Cervical Pain

Abstract

Cervical pain is described as the perception of pain in the region defined as below the superior nuchal line, between the lateral margins of the neck and above the level of the T1 spinous process (Merskey & Bogduk, 1994). Given the co-location of the neck with the head and upper extremities, pathologic conditions in the cervical spine may result in pain in other sites such as the jaw, head, shoulder, arms and upper back. For example, pain arising from the upper cervical zygapophyseal (or “facet”) joints tends to be perceived as headache in the suboccipital region (Cooper, Bailey, & Bogduk, 2007), and cervical radicular pain is perceived as upper extremity pain (Bogduk, 2011a). Thus, for the purposes of this chapter, the authors will focus on clinical states in which the patient’s perception of pain lies within the anatomic bounds of the neck. Of course, not all painful disorders involving the neck are constrained to this region; they may result in the perception of pain in other discrete anatomic sites or even generalized throughout the body. Therefore, such disorders will also be addressed insofar as they also result in the perception of pain in the neck.

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Overview

Cervical pain is described as the perception of pain in the region defined as below the superior nuchal line, between the lateral margins of the neck and above the level of the T1 spinous process (Merskey & Bogduk, 1994). Given the co-location of the neck with the head and upper extremities, pathologic conditions in the cervical spine may result in pain in other sites such as the jaw, head, shoulder, arms and upper back. For example, pain arising from the upper cervical zygapophyseal (or “facet”) joints tends to be perceived as headache in the suboccipital region (Cooper, Bailey, & Bogduk, 2007), and cervical radicular pain is perceived as upper extremity pain (Bogduk, 2011a). Thus, for the purposes of this chapter, the authors will focus on clinical states in which the patient’s perception of pain lies within the anatomic bounds of the neck. Of course, not all painful disorders involving the neck are constrained to this region; they may result in the perception of pain in other discrete anatomic sites or even generalized throughout the body. Therefore, such disorders will also be addressed insofar as they also result in the perception of pain in the neck.

Discussion of cervical pain is a key component to consider when undertaking a study of pain and disability in the workplace because cervical pain is a common source of occupation-related pain disorders, following only low back pain as a source of workplace absenteeism (Kvarnstrom, 1983). Spine pain, including the neck and lower back, is second only to arthritis and joint pains in terms of healthcare expenses utilized for musculoskeletal conditions. It is estimated that, from 2002 to 2004, approximately $194 billion was spent on spine pain alone. Furthermore, the vast majority (79 %) of spine pain occurs in adults of working age (18–64), thus accounting not only for large use of healthcare dollars but also a large source of lost workforce wages and productivity (Jacobs et al., 2008). One year prevalence of neck/shoulder pain has been reported to be in the 15–20 % range (Anderson, 1984; Kvarnstrom, 1983; Westerling & Jonsson, 1980), while lifetime prevalence has been reported to be nearly two-thirds (Cote, Cassidy, & Carroll, 1998). Also, the increasing automation and specialization in the modern workplace is thought to result in more homogeneous and repetitive work tasks that ultimately contribute to cumulative trauma and increased report of injury (Hagberg & Wegman, 1987; Nordin, Andersson, & Pope, 1997). Occupational cervical pain is more commonly reported in women than men and is a more frequent source of sick leave amongst women (Anderson, 1984; Westerling & Jonsson, 1980). Psychosocial factors may also contribute to the development of occupational musculoskeletal disorders. Stress, lack of control, monotony, poor job satisfaction, and low skill requirements have been reported to correlate with development of occupational musculoskeletal disorders (Nordin et al., 1997). Of note, though, is a recent literature review on the course and prognosis of neck pain in workers (Carroll, Hogg-Johnson, et al., 2011; Carroll, Holm, et al., 2011) which concluded that age, gender, and job-demand differences showed only small associations at best in predicting prognosis of cervical pain. The reviewers ultimately conclude that the strongest evidence for poor prognostic indicators included prior episodes of pain, prior sick leave, occupation (e.g., blue collar vs. white collar, enlisted personnel vs. officers), and, finally, the perception of little influence over one’s work situation. Further research on such prognostic factors is important because knowledge of such factors may allow for instituting changes in workplace policies or environments in order to avoid cervical pain, as well as to select for workers who may need specific interventions to ameliorate or altogether avoid episodes of cervical pain. Fortunately, the natural history of acute episodes of cervical pain tends toward resolution in the majority of cases, although some estimate that from 10 to 30 % of patients will go on to have chronic cervical pain (Bogduk, 2011a) and that, at any time, 4.6 % of adults have disabling neck pain (Cote et al., 1998).

Given the increasing personal and economic burden of chronic cervical pain, it has become increasingly important for the clinician to have a strong grasp of the various pathologic conditions resulting in chronic cervical pain. Proper evaluation and management of cervical pain require knowledge of the various anatomic elements that make up the cervical spine, their normal function, and the common pathologies that result in painful conditions. Special attention will be given in this chapter to the identification of the anatomic elements of the cervical spine and the pathologic conditions resulting in pain in this region. Treatment of such conditions will be addressed in other chapters in this handbook.

The Cervical Spine

The musculature of the neck is a common source of cervical pain, as well as headache and upper back or shoulder pain due to common insertions between the anatomic sites. Such myofascial pains will be addressed at length, as well as “whiplash” syndrome because it has become the subject of great interest due to its increasing commonality and levels of chronic pain and disability associated with this disorder. Specific anatomic topics and associated pathologic conditions that will be addressed in this chapter include the motion segments of the cervical spine, the bony and the intervertebral discs. Other conditions will be addressed insofar as they contribute to cervical pain and include fibromyalgia, rheumatologic conditions, neoplasms, vascular anomalies, and a variety of less common degenerative conditions.

Anatomy

The cervical spine begins at the base of the skull and ends at the first thoracic vertebra. It is comprised of seven vertebral segments that differ in morphology and articulation from the lower thoracic and lumbar segments. The upper two cervical vertebrae differ even more so due to their primary function, support, and axial motion of the skull. Each vertebra generally has an anterior body connected to paired pedicles which project posteriorly and form the lateral borders of the spinal canal. Posteriorly, the spinal canal is formed by the superior and inferior articular processes and the lamina. There are also bony projections posterior to the lamina (known as spinous processes) and lateral to the body (known as the transverse processes). The transverse processes contain a foramen that houses the vertebral artery as it projects up from the aortic arch to the skull. The vertebral bodies below C2 are separated by intervertebral discs, composed of a nucleus and an outer fibrous annular layer. The anterior annulus fibrosis is much thicker and stronger than the rest of the disc, which contributes to the lordotic curvature in this part of the spine. The primary role of the intervertebral discs is absorption of axial load.

