Show Summary Details
Page of

Intercostal Neuralgia and Thoracic Radiculopathy 

Intercostal Neuralgia and Thoracic Radiculopathy
Chapter:
Intercostal Neuralgia and Thoracic Radiculopathy
Author(s):

Yili Huang

, and Neel Mehta

DOI:
10.1093/med/9780199350940.003.0012
Page of

PRINTED FROM OXFORD MEDICINE ONLINE (www.oxfordmedicine.com). © Oxford University Press, 2016. All Rights Reserved. Under the terms of the licence agreement, an individual user may print out a PDF of a single chapter of a title in Oxford Medicine Online for personal use (for details see Privacy Policy and Legal Notice).

Subscriber: null; date: 23 October 2019

Key Points

  • Musculoskeletal thoracic pain, including intercostal neuralgia and thoracic radiculopathy, accounts for up to 50% of all chest pain cases.

  • The vertebral, skeletal, and neurologic components of the thoracic anatomy present many locations for painful pathology.

  • An algorithmic approach to the diagnosis of thoracic pain syndromes may be helpful.

  • It is important to consider life-threatening cardiopulmonary pain generators as well as acute infection and oncologic and traumatic causes of thoracic pain.

  • The most common form of thoracic radiculopathy is DTR. Fifteen percent of insulin-dependent diabetics and 13% of non–insulin-dependent diabetics have some form of DTR.

  • Upper thoracic radiculopathy must be considered in upper extremity neuropathies.

  • Lower thoracic radiculopathy is relatively rare and occurs most frequently in men between 30 and 50 years of age.

  • PHN is caused by neuronal injury of both the central and peripheral nervous systems leading to hyperalgesia and allodynia.

  • Tietze syndrome involves painful inflammation of the costal cartilages leading to tenderness in the costochondral junction.

  • Costochondritis is not associated with inflammation and represents 30% to 42% of musculoskeletal chest pain complaints in the primary care or emergency department settings.

  • Slipping rib syndrome involves fibrous loosening of the lower costal cartilages causing cephalic slippage of the tip into the adjacent rib, leading to intercostal neuralgia.

Introduction

Intercostal neuralgia and thoracic radiculopathy contribute significantly to musculoskeletal thoracic pain, which accounts for 50% of all chest pain cases.1 As many as 75% of these patients experience chronic pain leading to anxiety, depression, and decreased function.2 We will examine the thoracic anatomy, ruling out life-threatening cardiorespiratory pathology, and some common causes of neuropathic chest pain, including thoracic disc herniation, postherpetic neuralgia (PHN), costochondritis, Tietze syndrome, and slipping rib syndrome.

Thoracic Anatomy

The skeletal thoracic anatomy consists of the sternum, articulating ribs, and thoracic vertebrae. The sternum consists of the manubrium, body, and xiphoid process. The manubrium is bordered superiorly at the T3 vertebral level by the jugular notch and the medial end of the clavicle. The costal cartilage of the first rib is also adjacent to the lateral edge of the manubrium. The body articulates with the manubrium at the sternal angle, which is at about the T5 vertebral level. This articulation, also known as the manubriosternal junction, is the level of the second costal cartilage. The body of the sternum connects bilaterally with the second to the seventh ribs. The xiphoid process connects with the body of the sternum at the xiphosternal joint, usually at the 10th or 11th vertebral level.

There are 12 ribs on each side of the body. True ribs are ribs 1 to 7, which are connected to the sternum by their costal cartilages. False ribs are ribs 8 to 12. Ribs 8 to 10 join the costal cartilage above them, while ribs 11 and 12 are not connected to the sternum and are called floating ribs.

The thoracic vertebrae articulate with the corresponding ribs at the corresponding superior costal facet and at the level of the inferior costal facet of the vertebra above it (at the levels of T2 to T10). The heads of ribs 1, 11, and 12 articulate only with their corresponding vertebra. The increased articulation and the vertical medial orientation of the thoracic vertebral facets provide significant stability during movement and significantly lessen the risk for thoracic disc disease compared to that of the lumbar spine.

