the following:

    • The presence of clonus or a positive Babinski reflex

    • Bowel and bladder dysfunction (seen in up to 20% of symptomatic discs)

  • High thoracic (T2-T5) herniation mimics cervical disc disease. (See also the article Cervical Disc Disease.)

    • Patients can present with upper extremity involvement, including Horner syndrome. (See also the articles Horner Syndrome [in the Ophthalmology section] and Horner Syndrome [in the Oncology section].)

    • If myelopathy is present, a negative result from the Hoffmann test makes cervical spine involvement unlikely. A positive result from the Hoffmann test is seen when the middle-finger metacarpophalangeal joint and the proximal interphalangeal joints are kept extended; a flexion reflex of the thumb is seen when the distal interphalangeal joint is flicked or suddenly extended. This is known as the Hoffmann sign.

  • Radicular symptoms include pain/paresthesias or dysesthesias in a dermatomal distribution. Dermatome T10 is usually involved.

Physical

The physical examination for thoracic disc injuries includes the following: palpation over the thoracic spine; range-of-motion (ROM) examination of the hips, knees, and ankles; straight leg-raise test; motor and sensory examination; and reflex examination.

  • Palpation

    • Palpate the entire region of the thoracic spine.

    • Muscle spasms can be identified by palpation.

  • ROM examination

    • Assess the patient's ROM throughout the hips, knees, and ankles.

    • A ROM examination, especially of the hip, can confirm the presence of radiculopathy versus referred pain from hip/knee pathology (eg, arthritis). (See also the Arthritis Resource Center on Medscape.)

    • ROM in the thoracic spine can be affected by the type of pathology. Arthritic changes that cause mechanical pain usually limit extension; radiculopathy that is seen with disc herniation generally causes increasing pain with flexion.

    • Bilateral straight leg-raise tests should be completed, and the patient's available ROM and symptoms should be noted and documented.

  • Motor examination of all the lumbar roots, including L2-L4 (knee extension), L4 (inversion), L5 (dorsiflexion), and S1 (eversion and plantar flexion) is helpful for evaluating nerve root involvement in the lumbar spine and cord compression in the thoracic spine.

  • Sensory examination

    • Sensory examination of the dermatomes, especially in the thoracoabdominal region, can help the clinician identify the level of involvement.

    • The nipple is innervated by T4; the xiphoid, T7; the umbilicus, T10; and the inguinal region, T12.

  • Reflex testing

    • The knee (L4) and ankle (S1) reflexes should be tested.

    • The abdominal reflexes and cremasteric reflex (check for symmetry and presence) can help the clinician identify myelopathy and cord compression.

  • Vascular examination of the dorsalis pedis artery, posterior tibial artery, and femoral artery can rule out other causes of the patient's symptoms.

Causes

The progressive wear and tear that is noted with degenerative disc disease increases the risk of injury via trauma. Contributing factors to disc injury include the following:

  • Age

  • Trauma

  • Smoking

  • Obesity

  • Sedentary lifestyle

  • Poor physical fitness

 

DDx

 

Workup

Laboratory Studies

Laboratory testing is helpful in screening for the differential diagnosis.

  • Obtain a complete blood cell (CBC) count to check for the patient's white blood cell count and hematocrit level to rule out other disorders such as infection or multiple myeloma. Obtain serum protein electrophoresis results to evaluate for multiple myeloma.

  • Obtain a Westergren sedimentation rate measurement and C-reactive protein level to assess for osteomyelitis and/or infection.

Imaging Studies

Imaging studies are essential for making a diagnosis of disc injury.[4, 8, 9]

  • Radiography

    • Should be the initial examination that is ordered

    • Unable to distinguish actual disc herniation

    • May identify disc calcification (seen with degenerative disease in older patients)

    • May help to identify infectious or oncologic causes for the patient's pain

  • Magnetic resonance imaging (MRI)

    • Both T1- and T2-weighted imaging are needed.[10]

    • Sensitive for identification of disc herniation

    • T2-weighted images exaggerate findings.

    • Identifies calcification by low signal in T1- and T2-weighted images.

    • Can identify the bony inflammation that is seen with tumors/infection

  • Computed (CT) myelogram[11]

    • Has improved bony visualization compared with MRI

    • Not as sensitive for disc sequestration/migration

    • Invasive relative to MRI

 

Treatment

Acute Phase

Rehabilitation Program

Physical Therapy

For the acute phase of a thoracic disc injury, the focus of physical therapy is to decrease the patient's symptoms with cold/heat therapy, ultrasound, and rest. Mild ROM exercises and very low-impact exercises that do not worsen the patient's symptoms are acceptable.

Medical Issues/Complications

Activity modification to minimize the patient's symptoms is important. Proper posture can help to prevent further disc injury. If oral drug usage fails to alleviate the patient's symptoms, consider steroid injection for intercostal nerve blocks. An orthosis (ie, brace) is initially acceptable for pain control but causes deconditioning over time. Thus, long-term bracing should be avoided.