The first cervical vertebra (C1), also known as the atlas, is comprised of an anterior and posterior arch along with lateral masses. The lateral masses articulate with the occipital condyles of the skull superiorly and with the body of C2 inferiorly. The C2 vertebra, also known as the axis, has a bony projection (dens or odontoid process) that passes through the middle of C1 and articulates with the posterior aspect of its anterior arch. The atlanto-occipital joint (C1 to skull) allows for flexion and extension of the skull. It is important to note that normal range of flexion and extension at this joint can range up to 35° (Mercer & Bogduk, 2001), but further movement of the neck can be obtained with motion of inferior cervical segments. The atlantoaxial joint (C1–2) allows for axial rotation of the skull by pivoting on the odontoid process. The normal range of motion for this segment is about 45° of lateral rotation before low cervical segments begin moving.

Below this level, the cervical vertebra articulates via two separate joints bilaterally, allowing for anterior and posterior contact. This formation allows for transmission of axial load to the inferior spine. The uncovertebral joints, or joints of Luschka, are articulations of the uncinate process along the posterolateral borders of the vertebral body. The zygapophyseal, or facet, joints are articulations of the superior and inferior articular processes along the posterior element of the vertebra. The vertebrae are further stabilized by ligaments. The anterior longitudinal ligament runs anteriorly to the vertebral bodies and intervertebral discs, while the posterior longitudinal ligament runs posteriorly. The ligamentum flavum forms the posterior border of the epidural space and runs anterior to the lamina. The interspinous ligament runs between adjacent spinous processes while the supraspinous ligament runs along the distal ends of the spinous processes. Finally, the spinal canal protects the spinal cord as it descends from the foramen magnum, and it protects the nerve roots which exit the intervertebral foramina. There are eight paired cervical nerve roots, with the first exiting between the skull base and C1 (thus the C2 roots exit between C1/2 and so on).

Cervical Nerves

A thorough understanding of cervical nerves is necessary to interpret physical exam findings. Sensory dermatomes include the shoulder (C4), lateral arm to elbow (C5), thumb and index finger (C6), posterior forearm and middle finger (C7), and little finger (C8). Common muscle innervation includes the levator scapula tested with shrugging (C4), biceps tested with elbow flexion (C5), wrist extensors (C6), triceps tested with elbow extension (C7), and finger flexors (C8). Relevant deep tendon reflexes include the biceps (C5/6) and triceps (C7/8) (see Table 3.1).

Table 3.1 Cervical nerve roots

Cervical Musculature

The major posterior muscles of the neck include the trapezius, levator scapulae, splenius, semispinalis, and suboccipital muscles. The trapezius and levator scapulae muscles attach between the spine and the shoulders/back, and they are essentially involved in coordinated neck and shoulder movements. The splenius (capitis and cervicis) muscle attaches the head to the posterior spine and upper thoracic vertebrae. Its primary function is tilting the head backward and head rotation. The semispinalis (dorsi, cervicis, and capitis) is a large paraspinal muscle whose main action is extension of the neck. The suboccipitals (rectus capitis posterior major and minor, obliquus capitis superior and inferior) are involved in fine movements of the head including rotation and extension.

Laterally, the scalene muscles (anterior, middle, and posterior) attach from the cervical spine to the first and second ribs. They are involved in rotation, flexion, and lateral bending. Anteriorly, the sternocleidomastoid and prevertebral muscles are present. The sternocleidomastoid is mostly involved in flexion of the head and lateral movement. The prevertebral muscles (longus colli and capitis, rectus capitis anterior and lateralis) are mostly involved in neck flexion.

Cervical Zygapophyseal Joints

The cervical zygapophyseal (or “facet”) joints are formed by paired articular cartilaginous surfaces of corresponding upper and lower cervical vertebra to form one diarthrodial joint on each side of the cervical spine (Hertling & Kessler, 2006; Jaumard, Welch, & Winkelstein, 2011). These joints participate in bearing the weight of the head, and they allow motion in multiple planes including flexion, extension, axial rotation, and lateral bending. The upper cervical segments (i.e., C2 and above) have specialized anatomy allowing great range of motion and secure coupling with the head at the foramen magnum. The lower segments (i.e., C2–7) appear more similar to the thoracic and lumbar segments with specialized adaptations to bear the weight of the head and neck and facilitate the range of motion of the neck (Hertling & Kessler, 2006; Onan, Heggeness, & Hipp, 1998). Pain arising from the cervical zygapophyseal joints may be responsible for up to one-half of chronic pain associated with chronic whiplash injuries (Barnsley, Lord, & Bogduk, 1993; Lord, Barnsley, & Bogduk, 1995; Lord, Barnsley, Wallis, & Bogduk, 1996). It is unclear as to the incidence of zygapophyseal joint pain outside the setting of whiplash trauma (because such studies are lacking), but suspicion of these joints as a pain generator can be tested with diagnostic blocks of the suspected joints (Bogduk, 2011a).

Disorders of the Cervical Spine

Cervical Spondylosis

Spondylosis is a commonly utilized term and is often misunderstood in its role in neck pain. Cervical spondylosis denotes degenerative changes in various elements of the cervical spine, including the intervertebral discs, ligaments, and bony elements (i.e., pedicles, zygapophyseal joints). These degenerative changes become ubiquitous as population ages and are readily visible on imaging studies (Bogduk, 2011a; Hadler, 1999). Due to the ease with which such changes are noted by imaging and the exceedingly common nature of such degeneration, they are commonly implicated as the causative agent in neck pain. Unfortunately, such degenerative changes are not well correlated with physical signs and symptoms, and they are generally considered a normal part of the aging process, although they may be accelerated by trauma, heavy lifting, smoking, or operating vibrating equipment. Despite the fact that these degenerative changes are asymptomatic in most patients, if they are of sufficient severity, they may lead to stenosis of the neuroforamen or central canal and then to radicular symptoms (Bogduk, 2011a; Ehni, 1984; Kaplan & Tanner, 1989; Nordin et al., 1997).

Cervical Spondylolisthesis

Spondylolisthesis is anterior or posterior displacement of a vertebra in relation to the vertebra below it. Cervical spondylolisthesis, although less common than lumbar spondylolisthesis, still accounts for a significant portion of patients with neck pain. It is most often of degenerative etiology that can be due to trauma. Pain due to spondylosis or spondylolisthesis can be axial and/or radicular depending on the underlying pain generator. If the pain originates from the joints, it tends to be axial and localized (Van Eerd et al., 2010). Radicular pain could be due to irritation of nerve roots due to neuroforaminal stenosis or osteophytes. Degenerative spondylolisthesis is generally preceded by degeneration of the intervertebral disc and facet joints. The most common level of degenerative disease tends to be the C3/4 and C4/5 junctions (Jiang, Jiang, & Dai, 2011). Of concern is that patients may develop myelopathy. Although it has been noted that the severity of spondylolisthesis did not always correlate with myelopathy, others have argued that dynamic canal stenosis was of more importance in accounting for progression of myelopathy (Hayashi, Okada, Hashimoto, Tada, & Ueno, 1988).

Plain radiography of the cervical spine can help elucidate spondylosis and spondylolisthesis, while additional flexion/extension views can be obtained to determine any instability of the spine. MRI can be used to further assess for spinal cord or nerve compression, if suspected. Treatment options include physiotherapy, spinal manipulation (not for spondylolisthesis), pain management interventions, and surgery.

