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).

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.

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.

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.

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).

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 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.

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).

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.

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, 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).

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).