Interventions in Chronic Pain Management. 2. Diagnosis of Cervical and Thoracic Pain Syndromes

2.1 Clinical Activity: To differentiate the investigation for cervical radiculopathy from other upper-extremity syndromes in a 35-year-old patient with trapezius pain and radiation of pain into the upper extremity and scapula 

INNERVATED STRUCTURES in the vertebral column (facet, outer annulus of the intervertebral disk, dura mater, anterior or posterior longitudinal ligament, or paravertebral muscles) can cause localized or radiating pain. Differential diagnoses include cervical radiculopathy, cervical facet syndrome, cervical spondylosis, cervical stenosis, myelopathy, cervical herniated nucleus pulposis (HNP), myofascial pain or fibromyalgia, shoulder pathology including rotator cuff or joint pathology, scapular and humeral fractures, or visceral disease. Peripheral nerve lesions that can lead to cervical or trapezius pain include brachial plexopathy, dorsal scapular, suprascapular, spinal accessory, and axillary and long thoracic nerve lesions.

Cervical radiculopathy is a dysfunction of the cervical spinal nerve root caused by irritation or compression. The cervical nerve root may be compressed by an HNP, foraminal stenosis from osteophyte formation or facet hypertrophy, tumor, or infection. Inflammatory factors include phospholipase A2, prostaglandin E2, interleukin-6, matrix metalloproteinases, and nitric oxide. Cervical radiculopathies account for 5% to 36% of all radiculopathies.1 The incidence of cervical radiculopathy by level is as follows: 70% originate at C7, 9% to 25% at C6, 4% to 10% at C8, and 2% at C5.2

The examination should include observation and inspection of the trapezius and scapular musculature as well as palpation; range of motion (ROM) of the cervical spine; neurologic examination including testing of strength; deep tendon reflexes; and a sensory examination for pain, vibration, and light touch. Provocative maneuvers such as the Spurling test may help to reproduce symptoms arising from the cervical spine and differentiate radiculopathy from peripheral joint or nerve problems. Shoulder ROM must be evaluated. Furthermore, provocative shoulder testing should be evaluated to see if all or a portion of the pain is related to the cervical spine or the shoulder. The biceps tendon, subdeltoid bursa, and acromioclavicular joint must be palpated to look for secondary shoulder pathology. The medial and lateral epicondyle must be palpated; wrist flexors and extensors must be activated and stretched to evaluate for medial or lateral epicondylitis that can be confused with cervical radiculopathy or weak musculature associated with a peripheral nerve lesion. Percussion made over the median or ulnar nerve may be done to try to provoke the Tinel sign, which is a tingling or painful sensation in the distribution of the specific nerve that is being evaluated if that nerve is producing symptoms. This may help to rule out peripheral nerve lesions, which can be confused with cervical radiculopathy. The lower-extremity neurologic examination should be performed to rule out myelopathy, and the cranial nerves should be evaluated for upper motoneuron pathology arising from the brain. Peripheral pulses in the upper extremities should be evaluated to rule out vascular insufficiency.

Magnetic resonance imaging (MRI) is the study of choice to evaluate patients for a disk herniation; however, the presence of a disk herniation may or may not be significant. Boden et al2 found MRI abnormalities in 19% of asymptomatic patients. Fourteen percent of patients who are younger than age 40 have MRI abnormalities. Twenty-eight percent of patients over age 40 have MRI abnormalities.2

Cervical provocative diskography remains a controversial diagnostic test for patients with axial pain when other diagnostic studies fail to identify the patient’s pain generator. Provocative diskography may help to identify the painful disk, but the procedure is technically demanding; potential complications include diskitis, subdural hematoma, spinal cord injury, vascular injury, and prevertebral abscess.3

Electromyography is used to evaluate patients with suspected radiculopathies, plexopathies, peripheral neuropathies, or myopathies. The nerve conduction study evaluates the motor nerves by evoking a compound muscle action potential (CMAP), and sensory nerve action potential (SNAP) evaluates the sensory nerve. Patients with suspected radiculopathy rarely exhibit prolonged distal latency or reduced amplitudes in the SNAP. Lesions proximal to the cell body of the sensory nerve proximal to the dorsal root ganglia do not affect the SNAP; however, a lesion distal to the dorsal root ganglion will cause a decrement in the amplitude of the SNAP. In a suspected plexopathy, one should evaluate whether the sensory nerve emanates from a different trunk or cord to separate nerve root from plexus disease. Unlike the sensory nerve, the motor nerve’s cell bodies (anterior horn cells) are located in the gray matter of the ventral horn; therefore, the amplitude of the CMAP may be reduced if axonal degeneration has occurred with damage to the nerve root or distal to the nerve root. The sensitivity of needle electromyography to diagnose cervical radiculopathy is 61% to 67% compared with the criterion standards of clinical evaluation, myelogram, and intraoperative impression.4