Cervical Stenosis/Myelopathy

Stenosis refers to the narrowing of the spinal canal. Common causes include disc herniation/bulging, spondylosis, and ligamentous changes (such as hypertrophy and buckling). Canal stenosis is often asymptomatic; however, it can lead to compression of the spinal cord with possible myelopathy and cord changes. Occasionally, one may see an acute disc protrusion leading to myelopathy which requires surgical consultation. More likely, it is marked by the patient with clinically “silent disease” that progressively leads to decline in function. The clinical course is highly variable and can often be asymptomatic despite imaging findings (Alexander, 2011). There are several classification systems for severity of stenosis. One used involves the relation of the AP diameter at the affected level to normal: mild is classified as 75–99 % of normal, moderate is 50–74 %, and severe is less than 50 %.

Myelopathy refers to a disorder of the spinal cord with a neurologic deficit. It can be caused by stenosis, trauma, malignancy, infection, or autoimmune processes. Patients may often present with paresthesias, mild weakness, or clumsiness in the initial stages. Eventually, weakness of the extremities, sensory changes, ataxic gait, and bowel/bladder changes may be seen. In addition, hyperreflexia, Lhermitte’s sign, Hoffman’s sign, or a Babinski reflex may be elicited. A commonly seen disorder in a clinical setting is cervical spondylitic myelopathy. It most often presents as a slow decline in function, whereas acute changes are often a harbinger of some other etiology. It has been noted that long periods of severe cervical stenosis can be associated with demyelination of white matter and necrosis of grey and white matter, leading to potentially irreversible effects. It is important to recognize patients with severe symptoms and/or long-standing symptoms because the likelihood of improvement with nonoperative treatment is low (Matz et al., 2009). Imaging is helpful at delineating underlying etiologies. MRI or CT with or without myelography can be used. Treatment is generally surgical decompression of the affected area.

Nerve Compression

Spinal nerves can be compressed by disc disorders (herniation/bulges), spondylosis, tumors, and other less common etiologies. This often manifests as radicular pain that is felt extending from the neck into the upper back or extremities. This pain is due to activation of nociceptors by direct compression or due to inflammatory changes (Alexander, 2011). Patients may also develop radiculopathy (which is a sensory or motor deficit) of the upper extremity. It is important to note that patients may manifest with neck pain and intermittent upper extremity complaints or vice versa. In a study looking at patients from 1976 to 1990 within the Mayo clinic system (Van Zundert, Huntoon, & Patijn, 2010), it was noted that the highest incidence of cervical radiculopathy was seen in patients who were male, in the 50–54-year-old subgroup, and those who had prior lumbar radiculopathy. There has also been an association with heavy manual jobs, persons who operate vibrating equipment, frequent travel by automobile, and smoking (Alexander, 2011). The most commonly affected nerve dermatomes were at the C7 and C6 levels. If cervical disc herniation is the etiology, it is usually due to the intervertebral disc above the nerve root.

Diagnosis is mainly based on history and physical exam. Testing can include Spurling’s maneuver, which should reproduce radicular pain, and the axial manual traction test, which should alleviate pain (Nordin et al., 2009; Van Zundert et al., 2010). These tests have been found to have high specificity but low sensitivity (Van Zundert et al., 2010); there is consistent evidence that the clinical exam has higher negative predictive value than positive predictive value for cervical radiculopathy (Nordin et al., 2009). Overall, MRI is the imaging modality of choice due to its superior soft tissue resolution. However, many studies have shown that imaging abnormalities do not always equate with symptomatology (Alexander, 2011; Boden et al., 1990; Dai, 1998; Ernst, Stadnik, Peeters, Breucq, & Osteaux, 2005; Schellhas, Smith, Gundry, & Pollei, 1996; Sohn, You, & Lee, 2004; Zheng, Liew, & Simmons, 2004). Plain films can demonstrate spondylosis and potential neuroforaminal narrowing. Electrodiagnostic testing is useful in cases where the history and physical, and possibly the imaging, are inconclusive. Treatment usually includes physiotherapy, medications, pain management interventions, and surgery. Of note, in a review by the American Physical Therapy Association (Childs et al., 2008), patients with cervical radiculopathy had the best outcomes, relative to patients with other etiologies of neck pain.

Discogenic Pain

The prevalence of discogenic pain has been found to be near 20 % in patients presenting with neck pain (Manchikanti et al., 2009). Discogenic pain is presumed to be due to internal disc disruption characterized by nerve in-growth, inflammation, and mechanical hypermobility (Lotz & Ulrich, 2006). Disc degeneration begins in the second and third decade of life due to the aging process, axial loading stress, and of other uncertain etiologies (Alexander, 2011; Dvorak et al., 2007). Pain due to internal changes is mediated by several nerves depending on the portion of the disc. The outer posterior annulus is innervated by the sinuvertebral nerves, the outer lateral annulus is innervated by branches of the grey rami communicante nerves, and the outer ventral annulus is innervated by branches of the ventral rami (Bogduk, Windsor, & Inglis, 1989; Manchikanti et al., 2009; Walker, Spitzer, Veeramani, & Russell, 2005). Discogenic pain generally presents as axial neck pain, which is often hard to distinguish from facetogenic pain (Dwyer, Aprill, & Bogduk, 1990). Imaging studies (XR, CT, MRI) are often used to delineate abnormal discs. However, this information does not necessarily correlate with painful discs (Boden et al., 1990; Dai, 1998; Ernst et al., 2005; Nordin et al., 2009; Sohn et al., 2004; Zheng et al., 2004). In addition, it has been found that fissures in discs do not necessarily correlate with symptomatology (Oda, Tanaka, & Tsuzuki, 1998). Imaging findings indicative of degeneration can include disc space narrowing, vacuum phenomenon, desiccation, end plate sclerosis, osteophytosis, and herniations/bulges. Finally, cervical discography has been advocated as another tool for diagnostic evaluation of discogenic pain. While it does have value by provoking pain within discs and elucidating disc degeneration based on dye spread, there is significant controversy in the literature regarding its use due to a high false-positive rate and risk (Manchikanti et al., 2009; Nordin et al., 2009; Yin & Bogduk, 2008). In addition, there are no studies showing that outcomes are improved using this test in patients who are considering surgery (Margareta et al., 2008).