The intercostal nerves are somatic nerves that arise from the T1 through T11 thoracic nerve roots. After emerging from the intervertebral foramen, the spinal nerve divides into ventral and dorsal rami. The dorsal ramus innervates the musculature and skin of the paravertebral area, while the ventral ramus continues as the intercostal nerve. The nerve enters the subcostal groove between the ribs, the parietal pleura, and the most interior intercostal muscle and travels inferior along the intercostal artery and vein. The intercostal nerve gives rise to the lateral cutaneous branch, which passes through the intercostal muscles to supply the muscle and skin of the lateral trunk, while the remainder of the nerve gives rise to the anterior cutaneous branch supplying the skin and the muscles of the anterior trunk.

Approach to Patients with Thoracic Pain

The approach to patients presenting with thoracic pain may be challenging because of the multitude of pathologic causes (Fig. 12.1). Important factors to consider are the following:

Figure 12.1. Algorithmic guide to diagnosing causes of thoracic pain.

Figure 12.1. Algorithmic guide to diagnosing causes of thoracic pain.

  1. 1. Musculoskeletal chest pain must be distinguished from chest pain due to life-threatening cardiorespiratory disorders.

  2. 2. Evaluate for acute pathology:

    1. a. Infection

      1. i. Herpes zoster virus

      2. ii. Lyme disease

    2. b. Neoplastic

      1. i. Malignancy (breast, prostate, lung, kidney)

      2. ii. Benign (hemangioma)

    3. c. Fractures

  3. 3. Post-procedural: Vertebroplasty

  4. 4. History of comorbidities

    1. a. Diabetic thoracic polyradiculopathy (DTR)

    2. b. PHN

  5. 5. Thoracic vertebral versus anterior chest musculoskeletal pathology

    1. a. Thoracic disc herniation: T1 radiculopathy

    2. b. Tietze syndrome

    3. c. Costochondritis

    4. d. Slipping rib syndrome

The clinician must also consider the locations and generators of thoracic pain (Table 12.1).

Table 12.1. Locations and Generators of Thoracic Pain.

Spinal

Extraspinal

  • Infectious

  • Neoplastic: primary, metastatic

  • Degenerative: spondylosis, spinal stenosis, facet syndrome, disc disease/herniated nucleus pulposus

  • Metabolic: osteoporosis, osteomalacia

  • Deformity: kyphosis, scoliosis, compression fracture, somatic dysfunction

  • Neurogenic: radiculopathy, herpes zoster, anteriovenous malformation

  • Intrathoracic: cardiovascular, pulmonary, mediastinal

  • Intra-abdominal: hepatobiliary, gastrointestinal, retroperitoneal

  • Musculoskeletal: post-thoracotomy syndrome, polymyalgia rheumatica, myofascial pain syndrome, somatic dysfunction, rib fractures, costochondritis

  • Neurogenic: intercostal neuralgia, peripheral polyneuropathy, reflex sympathetic dystrophy syndrome/complex regional pain syndrome

Cardiorespiratory Causes of Thoracic Pain

Although the prevalence of musculoskeletal causes of chest pain is about 50%, it is important to rule out life-threatening cardiac (16%), respiratory (5%), and intra-abdominal (see Table 12.1) causes in the initial evaluation of chest pain.

The important features of acute coronary syndrome include the location of the substernal chest pain, exertional aggravation of the chest pain, and improvement with rest or nitroglycerin. If all three characteristics are present, there is a high risk of acute coronary syndrome for patients of all age groups. If two of the three are present, it is classified as atypical angina. If only one of the three is present, the pain is considered nonanginal chest pain.

Additional studies such as electrocardiography and common markers for myocardial damage such as creatine kinase (CK) and troponin can help diagnose acute cardiac chest pain. Imaging studies may be helpful in further elucidation of cardiorespiratory and gastrointestinal causes as well.

Acute Thoracic Radiculopathy

The typical mechanism of thoracic radiculopathy is mechanical nerve compression. It is important to consider and to rule out acute causes such as tumor, infection, or fractures.