In cervical spondylosis, the intervertebral disk, facet joints, and ligamentous structures degenerate, a situation that leads to central and foraminal stenosis. Predisposing factors include age, trauma, work activities, and family history. Patients may exhibit signs of myelopathy and/or radiculopathy. In addition, pain may be referred to the trapezius, base of skull, or shoulders. Acquired cervical stenosis may develop as a result of osteophyte formation, disk protrusion, ligamentum hypertrophy, or facet hypertrophy. Congenital cervical stenosis is most often associated with short pedicles.

Patients diagnosed with central cervical stenosis may exhibit neurologic changes including gait disturbance, bowel or bladder dysfunction, impotence, hand weakness, leg weakness, spasticity, clonus, or hyperrflexia. The diameter of the spinal canal in the cervical spine ranges from 15 to 25mm with a mean of 17mm,5, 6 whereas the average cervical spinal cord diameter ranges from 5 to 11.5mm with a mean of 10mm.7 A cervical spinal canal less than 13mm in diameter is considered stenotic,8 and a cervical canal less than 10mm is an absolute radiographic indicator of cervical spinal stenosis.9

Cervical facet syndrome is often characterized by neck, head, shoulder, and proximal upper-extremity pain and is associated with nondermatomal pattern. Aprill and Bogduk10 reported the prevalence of cervical zygapophyseal joint pain with intractable neck pain to be between 25% and 63%.

Referral patterns of the facet joints, which are innervated by the medial branches of the dorsal rami, were mapped out initially by Dwyer et al11 and later Aprill et al12 who anesthetized the medial branch above and below the symptomatic joint. Dwyer showed that C2-3 facet disease provoked occipital head pain; C4-5, C5-6, and C6-7 provoked shoulder pain; and C7-T1 provoked intrascapular pain. Windsor et al13 showed that stimulation of each medial branch created distinct referral patterns that are different from the mapping of the facet joints. The criterion standard for the diagnosis of pain generated by the zygapophyseal joint is diagnostic injection to the zygapophyseal joint or to the medial branch of the dorsal root since history; physical and imaging studies are unreliable.

Intra-articular injections are technically challenging in proportion to posttraumatic arthropathy, age, and surgical changes. An increased risk of false-positive results exists if the patient has extra-articular leakage into the interlaminar space or the interspinous, cervical epidural, or paraextradural space. Therefore, it is important that the local anesthetic always reaches the target nerve but does not affect any other diagnostically important structures. The patient must have between 50% and 80% pain relief with provocative pain maneuvers on 2 different occasions in order to diagnose the facet as the pain generator. Single uncontrolled injections carry a 27% false-positive rate.14 Comparative injection considerations include placebo versus local anesthetic or short-acting versus long-acting anesthetic. Comparative blocks are more specific but less sensitive than placebo-controlled blocks.15

Myofascial pain is often defined as a regional pain syndrome of soft-tissue origin. Patients with suspected myofascial pain may experience a hyperirritable spot in the skeletal muscle, which is classically defined as a trigger point. Active trigger points produce clinical complaints when digitally compressed, whereas latent trigger points do not produce spontaneous pain but can produce other effects characteristic of trigger points. Trigger points may refer pain in a peripheral, central, or local referral pattern.

The diagnosis of fibromyalgia is based on a history of widespread pain, defined as pain present bilaterally, in the upper and lower body, and in the axial skeleton. Furthermore, applying pressure to the specific tender point sites should reveal excessive tenderness at 11 of those 18 sites. By definition, these tender points become painful at 4kg of pressure.16 It is reported that 72% of patients with fibromyalgia have active trigger points and that 20% of patients with myofascial pain syndrome also have fibromyalgia.17 Two other criteria for the diagnosis of fibromyalgia are sleep disturbance and fatigue. Minor symptoms include paresthesias, anxiety, headache, and irritable bowel syndrome.