Myofascial Pain

The major muscle groups of the cervical region were discussed in detail earlier in this chapter. These muscles play a major role in both the mobilization and the stabilization of the neck. It is no surprise, then, that the cervical musculature and its associated fascia are a common source of neck pain. Myofascial pain syndrome is a regional pain disorder, characterized by muscle pain, stiffness, and decreased range of motion. Strain, overload, or trauma are primary causes, whereas coexisting arthropathies, neuropathies, radiculopathies, or visceral disease are potential secondary causes. Much of the literature addressing myofascial pain describes trigger points in the discussion of the pathogenesis of these disorders. Myofascial pain is traditionally defined as pain arising from one or more myofascial trigger points, which are hyperirritable spots in the skeletal muscle that are associated with hypersensitive palpable nodules in taut bands. They can be located at the muscle, fascia, or tendinous insertions. These points are painful on compression and can give rise to characteristic referred pain, referred tenderness, motor dysfunction, and, in some cases, even autonomic phenomena including abnormal sweating, lacrimation, dermal flushing, and vasomotor and temperature changes (Simons, Travell, & Simons, 1999). By comparison, fibromyalgia is a widespread chronic pain disorder with defined diagnostic criteria that includes widespread muscle pain, fatigue, sleep disturbance, and 18-paired tender points in the upper and lower body and in the axial skeleton (Mense, Simons, & Russell, 2001). 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. Although these studies suggest that there may be clinical overlap between these two conditions, this present section will focus specifically on myofascial pain.

There are several epidemiologic studies suggesting myofascial trigger-point pain as one of the major causes of neck pain and an important source of morbidity and disability in the community. Trigger points were the primary source of pain in 74 % of 96 patients with musculoskeletal pain seen by a neurologist in a community pain center and in 85 % of 283 patients consecutively admitted to a comprehensive pain center (Fishbain, Goldberg, Meagher, Steele, & Rosomoff, 1986; Gerwin, 1995). Over one-half of the 164 patients referred to a dental clinic for chronic head and neck pain were found to have active myofascial trigger points as the cause of their pain, as were nearly a third of those from a consecutive series of 172 patients presenting with pain to a university primary care internal medicine group (Fricton, Kroening, Haley, & Siegert, 1985; Skootsky, Jaeger, & Oye, 1989). Patients presenting with myofascial pain usually note localized or regional deep-aching sensations, which can vary in intensity from mild to severe. Cervical myofascial pain may be associated with neurologic and otologic symptoms, including imbalance, dizziness, and tinnitus. Functional complaints include decreased work tolerance, impaired muscle coordination, stiff joints, fatigue, and weakness. Other associated neurologic symptoms include paresthesias, numbness, blurred vision, twitches, and trembling (Fricton et al., 1985). Later stages can be compounded by sleep disturbance, mood changes, and stress. Patients with chronic trigger points must be carefully screened for perpetuating factors, such as postural abnormalities, ergonomic factors, or hypothyroidism (Borg-Stein & Simons, 2002). These symptoms can result in significant disability, at least temporarily.

The pathogenesis of trigger points remains unknown. Electromyographic studies have suggested that there are mini-end plate potentials found routinely in trigger points that may be used to characterize this phenomenon. However, these mini-end plate potentials are not found consistently enough to be considered pathognomonic. Other investigators have examined oxygen tension in trigger points and noted consistently lower oxygen levels in these muscle fibers (Borg-Stein & Simons, 2002). The mechanism that permits creation and maintenance of this lower level of muscle fiber oxygenation remains unclear. Another hypothesis of the pathogenesis of trigger points contends that uncontrolled acetylcholine release results in chronic muscle fiber contraction. This is the basis for the clinical use of botulinum toxin to break this cycle as a potential therapy (Lang, 2003). Overall, the pathophysiology of cervical myofascial pain appears to be complex and likely involves multiple levels of both the peripheral and central nervous systems.

Although there is very limited empirical evidence to guide therapy, there are many pharmacologic and nonpharmacologic treatments used in the management of myofascial pain by clinicians. Medications, such as nonsteroidal anti-inflammatory drugs, anticonvulsants, alpha-2 adrenergic agonists, antidepressants, and tramadol, have been used for this condition despite limited controlled data examining their efficacy. Stretching and range of motion exercises form the basis of the nonpharmacologic treatment of myofascial pain. This treatment addresses the muscle tightness and shortening that are closely associated with pain in this disorder, and it permits gradual return to normal activity (Borg-Stein & Simons, 2002). Trigger-point injections are a commonly used supplemental interventional option for the treatment of myofascial pain. There are many variations of these injections, including dry needling, local anesthetic-only injections, and the injection of local anesthetics combined with corticosteroid. These variations appear to have comparable efficacy. However, anecdotal clinical experience and the available literature on trigger-point injections suggest that the benefits achieved may not be sustained if performed in isolation. In general, pain relief lasts approximately 1–2 weeks when trigger-point injections are used as a stand-alone treatment. However, administration of these injections as one component of a comprehensive rehabilitation program, as mentioned above, may yield better results. The etiology, diagnosis, and treatment of myofascial cervical pain disorders will be discussed in greater detail elsewhere in this handbook.

Seronegative Spondyloarthropathies

Seronegative spondyloarthropathies are a group of inflammatory rheumatic diseases with common etiologic and clinical features. Clinically, patients have axial and peripheral inflammatory arthritis, enthesitis (inflammation at tendinous and ligamentous insertions points), extra-articular manifestations, and a close link with the presence of the HLA-B27 antigen (Olivieri, Barozzi, Padula, De Matteis, & Pavlica, 1998; Zochling & Smith, 2010). This group of arthropathies includes ankylosing spondylitis, Reiter’s syndrome and reactive arthritis, psoriatic arthritis, arthritis associated with inflammatory bowel disease (IBD), ulcerative colitis and Crohn’s disease, and other forms that do not meet criteria for definite categories, which are known as undifferentiated spondyloarthropathies (Zochling & Smith, 2010). Ankylosing spondylitis is by the far the most common of the seronegative spondyloarthropathies. It usually presents with lower back pain and stiffness. However, pain and stiffness in the cervical spine generally tend to develop after some years (Olivieri et al., 1998). Occasionally, neck pain may occur in the beginning stages of ankylosing spondylitis. However, some patients may complain of recurrent episodes of stiff neck or torticollis. Although an uncommon cause of cervical pain, seronegative arthritis should remain on the differential diagnosis list in cases that prove to be a diagnostic challenge.

Vascular Etiologies

Carotidynia is a historical diagnosis and an uncommon cause of neck pain that was first used by Fay, in 1927 (Stanbro, Gray, & Kellicut, 2011). The term is used to describe patients presenting with continuous or intermittent, dull, throbbing pain in the side of the neck located in the region of the carotid artery, sometimes radiating to the ipsilateral face and/or ear. The pain is typically exacerbated with light pressure. It can also be aggravated by neck movements, swallowing, or coughing. It has been related to various processes such as dissection, thrombosis, fibromuscular dysplasia, aneurysm, giant cell arteritis, or Takayasu’s arteritis, as well as other nonvascular processes such as lymphedema, sialadenitis, peritonsillar abscess, or neck neoplasm, amongst others (Castrillo Sanz, Mendoza Rodríguez, Gil Polo, & Gutiérrez Ríos, 2011). Carotidynia has since been removed as a distinct disease entity and reclassified by the International Headache Society into a syndrome of unilateral neck pain (Stanbro et al., 2011). Currently, carotidynia remains a poorly understood and controversial subject. Some authors continue to use the term to describe neck pain due to any etiology, whereas others maintain that it is a separate disease entity. It is important to recognize that the underlying vascular structures can be involved in the patient presenting with neck pain, and a high index of suspicion along with a thorough history and investigation must be performed by the clinician in order to rule out correctable or even life-threatening disease processes (Holland & Patel, 2010).