Bone is the third most common site for metastasis. The most common primary sites are breast, prostate, lung, and kidney.3 In addition, benign tumors such as vertebral hemangiomas may also lead to epidural soft tissue compression and radiculopathy.4 Diagnostic laboratory tests, biopsies, and serum calcium level as well as imaging such as plain radiographs, bone scan, computed tomography (CT), magnetic resonance imaging (MRI), and positron emission tomography may be useful in the diagnosis of metastatic compression.

The most common infectious form of thoracic radiculopathy is herpes zoster virus (HZV), which will be covered in detail here. Lyme disease may be another cause; within a month of the classic erythema migrans rash, radiculoneuritis may develop with severe pain in the thoracic dermatome with associated motor and reflex changes.5 Tuberculosis involvement of the vertebral body (Pott’s disease) may spread to the intervertebral discs and lead to irritation of the nerve roots.6

Vertebral compression fractures may be another cause of thoracic radicular pain. As the bony structure of the thoracic spine becomes compromised, nerve root compression may result. Because the thoracic spine is less mobile than the lumbar spine, trauma can lead to fractures in the lower thoracic vertebrae. T10 through L2 is the most common fracture site in the spinal column.7

One of the most widely accepted treatments for vertebral compression fractures is percutaneous vertebroplasty. However, its most common complication can lead to further radiculopathy: cement extravasation is seen in 5% to 15% of routine percutaneous vertebroplasty cases, but these leaks are generally small and clinically inconsequential. The most common sequela of symptomatic cement leaks is radiculopathy from local nerve irritation (Fig. 12.2). This may result in pain within the dermatome of the lower thoracic region. Most cases are transient, and symptomatic treatment includes nonsteroidal anti-inflammatories (NSAIDs) and epidural steroid injections. Large leakage, persistent pain, neurologic deficits, and cord compression, however, may necessitate surgical cement extraction.8

Figure 12.2. Post-vertebroplasty CT scan demonstrating large symptomatic cement leak (arrow) leading to radiculopathy from local nerve irritation.

Figure 12.2. Post-vertebroplasty CT scan demonstrating large symptomatic cement leak (arrow) leading to radiculopathy from local nerve irritation.

Diabetic Thoracic Radiculopathy

The most common form of thoracic radiculopathy is DTR. Fifteen percent of insulin-dependent diabetics and 13% of non–insulin-dependent diabetics have some form of DTR. DTR usually causes severe, chronic abdominal pain in patients with type 2 diabetes of variable duration. Other diabetic complications, weight loss, and paretic abdominal wall protrusion are common. Sensory, motor, and autonomic functions are affected. The diagnosis can be made from the characteristic history, physical examination findings, paraspinal electromyography, and other procedures. The differential diagnosis includes PHN, abdominal wall pain, malignancy, and other spinal disorders.9 The pathology appears to be immune-mediated neurovasculitis resulting in ischemic injury. Traditional therapy is symptomatic, but recent pathologic findings and clinical experience suggest that immunotherapy may be effective.10

Upper Thoracic Radiculopathy

Because of the thoracic innervations of the upper extremities, upper thoracic radiculopathy must be considered in pain and dysfunctions of the arms and hands (Table 12.2). T1 radiculopathy is difficult to differentiate from C8 radiculopathy. Several characteristics, such as diminished sensation in the axilla, motor deficit involving only the intrinsic muscles of the hand, and Horner syndrome, may help distinguish T1 radiculopathy. By contrast, T2 radiculopathy can be distinguished by cutaneous representations of the T2 nerve root to the axilla, posteromedial arm, and lateral forearm, suggesting yet another source of upper extremity radicular pain.11

Table 12.2 Location of Upper Thoracic Radiculopathy.