There are no universally accepted tests that are diagnostic for the identification of a trigger point. Several studies have investigated the use of electromyography as a diagnostic test, but the results remain controversial. Both Weeks and Travell18 and Hubbard and Berkoff19 identified high-frequency potentials in trigger points while the remainder of the muscle was electrically silent. Simons et al20 identified high-amplitude endplate spike potentials in addition to low-voltage endplate potentials after increasing the amplification 5-fold and the sweep speed 10-fold. Electromyographers often identify these same findings as normal endplate potentials or endplate noise.

2.2 Clinical Activity: To investigate the reason for burning midthoracic pain that is followed by a rash in a 55-year-old woman 

2.3 Clinical Activity: To differentiate cervicogenic headache from other headache syndromes in a 25-year-old woman with chronic migraines who is experiencing recent exacerbation of her headaches after a motor vehicle collision 

In 1983, Sjaastad et al44 introduced the term cervicogenic headache. The concept was that the pain was perceived in the head but that the underlying source of the pain originates in the neck. The International Headache Society (IHS) has designated cervicogenic headache as a secondary headache.45 According to IHS, the types of headaches designated as primary are migraine, tension-type headache, cluster headache, and “other primary headaches.” The primary headaches are based on clinical and descriptive criteria for the most part. The diagnosis of the primary headache requires the exclusion of any other disorder that might be the cause of the headache. Secondary headaches are, by definition, attributed to another disorder when a new type of headache develops for the first time soon after the onset of the given disorder.

IHS has 4 diagnostic criteria for cervicogenic headache. Pain must be referred from a source in the neck and be perceived in the head and/or face. Clinical, laboratory, and/or imaging evidence of a disorder or lesion within the neck is generally accepted as a valid cause of headache. There must be evidence that the pain can be attributed to a cervical lesion. Evidence is obtained in 2 ways: (1) demonstration of clinical signs that implicate a source of pain in the neck or (2) abolition of headache after a diagnostic block of a cervical structure or its nerve supply along with the use of a placebo or other adequate control. Also, pain should resolve within 3 months of successful treatment of the underlying lesion. Spondylosis of the upper cervical spine is not formally accepted as valid imaging evidence of a disorder. Also, if myofascial tender points in the cervical spine are believed to be the cause of the headache, then the headache should be coded under tension-type headache.45

The Cervicogenic Headache International Study Group described the clinical features of cervicogenic headache.46 Typical headache must be precipitated by neck movement or by external pressure applied over the upper cervical spine or occiput on the symptomatic side. Cervical ROM is restricted. There must be ipsilateral neck and/or shoulder or arm pain, which is typically vague and generally nonradicular. The head pain is consistently unilateral and does not switch sides. Confirmatory evidence by diagnostic anesthetic blockade is essential.

Pain is usually moderate and achy more than throbbing. Initially, it is episodic, but over time it can become constant. It starts in the neck but spreads to ipsilateral orbital, frontal, and temporal areas. Classic signs of migraine such as nausea and vomiting and photophobia and phonophobia do not occur commonly. There is often a history of head or neck trauma.

The prevalence of cervicogenic headache is 0.4% to 2.5% in the general headache population and affects 15% to 20% of patients with chronic headaches. It is more prevalent in females by a 4:1 ratio, and the mean age is 42.9 years.47, 48

The etiology of cervicogenic pain has been debated. Generic possibilities include muscular, neurogenic, osseous, and vascular etiologies. The zygapophyseal joints (particularly C1-2, C2-3, C3-4) can be proven to be pain generators by anesthetic block of the joint or by blocking the medial branch of the dorsal root supplying the joint. The C2 and C3 spinal nerves and the greater and lesser occipital nerves are potential pain generators that can be diagnosed by diagnostic blocks. Cervical diskography may be a diagnostic tool to establish whether the intervertebral disk may be the cause of cervicogenic headache. Myofascial pain may or may not be diagnosed with trigger point injections. Vertebral fractures, tumors, infections, and rheumatoid arthritis of the upper cervical spine have not been formally validated as causes of cervicogenic headache but are accepted as valid causes in individual cases by IHS. Because facet and diskogenic changes are commonly seen without painful symptoms, radiologic findings may or may not be helpful, depending on the clinical presentation.