Fracture/Trauma

As this handbook is not intended to be for emergent evaluation and treatment, our discussion of fracture and trauma will be mostly limited to the clinic setting. Patients may present after a fall, blunt trauma, workplace accident, or motor-vehicle accident. Any subsequent neck pain should be evaluated seriously. One must be aware of potential cervical fracture, instability, and possible cord or nerve compromise. Suspicion should be particularly high in patients with predisposing factors, or “red flags,” that signify underlying pathologies that alter the spine, such as malignancy (unexplained weight loss, prior cancer history, failure to improve with conservative therapy), systemic diseases (osteoporosis, inflammatory arthritis), infection (history of intravenous drug abuse, fever), and medication use (corticosteroid). In such patients, increased axial loading of the spine can lead to end plate compression or burst fractures. However, fractures of any bony element of the spine can be seen. Bone pain is mediated by interosseous and periosteal C nerve fibers. Additionally, fracture of bony elements or alteration of intervertebral disc or ligamentous structures can lead to canal compromise or nerve compression. Neurologic changes along with cord compression should prompt early surgical intervention (Dvorak et al., 2007). Appropriate referral to a surgical specialist is based on clinical exam and imaging findings.

If trauma has occurred, patients can be stratified with the Canadian Cervical Spine Rule, assuming they are alert and have a Glasgow Coma Scale score of 15. High-risk patients include those older than 65 years of age, persons who have had a dangerous mechanism of injury (essentially any incident other than simple rear-end motor-vehicle collision, but please refer to reference), or who have upper extremity paresthesia (Margareta et al., 2008). These patients should undergo CT imaging (Margareta et al., 2008) which has better bony resolution than MRI, or if not available, then cervical plain films should be taken. Referral to an acute care setting should be made based on history and exam. Low-risk patients are screened initially as being able to sit in the waiting room, being ambulatory at any time, having had a simple rear-end collision, those who have delayed onset of neck pain, or those who do not have midline spinal tenderness. Patients who fit any of these criteria, and who are then able to actively rotate their head 45° in each direction, are deemed low risk and do not acutely require imaging (Childs et al., 2008; Margareta et al., 2008). If pain persists beyond 4–6 weeks despite symptomatic treatment, plain films can be taken to evaluate further.

There are no physical exam findings that are pathognomonic for fracture. However, tenderness with palpation over the spine is a commonly used sign. Interestingly, it has been found that return-to-work after surgery for cervical spine fracture can range anywhere from 1 to 26 weeks, depending on the injury (Lewkonia et al., 2012). In addition, there is significant controversy regarding expected functional limitations after such injuries, with surgeon opinions differing in literature.

Neoplasm

Neoplastic conditions represent a rare, albeit serious, etiology of neck pain. Estimates based on population studies calculate that neck pain due to serious conditions, such as infection or neoplasm, represents less than 0.4 % of all cases of neck pain (Bogduk, 2011a). Pain associated with neoplastic lesions is commonly noted to worsen with motion and at night. This is thought to be due to vascular engorgement while maintaining a recumbent position for a long period of time. The symptoms will vary widely depending on the location and size of tumors within or around the spine, although patients often display other constitutional symptoms not commonly seen with other etiologies of neck pain. Neoplastic lesions in the cervical spine may represent primary or metastatic processes. Metastatic lesions are often due to breast, prostate, lung, or kidney cancer. Imaging studies often confirm the presence of a lesion, although biopsy may be required in order to determine the type of neoplasm and appropriate course of treatment (Hadler, 1999; Tollison & Satterthwaite, 1992).

Whiplash

Whiplash, as a clinical entity, was first introduced by H. E. Crowe in 1928 and has been a source of confusion and controversy since that time in both the medical and legal communities (Bannister, Amirfeyz, Kelley, & Gargan, 2009; Ferrari, 1999). Even the term “whiplash” has been a source of controversy. Originally, it described the mechanism of injury, namely rear-end collision in a motor-vehicle accident, but the term has grown to be synonymous with the injury resulting from this mechanism, as well as the constellation of symptoms surrounding the injury associated with the mechanism. At least there is some agreement at this time that the elements which define whiplash include neck pain, possibly resulting from injury, along with a variety of related symptoms that occur as a result of the forces applied to the head and neck during a motor-vehicle collision, usually a rear-end collision (Bannister, Amirfeyz, Kelley, & Gargan, 2009; Barnsley, Lord, & Bogduk, 1994; Ferrari, 1999). In fact, now terms such as “whiplash-associated disorder” or “late whiplash syndrome” have been coined to describe the spectrum of signs and symptoms seen after a whiplash injury, especially in the chronic setting. Gradations of severity have been proposed to further characterize the severity of whiplash-associated disorder (WAD) (Carroll et al., 2008; Poorbaugh, Brismee, Phelps, & Sizer, 2008). In Grade 0 WAD, the patient has no neck complaints and there are no physical signs of injury; thus, there is no whiplash. Grade I WAD indicates complaints of neck pain, stiffness, or tenderness without any physical signs, while Grade II WAD notes similar complaints, along with musculoskeletal physical signs such as decreased range of motion or point tenderness. Grade III WAD refers to neck complaints along with neurologic physical signs such as diminished deep tendon reflexes, weakness, and/or sensory deficits. Finally, Grade IV WAD indicates neck complaints in the setting of fractures or dislocations (see Table 3.2). Interest in the prevention, prognosis, and treatment of WAD has grown as its incidence has increased. While all agree that the syndrome is quite common, estimates vary on the actual incidence, ranging from 70 to 328 per 100,000 in North America (Walton, Pretty, Macdermid, & Teasell, 2009). Other authors have noted that estimation of the incidence is challenging due to the possibility of selection bias when utilizing insurance claims as a source for estimating true incidence (Barnsley et al., 1994). Further complicating the issue is that neck pain is exceedingly common, affecting up to 40 % of the general population at any one time, and may lead to overestimation of the true incidence (Hogg-Johnson et al., 2008). The economic burden associated with whiplash disorders has also drawn the interest of insurance providers and government policy makers to begin to make headway effective prevention and treatment strategies. In the USA, it is estimated that approximately 6 % of the population may suffer from chronic whiplash symptoms, with an annual medical cost of $10 billion (Poorbaugh et al., 2008) while in the UK, such costs are estimated to be $3.6 billion per year and represent 76 % of auto-insurance claims in that country (Bannister et al., 2009).