Surgical Intervention

Surgical decompression is indicated in patients with myelopathy (unless improving), progressive neurologic symptoms, and worsening symptoms[12, 13, 14] or lack of improvement in the patient's symptoms by 4-6 weeks of conservative management.[10, 15]

An analysis of 25,413 patients who were treated surgically for thoracic disc herniation by Yoshihara et al compared anterior and nonanterior approach procedures and reported that anterior approach procedures were associated with a higher overall in-hospital complication rate (26.8% vs. 9.6%), mortality rate (0.7% vs. 0.2%), longer hospital stays (7.6 vs. 4.8 d) and increased hospital charges ($84,199 vs. $46,837).[16]

Consultations

Myelopathy and progressive neurologic symptoms require emergent neurosurgical/orthopedic consultation.

Recovery Phase

Rehabilitation Program

Physical Therapy

When the patient's acute symptoms have resolved, general cardiovascular conditioning and abdominal muscle strengthening with ROM may be introduced.[17]

Maintenance Phase

Rehabilitation Program

Physical Therapy

Home exercises for abdominal and paraspinal muscle strengthening and cardiovascular conditioning is helpful in preventing recurrences.[17]

 

Medication

Medication Summary

Medications are used to minimize pain and inflammation. In the early phase of a disc herniation, nonsteroidal anti-inflammatory drugs (NSAIDs) are recommended. If NSAIDs are not effective, a tapering course of steroids, such as with methylprednisolone, can be used to try to minimize the inflammatory process. In cases of severe pain, narcotics can be used in the acute phases; if pain has become a chronic problem, narcotics then become the primary modality for pain control. Muscle relaxants can be utilized to potentiate the effectiveness of NSAIDs, narcotics, or steroids.

Nonsteroidal anti-inflammatory drugs

Class Summary

NSAIDs are used to decrease the inflammatory process that is involved in disc herniation and nerve root irritation; furthermore, NSAIDs can help to decrease the pain that is associated with disc herniation.

Ibuprofen (Motrin, Ibuprin)

Drug of choice (DOC) for patients with mild to moderate pain. Inhibits inflammatory reactions and pain by decreasing prostaglandin synthesis.

Naproxen (Naprosyn, Anaprox, Naprelan)

For relief of mild to moderate pain; inhibits inflammatory reactions and pain by decreasing the activity of cyclooxygenase, which is responsible for prostaglandin synthesis.

Diclofenac (Voltaren)

Inhibits prostaglandin synthesis by decreasing the activity of the enzyme cyclooxygenase, which, in turn, decreases formation of prostaglandin precursors.

Celecoxib (Celebrex)

Inhibits primarily COX-2. COX-2 is considered an inducible isoenzyme; it is induced during pain and inflammatory stimuli. Inhibition of COX-1 may contribute to NSAID GI toxicity. At therapeutic concentrations, COX-1 isoenzyme is not inhibited; thus, GI toxicity may be decreased. Seek the lowest dose of celecoxib for each patient.

Corticosteroids

Class Summary

Corticosteroids are potent anti-inflammatory agents that are used to relieve inflammation of the nerve roots and surrounding tissue.

Prednisone (Deltasone, Meticorten, Orasone)

May decrease inflammation by reversing increased capillary permeability and suppressing polymorphonuclear leukocyte activity.

Methylprednisolone (Medrol, Solu-Medrol, Depo-Medrol)

Decreases inflammation by suppressing migration of polymorphonuclear leukocytes and reversing increased capillary permeability.

Muscle relaxants

Class Summary

Muscle relaxants reduce muscle spasms in the paraspinal muscles.

Carisoprodol (Soma)

Short-acting medication that may have depressant effects at the spinal cord level.

Cyclobenzaprine (Flexeril)

Skeletal muscle relaxant that acts centrally and reduces the motor activity of tonic somatic origins that influence both alpha and gamma motor neurons.

Structurally related to tricyclic antidepressants and, thus, carries some of their same risks.

Narcotic analgesics

Class Summary

Narcotic analgesics are used for short-term pain control.

Hydrocodone and acetaminophen (Vicodin, Lortab, Norcet)

Drug combination indicated for short-term (< 10 d) relief of moderate to severe acute pain.

Oxycodone and acetaminophen (Percocet, Roxicet, Roxilox, Tylox)

Drug combination indicated for the relief of moderate to severe pain.

 

Follow-up

Return to Play

Thoracic disc disease is usually self-limiting; return to play depends on the success of conservative management in controlling the pain/radiculopathy that is associated with the disc herniation.

Complications

The most serious but rare complication of thoracic disc disease is myelopathy. Myelopathic features, including hyperreflexia, weakness, and bowel/bladder dysfunction, may not improve after surgical decompression. Worsening myelopathic findings are an absolute indication for surgical decompression.

Prevention

Exercises, including cardiovascular training and abdominal/lumbar muscle training, are the primary preventive measure for thoracic disc disease.

Prognosis

Thoracic disc disease is essentially self-limiting and rarely requires surgical intervention. Most cases resolve within the first 4-6 weeks following onset.