Disk Space

Nerve Root

Muscle

Sensory

C7–T1

C8

Finger flexors

4th and 5th fingers

T1–2

T1

Finger abductors

Ulnar forearm

T2–3

T2

Intrinsic back muscles

Axilla, posteromedial arm, lateral forearm

Lower Thoracic Disc Herniation

Thoracic disc radiculopathy accounts for only 0.2% to 0.7% of all disc disease cases. Because of the relative stability of the thoracic spine, its prevalence is significantly lower than that of the cervical or lumbar region. It most frequently occurs in men between the ages of 30 and 50 years, with most herniations of the nucleus pulposus being central or paracentral. Because there is increased mobility and torsion stresses in the lower thoracic levels, 75% of all thoracic disc herniations occur below T8, with the majority being between T11 and T12.12 Another important distinction is the presence of calcification. As many as 30% to 70% of thoracic disc herniations show calcification, and 5% to 10% of these calcified discs are associated with intradural extension.13

Similar to any vertebral disc herniation, thoracic herniations may also be completely asymptomatic. As many as 9.2% to 11% of patients with myelographic evidence of thoracic disc herniations do not exhibit any associated complains.14

Patients with symptomatic thoracic disc disease generally have three distinct presentations. The most common presenting symptom of thoracic disc herniation is pain, occurring in 76% of patients. One group complains of radicular pain, often in a band-like dermatomal distribution. The spinal nerves exit through the intervertebral foramen in proximity to the disc space. The exiting nerve root occupies essentially the entire thoracic intervertebral foramen, leaving only a third of the cranial portion for vascular passage; thus, thoracic disc herniation may cause compression of these nerves. Because each nerve in the thoracic spine travels a level down prior to exiting the foramen, a central disc protrusion will likely cause symptoms in the dermatomal level corresponding to the lower nerve, while lateral herniation will cause symptoms at the spinal level.15

In addition to radicular pain caused by foraminal stenosis, thoracic disc herniations may also generate nociceptive pain by irritation of the unmyelinated neurons surrounding the intervertebral disc, including the anterior longitudinal ligament, the posterior longitudinal ligament, the ligamentum flavum, the supraspinous ligament, the interspinous ligament, the synovial capsule, and the vertebral periosteum.16 These patients often complain of well-localized mid- or lower thoracic axial pain.

Less common but worrisome are sensory disturbances or motor impairment, which were present in 61% of patients, resulting in paresthesia, dysesthesia, sensory loss, or paraparesis. Signs of myelopathy such as a positive Babinski sign, clonus, or wide-based gait may indicate thoracic cord compression. Additionally, bladder dysfunction, usually resulting in urgency, was present in 24% of patients.13

In addition to a detailed history and physical, neuroimaging studies are essential for the diagnosis of thoracic disc disease. Plain radiographs must be obtained to rule out neoplastic and acute osseous injury. Radiography may also be able to reveal the presence of calcification. Because it is both noninvasive and sensitive, MRI is an ideal study to evaluate thoracic radiculopathy. CT myelography is a high-sensitivity study to evaluate for thoracic disc herniation. A thoracic provocative discogram may be useful in helping to elucidate and localize the source of the thoracic disc pain.17

Treatment for patients with thoracic disc pain, like that of lumbar disc pain, should begin with pharmacotherapy and physical therapy. Medications should begin with NSAIDs and may be elevated to a short course of opioid pain medications and muscle relaxants.18 Adjuvant medications such as membrane stabilizers or antidepressants may also be helpful in the treatment of thoracic radicular pain. In acute thoracic radiculopathy, an oral corticosteroid taper for about 3 to 5 days may provide adequate anti-inflammatory relief.

Short-term therapeutic modalities include manipulation, ice, heat, range of motion, flexibility, strengthening, and transcutaneous electrical nerve stimulation (TENS). However, there is little evidence that these techniques provide any long-term relief for thoracic radiculopathy.19 Brief bracing may also be helpful, but prolonged reliance may cause deconditioning and become harmful.