Table 3.2 Whiplash-associated disorder grading

While a variety of symptoms have been described, all agree that the predominant feature of whiplash injury is neck pain. The neck pain should occur in conjunction with a motor-vehicle accident, although the pain may not occur immediately after the collision. It is quite common for the pain to begin several hours, or even a day, later (Bannister et al., 2009; Barnsley et al., 1994; Schofferman, Bogduk, & Slosar, 2007; Tollison & Satterthwaite, 1992). The next most common symptom seen in the acute phase of whiplash is headache. They may be unilateral or bilateral and are most commonly reported in the suboccipital region, although patients may describe referral patterns into other parts of the head (Schofferman et al., 2007). Other symptoms include neck stiffness, arm pain, low back pain, dizziness, visual disturbances, weakness, cognitive dysfunction, and psychological disturbances (Bannister et al., 2009; Barnsley et al., 1994; Tollison & Satterthwaite, 1992).

Of note, there has been much interest in pursuing the role of psychosocial disorders in whiplash disorders. An all-encompassing clinical description that ties together the mechanism of injury with quantifiable tissue injury has been largely lacking throughout most of the course of investigation of whiplash injuries. Such a lack of quantifiable injuries for so long led many to conclude that the pain reported from whiplash injuries was due to psychosomatic origin or malingering. This concept was sometimes referred to as “traumatic neurosis,” in which symptoms were real but were not a result of actual physical injury (Barnsley et al., 1994; Ferrari, 1999). Comparisons of patients with chronic whiplash symptoms with patients who had non-whiplash chronic musculoskeletal pain displayed no difference in the prevalence or type of psychosocial conditions, and, furthermore, patients with chronic whiplash pain who obtained improvement with radio-frequency neurotomy also showed improvement with psychosocial testing as well (Wallis, Lord, & Bogduk, 1997). This would indicate that pain was driving the psychosocial disturbances, not the other way around. For decades, the lack of quantifiable tissue injury in whiplash drove many to discount the veracity of the diagnosis and led to the conclusion that whiplash syndromes were born from psychological, not physical, factors. This idea was bound to persist until researchers could posit a likely site or sites of physical injury to explain the symptoms seen in the clinical setting.

In a rear-end collision, the initial result of impact is forward acceleration of the target vehicle within 100 ms of impact. The force of the impact causes the vehicle to travel forward and, by extension, the car seat followed by the seated passenger’s trunk and shoulders. Initially, the head has no force acting upon it and remains stationary due to its inertia. Studies have shown that such forces cause upward and forward displacement of the torso resulting in a sigmoid, or “S”-shaped, deformation where the lower cervical segments are in extension while the upper cervical segments are in flexion. As the head’s inertia is overcome, it begins forward acceleration, mainly at the base of the skull where the cervical spine attaches, thus resulting in rearward rotation of the head. Following this, the head is “whipped” forward, using the neck as a lever and placing the neck in flexion. Any rotation of the neck present at the time of impact will place stress on the cervical elements, such as zygapophyseal joints, intervertebral discs, and ligaments, and the force of the impact will result in further rotation of the cervical spine and place further stresses on the said structures (Barnsley et al., 1994; Bogduk, 2011b; Poorbaugh et al., 2008; Schofferman et al., 2007). Studies have attempted to recreate such movements in an experimental environment in animal, human cadaver, and live human volunteer tests. One important concept born from such experiments is that of the change in velocity as a result of a collision, or the delta-V. This refers to the positive change in the velocity of the vehicle that is struck in a rear-end collision or, in contrast, the negative change in the velocity of the striking vehicle. The speed with which such a change in velocity occurs denotes acceleration and it is denoted in multiples of the acceleration of gravity, or g. For example, dropping an object results in acceleration of 1 g relative to the object. A more rapid acceleration requires greater force, thus researchers looked at the delta-V and g-forces sustained in collisions to try to determine the magnitude of such forces required to induce pain and/or injury. Also note that the mass of the vehicles involved will affect the relative transfer of force in a collision. For example, if a kindergartener and an NFL offensive lineman ran at the same speed and attempted to tackle the author, the force expended on the author would be drastically different due to the differences in mass of the striking objects. One could surmise that such differences in force expended would translate into greater delta-V and g-forces after being struck by the lineman and could, hypothetically, result in greater pain and/or injury in the author. Based on experimental studies, it appears that delta-V over 5 mph and acceleration in the 12–20 g range result only in mild, temporary pain in experimental models and would represent the minimum forces required to cause whiplash syndrome. In comparison, sneezing can induce 3 g acceleration on the neck, and falling from standing into a chair can result in 8 g acceleration on the neck (Ferrari, 1999). Review of postmortem studies of fatal MVC victims did show nonlethal injuries to the C-spine that were not visible on radiography. These included lesions to the zygapophyseal joints, intervertebral discs, and nerve roots (Bogduk, 2011b). While it is unclear whether such injuries would result in whiplash-like pain, as the studies were postmortem analyses, it is interesting to note that such injuries were unable to be visualized with radiographic imaging. Biomechanical studies show that the abnormal sigmoid deformation of the cervical spine in experimental whiplash models causes nonphysiologic movement of the cervical motion segment, such that there is rotation of the upper cervical segment relative to the lower segment, causing a pinching or grinding motion of the cervical zygapophyseal joint and a simultaneous distraction of the anterior longitudinal ligament and annulus fibrosis (Bogduk, 2011b; Poorbaugh et al., 2008; Schofferman et al., 2007). Such non-physiologic motions may result in articular or capsular injury of the zygapophyseal joints, as well as annular tears or disruption of the anterior longitudinal ligaments. Damage to the alar and transverse ligaments has been described in whiplash patients (Barnsley et al., 1994; Poorbaugh et al., 2008). Such injuries can contribute to pain and hypermobility in the atlantoaxial joints, though if such injuries are severe, it may result in compromise of the atlantoaxial joints causing severe neurologic injury or even death. Muscular injuries are commonly implicated in whiplash given the description of pain after whiplash injuries. Studies have shown elevated creatine kinase levels at 24 h post-injury in whiplash patients, although not at 48 h (Scott & Sanderson, 2002). Acute whiplash pain is thought to be due to muscular strain and tears which subsequently heal within 2 or 3 months, explaining the short course of pain experienced by most whiplash patients (Barnsley et al., 1994; Schofferman et al., 2007). The role of chronic muscular pathology in whiplash is poorly understood. There has been evidence in whiplash patients of transformation of neck muscle fibers from slower twitch, oxidative fibers to fast twitch, glycolytic fibers. While the causative factor for such transformation is unclear, it is theorized that since one of the primary responsibilities of neck musculature is the stabilization of the cervical spine, the overabundance of fast twitch fibers results in more rapid fatigue of these muscles. This fatigue limits muscular endurance, and it is thought to contribute to decreased cervical stability and worsening of muscle spasms (Poorbaugh et al., 2008). There is some evidence showing fatty infiltrates by T1-weighted MRI in the neck muscles of patients with chronic whiplash pain and, interestingly, not in the neck muscles of patients with chronic idiopathic neck pain nor in patients with only acute whiplash pains (Sterling, McLean, et al., 2011). While the development of a radiologically identifiable muscular lesion is interesting, to say the least, its role in the development of chronic whiplash pain is unclear and requires further study. Other reviewers conclude that, because cervical musculature overlies the zygapophyseal joints, tenderness elicited over these muscles may be due to those joints, especially if the clinician is unable to palpate bands or twitch response over the painful site (Barnsley et al., 1994). Insertion of the cervical multifidi muscles on cervical facet capsules are thought to contribute to pain with neck movement in the setting of zygapophyseal joint injury; thus, neck pain with movement may be more of a function of zygapophyseal pathology rather than muscular pathology (Anderson, Hsu, & Vasavad, 2005). Headache is the second-most commonly reported symptom in whiplash and is thought to be due to injury in the upper cervical segments because C2–3 zygapophyseal joint pain is often referred to the suboccipital region (Cooper et al., 2007) and the trigeminal nucleus has inputs from the C1–3 nerves which may result in referred pain in the trigeminal distribution from damage to these structures (Barnsley et al., 1994; Poorbaugh et al., 2008).