The trigeminocervical nucleus is a region of the spinal cord where descending sensory nerve fibers of the trigeminal nerve interact with sensory fibers of the upper cervical roots. The trigeminal nucleus caudalis descends as low as the C3 or C4 spinous segments and is continuous with the spinal dorsal horn gray matter. Afferent spinal sensory neurons ascend or descend for 3 segments in the dorsilateral tract and substantia gelatinosa before entering the dorsal horn. This would allow pain from even the lower cervical segments to radiate to the head and vice versa. It is an area that could account for overlap between cervicogenic and migraine headaches.49

Certain issues raise the red warning flag of a possibly emergent condition. Sudden onset of severe headache raises the question of subarachnoid hemorrhage, a mass, or an arteriovenous malformation (AVM). Headache caused by masses or subarachnoid lesions may also be triggered by the Valsalva maneuver. A worsening pattern of headache is suspicious for mass, subdural hematoma, or medication overuse. Headache with systemic illness (fever, rash, neck stiffness) raises concerns about meningitis, encephalitis, Lyme disease, systemic infection, arteritis, and collagen vascular disease. Focal neurologic signs or symptoms may be found in mass lesions, AVM, and collagen vascular diseases. New headaches in pregnancy or postpartum patients can be caused by cortical vein/sinus thrombosis, carotid dissection, and pituitary apoplexy. Papilloedema raises concerns about pseudotumor, encephalitis, meningitis, or mass lesion.50

Primary headaches to be considered in the differential diagnosis include migraine headaches, tension-type headaches, cluster headaches, benign paroxysmal hemicranias, and hemicrania continua. The diagnosis of a secondary headache in a patient with a preexisting primary headache is challenging. Worsening may represent exacerbation of a preexisting primary headache or a new type of secondary headache. A secondary headache is more likely if a close temporal relationship to a causal disorder exists, if evidence that the causal disorder can cause the headache is strong, or if treatment of that disorder is successful. Also, a secondary headache is more likely if its symptoms are distinctly different from those of the primary headache.45

Further complicating the issue is the fact that a migraine headache is a common condition that affects up to 12% of the population. Thus, up to 12% of patients with cervicogenic headaches may also have migraines.51 Conversely, up to 75% of patients with a migraine have concurrent neck pain. Muscle tension in the head and neck is likewise common in tension-type headaches.52 Furthermore, a medication-overuse headache may be of concern.

A migraine headache may occur with and without aura. A migraine without aura must have at least 2 of the 4 following criteria: unilateral location, pulsating quality, moderate or severe intensity, and aggravation by or causing avoidance of routine physical activity. During the headache, either photophobia/phonophobia or nausea and/or vomiting must be present. Attacks last for 4 to 72 hours. In a migraine with aura, the migraine begins during the aura or follows the aura within 60 minutes. Aura consists of at least 1 of the following phenomena: reversible visual symptoms (eg, loss of vision, spots, lines), reversible paresthesias or numbness, or reversible dysphasic speech disturbance. At least 2 of the following symptoms must be present: homonymous visual symptoms and/or unilateral sensory symptoms, at least 1 or more aura symptoms either alone or in succession for more than 5 minutes, and each symptom must last between 5 and 60 minutes.45, 50

Tension-type headaches have at least 2 of the following symptoms: bilateral location, pressing or tightening (nonpulsating) quality, mild to moderate intensity, and not aggravated by routine physical activity. Nausea and vomiting does not occur, and there should not be more than 1 of either phonophobia or photophobia. It can last for 30 minutes to 7 days. To be designated an “infrequent episodic tension-type headache,” the patient must have at least 10 episodes that occur less often than 1 day a month. Patients with a “frequent episodic tension-type headache” have at least 10 episodes that occur between 1 and 15 days a month for at least 3 months. A “chronic tension-type headache” happens 15 or more days monthly for more than 3 months.45, 50

Cluster headaches are intermittent and brief. Pain peaks in 10 to 15 minutes but remains intense for 1 hour. Excruciating unilateral head pain is accompanied by autonomic dysfunction. Pain is sharp, boring, and piercing more than pulsating. Episodic cluster headaches last for 7 days to 1 year, and the patient may have attack-free periods of 1 month or more. Chronic cluster headache attacks occur for 1 year without remission or with remissions of less than 1 month.45, 50

Paroxysmal hemicrania has 3 main features. It is characterized by more than 5 attacks daily and 20 overall attacks that last 2 to 30 minutes and are severe and unilateral in the orbital, supraorbital, or temporal regions. Symptoms of autonomic dysfunction ipsilateral to the pain are present. Indomethacin relieves the headache.

Hemicrania continua is a headache that is unilateral and of moderate intensity. It may be accompanied by autonomic symptoms. It is responsive to indomethacin. It occurs daily and may have exacerbations.45, 50