Interventional nonsurgical treatments may also be effective. The most widely used intervention for thoracic radiculopathy is thoracic epidural steroid injection. Epidural injections are performed via the interlaminar or transforaminal route. A review of 17 studies showed that there was fair evidence for thoracic epidural injection in the treatment of chronic thoracic radiculopathy.20 While not likely contributing to radicular pain, another potential pain generator in thoracic axial pain is the thoracic facet joint. The evidence for medial branch local anesthesia blocks to the innervation to the joint has also been fair, while there is still limited evidence for radiofrequency neurotomy of the thoracic medial branches due to insufficient literature.21 Spinal cord stimulation may be helpful in the treatment of refractory thoracic radiculopathy. Electrical stimulation of the dorsal column may prevent neuronal conduction through inhibition of the C-fibers attributed to the gate control theory of pain.22 Interestingly, a retrospective analysis demonstrated that 11 of 172 patients (6%) undergoing implantation of a spinal cord stimulator actually developed post-implantation thoracic radiculopathy, which was reversible by surgical revision.23

Surgical options become appropriate if nonsurgical modalities are insufficient to improve the pain for a prolonged time or if there is coexisting progressive myelopathy. Thoracic discectomy may be performed via the anterior, posterior, or lateral approach. A thoracotomy may be necessary in the anterior approach, so the pulmonary status of the patient must be considered: a patient with significantly decreased vital capacity may require an alternative approach. Posterior approaches would involve laminectomy, while lateral approaches include costotransversectomy.24

Postherpetic Neuralgia

PHN is a common cause of neuropathic thoracic pain. Many people in the world have been exposed to VZV. The virus remains dormant in the dorsal root ganglia, and there is a 30% chance that it may reemerge later in life as acute herpes zoster (AHZ) or shingles. AHZ is a transient condition associated with a dermatomal rash (Fig. 12.3) and associated pain. The pain persists for 120 days after the initial rash in 10% to 20% of cases when PHN develops.25 Although the trigeminal, cervical, and lumbar regions may be affected as well, the thoracic dermatomes are most frequently affected.26 Because of cell-mediated immunity depression, elderly patients tend have a 20% to 35% increased risk of developing PHN and more severe symptoms.27

Figure 12.3. Acute herpes zoster or shingles showing associated dermatomal rash.

Figure 12.3. Acute herpes zoster or shingles showing associated dermatomal rash.

Reprinted with permission from the Centers for Disease Control and Prevention’s Public Health Image Library (PHIL).

PHN is caused by neuronal injury of both the central and peripheral nervous systems leading to hyperalgesia and allodynia. Cellular changes lead to increased irritability and sensitization of C-fiber nociceptors. Further, these sensitized C-fibers lead to deafferentation and connection with physiologically non-nociceptive A-beta fibers, progressing to further allodynia due to the rewiring of the peripheral and central nervous systems. Transient receptor potential vanilloid-1 (TRPV1) receptors are upregulated, leading to further peripheral sensitization.

AHZ vaccines decrease the incidence and severity of PHN, and nearly universal VZV vaccination has dramatically decreased the number of acute infections. Early antiviral treatment within the first 3 days of the appearance of the AHZ rash can decrease the extent of the neuronal damage and therefore decrease the intensity and duration of PHN.28

Management of PHN is symptomatic and may be chronic as pain may persist for an extended time. Topical treatment is usually the first option. The 5% lidocaine patch is approved in the US for the treatment of PHN and has been shown to be beneficial in the treatment of PHN pain.29 Because TRPV1 receptor upregulation has been implicated in the development of PHN, topical capsaicin may have a role in its treatment. Capsaicin initially activates TRPV1 but then renders the receptor inactive. Capsaicin cream in a 0.075% strength may be applied, but a high-concentration (8%) capsaicin patch, when applied for about an hour along with the topical anesthetic, has been shown to relieve PHN for about 3 months.30 Because of the significant concentration, 8% capsaicin should be administered only at specialty clinics.

Systemic treatments include the use of tricyclic antidepressants and antiepileptic drugs such as gabapentin and pregabalin. The effectiveness of opioids is questionable and they are generally considered third-line treatments. Because the prevalence of PHN is highest among the elderly, it is important to be cautious about the sedative effects of systemic medications.