Vertebral artery dissection has also been shown to be more common in whiplash patients (Hauser, Zangger, Winter, Oertel, & Kesselring, 2010) and is postulated to be due to a combination of the non-physiologic movements of the cervical spine seen in whiplash patients and the torturous course of the vertebral arteries through the cervical region. While there is an association between vertebral artery flow anomalies and chronic whiplash symptoms, there is no diagnostic tool showing that such injuries contribute to neck pain in the setting of whiplash (Curatolo et al., 2011). Thus, acute whiplash pain is thought to be due to muscle strain which resolves with time, accounting for the majority of patients who have mild pain that resolves within 3 months. Other sites may be injured as a result of a motor-vehicle collision due to the abnormal physiologic movement of the spine and mainly include the cervical zygapophyseal joint, cervical intervertebral discs, and cervical ligaments, although muscles and vascular structures may also be damaged.

Many of the proposed sites of tissue injury in whiplash injury models are difficult to study in vivo as there are few diagnostic tools to rule in or rule out various structures. This is not the case, however, with the cervical zygapophyseal joints and, to a lesser degree, with the cervical intervertebral discs. The use of cervical medial branch nerve blocks to diagnose zygapophyseal joint pain is well established (Barnsley et al., 1993; Lord et al., 1995, 1996). These studies show that cervical zygapophyseal joint pain is responsible for approximately 50 % of chronic whiplash pain, as evidenced by relief with diagnostic blocks. These patients can then pursue cervical medial branch radio-frequency neurotomy for more long-lasting relief. Discogenic pain is thought to be mediated by its innervation from the sinuvertebral nerves from the ventral primary ramus of the spinal nerve (Bogduk, Windsor, & Inglis, 1988). Provocation discography can be used to diagnose pain arising from the cervical intervertebral discs in which distension of the disc by injection of contrast elicits pain concordant with the patient’s usual pain, thus establishing the problem disc. The problem arises in that it can be difficult for the patient to determine whether pain elicited with discography is their usual pain (Barnsley et al., 1994). Furthermore, pain reproduced on discography has been effectively treated with zygapophyseal joint blocks (Aprill & Bogduk, 1992), thus calling into question the reliability of discography in the diagnosis of discogenic pain. One model presented recommends diagnostic cervical medial branch nerve blocks in patients with chronic whiplash symptoms, as this represents the best studied diagnostic procedure and may reveal the source of up to one-half of chronic whiplash cases. If positive, radio-frequency neurotomy can be pursued and, if negative, consideration can be given to pursue provocative discography (Barnsley et al., 1994). Other potential sites of injury, such as ligaments, muscles, and vascular structures, do not have similar diagnostic tests of sufficient reliability to recommend at this time (Fig. 3.1).

Fig. 3.1

Lateral radiographic image of diagnostic blockade of the C5 medial branch nerve for treatment of facetogenic pain. SP spinous process. Arrow needle. The needle tip can be visualized at the midsection of the C5 articular pillar

While the natural course of whiplash injuries tends toward complete recovery in the majority of affected individuals, an alarming number of patients continue to experience pain many months or even years later. Estimates of the percentage of patients who reports acute whiplash symptoms that go on to have chronic symptoms vary greatly. Difficulty arises in defining the chronicity of whiplash syndromes in that studies utilize different end points and different populations to make such estimates. There is widespread agreement that the percentage of whiplash patients that go on to note symptoms on a chronic basis ranges from 14 to 42 % and that up to 10 % will have severe pain and/or disability (Barnsley et al., 1994; Poorbaugh et al., 2008; Schofferman et al., 2007). Aside from potential anatomic lesions that may provide a source of pain, some theorize that other factors may contribute to the development of chronic whiplash syndromes. One such possibility is that hypersensitivity occurs due to augmentation of central nociceptive processing. Such changes can result in hyperalgesia and allodynia and are commonly seen in other chronic pain syndromes (Sterling, McLean, et al., 2011). A study comparing patients who had recovered from whiplash injury after 1 year to non-recovered patients showed increased peak pain and decreased endurance to cold pressor test (Kasch, Qerama, Bach, & Jensen, 2005). While not completely understood, such changes are thought to be multifactorial in origin depending on the nature of the inciting injury, psychosocial conditions, and stress-response systems. One interesting report studied whiplash patients and the genetic variation of the catechol-O-methyltransferase (COMT) gene, which is an enzyme that breaks down catecholamines. There was an association between the haplotype coding for the least enzyme activity, and thus the highest catecholamine levels, and the highest pain sensitivity (Diatchenko et al., 2005).

Much research has gone toward determining prognostic factors that may predict which patients will continue on to develop chronic whiplash pain. To be able to make such predictions with accuracy, it would help to identify at-risk patients and develop strategies to intervene prior to the development of chronic symptoms and, perhaps, blunt the course of the disease process. High initial levels of acute pain after collision are considered to be the best predictor of chronic symptoms (Bannister et al., 2009; Schofferman et al., 2007; Sterling, Carroll, Kasch, Kamper, & Stemper, 2011; Walton et al., 2009). Meta-analysis comparing WAD Grade III patients to WAD Grade II patients showed significant differences in initial symptom, but such differences lost significance by 24 months (Walton et al., 2009). Patients with Grade II or III WAD symptoms reported greater pain and functional limitations from 6 to 24 months post-collision when compared with Grade 0 or I WAD, although the inclusion of Grade 0 patients may skew the results as these patients do not have symptoms and, therefore, do not have whiplash (Sterner, Toolanen, Gerdle, & Hildingsson, 2003; Walton et al., 2009). Despite such limitations, high initial pain levels are still considered the strongest predictor of chronic whiplash symptoms. Age and gender are commonly studied variables as well. Age, in particular, has been a difficult factor to draw conclusions about due to different age cutoffs used in various studies. Many have found a positive association between either female gender or older age and chronic whiplash symptoms (Bannister et al., 2009; Barnsley et al., 1994; Carroll et al., 2008; Radanov, Stefano, Schnidrig, & Ballinari, 1991; Schofferman et al., 2007; Walton et al., 2009). The effect of age, though, was only modest in predicting persistent disability or speed of recovery, and there was no significant difference in persistent pain in patients over 50 (Carroll et al., 2008; Walton et al., 2009). Female gender was found to have, at best, modest predictive ability for chronic whiplash pain, although some studies showed no difference (Carroll et al., 2008). Lower educational status, usually defined as lack of postsecondary education, is noted to be another predictor for chronic whiplash pain and/or disability (Bannister et al., 2009; Carroll et al., 2008; Walton et al., 2009). Preexisting neck pain has also been found to be a strong predictor of chronic whiplash symptoms, but studies of this factor often used patient self-report to establish such a history, thus introducing a possible source of recall bias (Walton et al., 2009).

Passengers not wearing seat belts at the time of collision have also been found to be at higher risk for developing whiplash (Walton et al., 2009), but passengers in vehicles utilizing specialized seats and head restraint systems designed to absorb more of the force of impact have 50 % less permanent impairment (Kullgren, Krafft, Lie, & Tingvall, 2007). There is some concern regarding the veracity of such claims because the studies were supported by manufacturers, thus introducing a potential source of bias (Curatolo et al., 2011). As noted above, the presence of psychosocial disturbances in patients with chronic whiplash pain is more likely to be a result of chronic pain, rather than a causative factor. There is evidence that some psychosocial factors are associated with the development of chronic symptoms following whiplash. Depressive symptoms prior to whiplash injury may predict slower recovery (Carroll et al., 2008), but other reviewers report no significant difference based on this factor (Walton et al., 2009). Catastrophizing behaviors, on the other hand, are strongly associated with poor outcome following whiplash injury and indeed amongst many chronic pain syndromes. Such behaviors are characterized by focus on somatic symptoms, emotional distress, pronounced pain behaviors, and a defeatist attitude regarding outcomes (Nederhand, Ijzerman, Hermens, Turk, & Zilvold, 2004; Sterling, McLean, et al., 2011; Walton et al., 2009). Fear-avoidance behaviors are another potentially confounding psychosocial factor contributing to impairment in the setting of chronic pain. Such behaviors are characterized by a patient’s fear and anxiety related to exacerbating pain leading to avoidance of physical activity, disuse, and deconditioning (Vlaeyen & Linton, 2000). Thus, many factors have been explored to attempt to find which ones will allow prediction of the development of chronic symptoms in whiplash patients. As research efforts continue, this list will likely change, but it appears that the best prognostic indicators of progression to chronic whiplash pain are higher initial pain intensity, WAD Grades II or III, prior history of neck pain, presence of abnormal cold pressor tests, and psychosocial disturbances such as catastrophizing or fear-avoidance behaviors. Some weaker prognostic indicators would include female gender, age >50 years, and lack of postsecondary education.

The effect of litigation related to chronic whiplash pain is another source of controversy as it represents a potential source of secondary gain. Contributing to this issue is the finding of vast differences in reporting of chronic whiplash in various countries that is often dependent on whether there is a legal means by which patients may seek financial compensation or disability status following motor-vehicle collisions resulting in chronic WADs. For example, recent data show that 76 % of personal injury claims in the UK are for whiplash disorders vs. about 5 % in France (Haddrill, 2008). The presence of such a disparity in chronic whiplash claims in societies where the medicolegal framework allows compensation for such issues has led to the belief that secondary gain or malingering is the cause of such differences. Such implications would suggest that post-litigants would show improvement in pain and disability as they have achieved their conscious or unconscious goal of obtaining compensation for the purported injury. A study comparing current and post-litigants, though, showed no difference in pain-related disability or psychosocial distress, but current litigants did report greater pain intensity in more locations and with greater impact on daily activities (Swartzman, Teasell, Shapiro, & McDermid, 1996). Prior reviews also refute the assertion that symptoms will improve following closing of litigation (Bannister et al., 2009; Mendelson, 1992; Schofferman et al., 2007). In fact, one prospective study comparing litigants and non-litigants with persistent whiplash symptoms undergoing radio-frequency medial branch neurotomy showed similar reductions in pain following the procedure, thus providing further evidence refuting the purported link between litigation status as a marker for secondary gain or malingering in chronic whiplash patients (Sapir & Gorup, 2001).

As treatment measures for chronic whiplash pain remain limited, some have focused on prevention to try to decrease the societal burden of such injuries. A consortium, representing the insurance industry in Britain, has four recommendations to help prevent motor-vehicle collisions which result in whiplash injuries or to mitigate the damage sustained in such collisions (Haddrill, 2008). The first recommendation involves changing driver behaviors, mainly in discouraging tailgating. This mainly involves teaching new driver tactics to estimate proper following distances, encouraging employers to institute similar policies in the workplace, and public awareness campaigns regarding the risk of tailgating behaviors. The second recommendation involves encouraging vehicle manufacturers to utilize anti-collision technologies utilizing systems akin to radar which determines the location of objects around a vehicle and coupled with alarms that alert the driver that collision is imminent or automated-braking systems that attempt to avoid such collisions. The third, proper head restraint positioning was recommended in which the top of the restraint is level with the top of the head and the back of the head is as close to the restraint as possible. Such positions allow the restraint to stop the motion of the head and neck during a collision and may decrease the risk of sustaining a whiplash injury by up to 24 % (Farmer, Wells, & Werner, 1999). Finally, manufacturers were encouraged to develop seats that more effectively absorb the force of a collision and potentially decrease the forces transmitted to passengers thus decreasing whiplash injuries. Such systems are widely utilized and advertised in European automobile fleets.

In conclusion, WADs are a common form of injury sustained mainly during motor-vehicle collisions. Such injuries are normally self-limited and resolve without intervention, but a substantial portion of patients reporting such injuries go on to report chronic pain and, less commonly, disability. While multiple potential sites of injury exist based on experimental data, the most clearly studied are the cervical zygapophyseal joints which appear to be responsible for roughly one-half of all chronic whiplash pain. While issues, such as underlying psychosocial problems and secondary gain or malingering, have been implicated as a source of these chronic pains, the evidence does not support such claims. High initial pain complaints, prior history of neck pain, evidence of hyperalgesic responses, and specific pain behaviors (such as catastrophizing or fear avoidance) are the best prognostic factors to date. Collision prevention and mitigation of injury during collisions represent a significant opportunity to prevent whiplash injuries or to limit the severity of such injuries.

Conclusions

In conclusion, cervical pain is a common complaint in the population and is a frequent source of disability amongst those of working age. The source of cervical pain is variable, and diagnosis requires knowledge of relevant anatomy, neurology, referral patterns, and mechanisms. Many times an in-depth history and physical exam is sufficient to establish the diagnosis, but at other times it may be necessary to obtain imaging, laboratory studies, electrophysiologic studies, or diagnostic procedures to establish the diagnosis. On a larger scale, it is important to consider other prognostic factors that contribute to development of cervical pain, from one’s perception of the work environment to the design and manufacture of work implements. Careful evaluation of such elements by healthcare providers and policy makers could potentially result in improved outcomes following injury or perhaps even prevention of injury or disability.