Invasive treatments can be used for cases refractory to medical therapy. Because most cases of PHN involve thoracic dermatomes, intercostal nerve blocks have demonstrated up to 80% symptomatic improvement for up to 3 months.31 Intrathecal steroids may also help to achieve more than 50% pain relief, but they have been associated with an increased risk of arachnoiditis.32 Epidural steroid injections are associated with immediate reduction of symptoms but do not seem to have a lasting analgesic effect at 1 to 5 months of follow-up.33

Tietze Syndrome

Tietze syndrome involves painful inflammation of the costal cartilages leading to tenderness in the costochondral junction. This inflammation leads to muscular imbalance and neuronal inflammation.34 It usually is seen in the unilateral upper ribs of younger patients of either sex and is usually a result of physical strain or injury.35 Diagnosis is mainly clinical, although bone scintigraphy and ultrasound evaluation may be helpful.36

Treatment includes anti-inflammatory medications such as NSAIDs as well as reassurance. Ultrasound-guided steroid or lidocaine injections into the costal cartilage have been effective in the treatment of persistent pain. The pain is often self-limiting in a couple of months.

Costochondritis

Like Tietze syndrome, costochondritis is characterized by costochondral junction tenderness in the upper ribs, but in costochondritis there are no signs of inflammation (Table 12.3). Costochondritis represents 30% to 42% of musculoskeletal chest pain complaints in primary care or emergency department settings.37 Costochondritis is associated with seronegative arthropathies.

Table 12.3 Characteristics of Tietze Syndrome versus Costochondritis.

Inflammation

Sites Affected

Age

Prevalence

Tietze syndrome

Present

Mostly 1 site affected

<40 years old

Rare

Costochondritis

Absent

>1 site affected

>40 years old

Common

Pain that is reproducible on palpation suggests costochondritis, other causes of chest wall tenderness need to be excluded, including cardiac, infectious, and oncologic. Electrocardiography and echocardiography can help exclude cardiac causes, while diagnostic imaging (radiologic imaging and bone scan) can rule out the latter.

Treatment centers on symptomatic pain relief with NSAIDs and acetaminophen. Local anesthetic, steroid, and sulfasalazine injections to the costochondral junction may lead to prolonged symptomatic relief.38

Slipping Rib Syndrome

Slipping rib syndrome accounts for 5% of musculoskeletal chest pain cases.37 Fibrous loosening of the lower costal cartilages causes cephalic slippage of the tip into the adjacent rib, leading to intercostal neuralgia. There is a painful click over the tip of the slipped rib associated with tenderness and laxity. The cause is often progression of previous trauma or repetitive trunk motion.39

Clinical examination of the chest wall reveals hypermobility and tenderness of the costal cartilage. This often results in painful clicking and pain reproduced by the hooking maneuver (hooking the clinician’s fingers under the lowest costal cartilage margin).40

Treatment starts with NSAIDs with physical and behavioral therapy to avoid the positions that would produce the slippage. Second-line therapy would involve intercostal nerve blocks with local anesthetic and steroids. Subperichondrial resection may be indicated for refractory pathology. The point of tenderness and offending ribs are identified and the cartilage is resected while preserving the perichondrium.41

References

1. Klinkman MS, Stevens D, Gorenflo DW. Episodes of care for chest pain: a preliminary report from MIRNET. Michigan Research Network J Fam Pract. 1994;38:345–352.Find this resource:

    2. Janson Fagring A, Gaston-Johansson F, Danielson E. Description of unexplained chest pain and its influence on daily life in men and women. Eur J Cardiovasc Nurs. 2005 Dec;4(4):337–344.Find this resource:

      3. Society of Interventional Radiology. Nonsurgical treatments for metastatic cancer in nones. http://www.sirweb.org (accessed March 26, 2013).

      4. Jiang L, Liu XG, Yuan HS, Yang SM, Li J, Wei F, Liu C, Dang L, Liu ZJ. Diagnosis and treatment of vertebral hemangiomas with neurologic deficit: a report of 29 cases and literature review. Spine J. 2014 Jun 1;14(6):944–954.Find this resource:

        5. Hehir MK 2nd, Logigian EL. Infectious neuropathies. Continuum (Minneap Minn). 2014 Oct;20(5 Peripheral Nervous System Disorders):1274–1292.Find this resource:

          6. Goodman C, Fuller K. Infectious diseases of the musculoskeletal system. In: Goodman CC, Fuller K, eds. Pathology: Implications for the Physical Therapist, 3rd ed. (pp. 1198–1199). St. Louis, MO: Saunders; 2009.Find this resource:

            7. Wood KB, Li W, Lebl DR, Ploumis A. Management of thoracolumbar spine fractures. Spine J. 2014 Jan;14(1):145–164.Find this resource:

              8. Mathis JM. Percutaneous vertebroplasty: complication avoidance and technique optimization. AJNR Am J Neuroradiol. 2003 Sep;24(8):1697–1706.Find this resource:

                9. Giles LGF, Singer K. Elements of the physical examination. In: Giles LGF, Singer K, eds. The Clinical Anatomy and Management of Thoracic Spine Pain (Table 18, p. 288). Oxford, UK: Butterworth-Heinemann; 2000.Find this resource:

                  10. Longstreth GF. Diabetic thoracic polyradiculopathy. Best Pract Res Clin Gastroenterol. 2005 Apr;19(2):275–281.Find this resource:

                    11. Sebastian D. T2 radiculopathy: a differential screen for upper extremity radicular pain. Physiother Theory Pract. 2013 Jan;29(1):75–85.Find this resource:

                      12. Arce CA, Dohrmann GJ. Herniated thoracic disks. Neurol Clin. 1985;3:383–392.Find this resource:

                        13. Stillerman CB, Chen TC, Couldwell WT, et al. Experience in the surgical management of 82 symptomatic herniated thoracic discs and review of the literature. J Neurosurg. 1998;88:623–633.Find this resource:

                          14. Awwad EE, Martin DS, Smith KR Jr, et al. Asymptomatic versus symptomatic herniated thoracic discs: their frequency and characteristics as detected by computed tomography after myelography. Neurosurgery. 1991;28:180–186.Find this resource:

                            15. DePalma AF, Rothman RH.The Intervertebral Disc. Philadelphia: WB Saunders; 1970.Find this resource:

                              16. Hirsch C, et al. The anatomical basis for low back pain. Studies on the presence of sensory nerve endings in ligamentous, capsular and intervertebral disc structures in the human lumbar spine. Acta Orthop Scand. 1963;33:1–17.Find this resource:

                                17. Schellhas KP, Pollei SR, Dorwart RH. Thoracic discography: a safe and reliable technique. Spine. 1994;19:2103–2109.Find this resource:

                                  18. Brown CW, Deffer PA Jr, Akmakjian J, Donaldson DH, Brugman JL. The natural history of thoracic disc herniation. Spine. 1992;17(suppl 6):S97–S102.Find this resource:

                                    19. O’Connor RC, et al. Thoracic radiculopathy. Phys Med Rehab Clin North Am. 2002;13(3):623–644.Find this resource:

                                      20. Benyamin RM, Wang VC, Vallejo R, Singh V, Helm S II. A systematic evaluation of thoracic interlaminar epidural injections. Pain Physician. 2012 Jul-Aug;15(4):E497–E514.Find this resource:

                                        21. Manchikanti KN, Atluri S, Singh V, Geffert S, Sehgal N, Falco FJ. An update of Evaluation of therapeutic thoracic facet joint interventions. Pain Physician. 2012 Jul-Aug;15(4):E463–E481.Find this resource:

                                          22. Melzack R, Wall PD. Pain mechanisms: a new theory. Science. 1965 Nov 19;150(3699):971–979.Find this resource:

                                            23. Mammis A, Bonsignore C, Mogilner AY. Thoracic radiculopathy following spinal cord stimulator placement: case series. Neuromodulation. 2013 Sep-Oct;16(5):443–448.Find this resource:

                                              24. Vanichkachorn JS, Vaccaro AR. Thoracic disk disease: diagnosis and treatment. J Am Acad Orthop Surg. 2000 May-Jun;8(3):159–169.Find this resource:

                                                25. Dworkin RH, Gnann JW Jr, Oaklander A, Raja SN, Schmader KE, Whitley RJ. Diagnosis and assessment of pain associated with herpes zoster and postherpetic neuralgia. J Pain. 2008; 9(1 suppl 1):S37–S44.Find this resource:

                                                  26. Kost R, Straus S. Postherpetic neuralgia—pathogenesis, treatment, and prevention. N Engl J Med. 1996;335(1):32–42.Find this resource:

                                                    27. Levin MJ, Gershon AA, Dworkin RH, Brisson M, Stanberry L. Prevention strategies for herpes zoster and post-herpetic neuralgia. J Clin Virol. 2010;48(suppl 1):S14–S19.Find this resource:

                                                      28. Jung BF, Johnson RW, Griffin DR, Dworkin RH. Risk factors for postherpetic neuralgia in patients with herpes zoster. Neurology. 2004 May 11;62(9):1545–1551.Find this resource:

                                                        29. Binder A, Bruxelle J, Rogers P, Hans G, Bosl I, Baron R. Topical 5% lidocaine (lignocaine) medicated plaster treatment for post-herpetic neuralgia: results of a double-blind, placebo-controlled, multinational efficacy and safety trial. Clin Drug Investig. 2009;29:393–408.Find this resource:

                                                          30. Derry S, Sven-Rice A, Cole P, Tan T, Moore RA. Topical capsaicin (high concentration) for chronic neuropathic pain in adults. Cochrane Database Syst Rev. 2013;2:CD007393–CD007393.Find this resource:

                                                            31. Shannon HJ, Anderson J, Damle JS. Evidence for interventional procedures as an adjunct therapy in the treatment of shingles pain. Adv Skin Wound Care. 2012;25:276–286.Find this resource:

                                                              32. Kotani N, Kushikata T, Hashimoto H, Kimura F, Muraoka M, Yodono M, Asai M, Matsuki A. Intrathecal methylprednisolone for intractable postherpetic neuralgia. N Engl J Med. 2000;343:1514–1519.Find this resource:

                                                                33. Perkins HM, Hanlon PR. Epidural injection of local anesthetic and steroids for relief of pain secondary to herpes zoster. Arch Surg. 1978;113:253–254.Find this resource:

                                                                  34. Rovetta G, Sessarego P, Monteforte P. Stretching exercises for costochondritis pain. G Ital Med Lav Ergon. 2009;31(2):169–171.Find this resource:

                                                                    35. Semble EL, Wise CM. Chest pain: a rheumatologist’s perspective South Med J. 1988;81:64–68.Find this resource:

                                                                      36. Kamel M, Kotob H. Ultrasonographic assessment of local steroid injection in Tietze’s syndrome. Br J Rheumatol. 1997;36:547–550.Find this resource:

                                                                        37. Verdon F, Herzig L, Burnand B. Chest pain in daily practice: occurrence, causes and management. Swiss Med Wkly. 2008;138:340–347.Find this resource:

                                                                          38. Freeston J, Karim Z, Lindsay K. Can early diagnosis and management of costochondritis reduce acute chest pain admissions? J Rheumatol, 2004;31:2269–2271.Find this resource:

                                                                            39. Karlson K. Thoracic region pain in athletes. Curr Sports Med Rep. 2004;3(1):53–57.Find this resource:

                                                                              40. Fu R, Iqbal CW, Jaroszewski DE. Costal cartilage excision for the treatment of pediatric slipping rib syndrome. J Pediatr Surg. 2012;47(10):1825–1827.Find this resource:

                                                                                41. Mooney DP, Shorter HA. Slipping rib syndrome in childhood. J Pediatr Surg. 1997; 32(7):1081–1082.Find this resource: