Pathophysiology of Axial Neck Pain

Axial neck pain results from a multitude of potential causes and can be divided geographically into anterior neck pain, which usually stems from sprains and strains of the sternocleidomastoid and other strap muscles and their attachments, and posterior neck pain, which can be subdivided further into subaxial and suboccipital locations.⁸ In many patients, subaxial neck pain results from muscular or ligamentous imbalances related to poor posture, faulty ergonomics, or muscle fatigue or stress or both. Muscular pain often occurs as a result of postural adaptations to a primary pain source located in the shoulder, the craniovertebral junction, or the temporomandibular joint.⁵

The physiology of this pain process is not yet fully delineated. Patients with chronic myofascial pain have significantly lower levels of high-energy phosphates in the involved muscle tissue.⁹ It is unknown whether the diminished level of high-energy phosphates causes the pain or if it is a result of the pain. Unencapsulated free nerve endings in the neck musculature function as chemonociceptive units. Fatigued muscle generates anaerobic metabolites, which accumulate and can stimulate these chemonociceptive nerve endings. These free nerve endings also respond to non-neurogenic pain mediators released as a result of ischemia or injury, such as bradykinin, histamine, serotonin, and potassium ions. Primary muscle pain may result from sensitization of these nerve endings.

Axial neck pain should be attributed to degenerative changes in the cervical discs or facet joints only after careful consideration, owing to the ubiquitous nature of these changes in the spine. Nevertheless, multiple studies suggest that cervical discs and facet joints can generate pain.^10–14 Nerve fibers and nerve endings, containing somatic afferent fibers, innervate the peripheral portion of the intervertebral disc (the outer third of the anulus) and offer a potential mechanism by which degenerative cervical discs generate pain directly. The sinuvertebral nerve, formed by branches of the ventral nerve root and by the sympathetic plexus, innervates the intervertebral disc (Fig. 36–1). When formed, the sinuvertebral nerve turns back into the intervertebral foramen along the posterior aspect of the disc, supplying portions of the anulus, posterior longitudinal ligament, periosteum of the vertebral body and pedicle, adjacent epidural veins, and dura mater.¹⁰ A review of a 12-year cervical discography experience suggests that stimulation of each disc results in consistent and predictable patterns of neck pain (Fig. 36–2).¹⁴

FIGURE 36–1 Cross-sectional anatomy showing dorsal and ventral primary branches of cervical nerve root, origin of sinuvertebral nerve (also known as recurrent meningeal nerve) from the nerve root, and sympathetic plexus. Note proximity of disc, uncovertebral and facet joints, and vertebral artery.

FIGURE 36–2 Axial pain patterns provoked during discography at each cervical level. A, C2-3. B, C3-4. C, C4-5. D, C5-6. E, C6-7.

(From Grubb SA, Kelly CK, Bogduk N: Cervical discography: Clinical implications from 12 years of experience. Spine [Phila Pa 1976] 25:1382-1389, 2000.)

Degenerative changes at a cervical facet joint can be a source of axial neck pain. Provocative injections into the facet joints of asymptomatic volunteers result in a reproducible pattern of axial neck pain and shoulder girdle pain (Fig. 36–3).¹² Controlled injection of anesthetic into the symptomatic facet joint or into the dorsal primary rami blocks these patterns of facet pain, suggesting that the facet joint plays a role in the development of axial neck pain. C3-4 to C8-T1 facet joints receive their innervation from the medial branches of the cervical dorsal rami above and below each joint, whereas the third occipital nerve innervates the C2-3 facet joint.¹¹ The presence of mechanoreceptors and nociceptive nerve endings in cervical facet joint capsules further supports a possible role for these structures in the pathogenesis of cervical spine pain.¹⁵ Immunohistochemical studies show the presence of free nerve endings reactive for pain-related peptides located in the synovial folds of the human cervical facet joint.

FIGURE 36–3 Composite map of axial pain patterns from facet joints at C2-3 to C6-7.

(From Dwyer A, Aprill C, Bogduk N: Cervical zygapophyseal joint pain patterns. I. A study in normal volunteers. Spine [Phila Pa 1976] 15:453-457, 1990.)

Suboccipital pain radiating down into the neck or to the back of the ear may be a manifestation of degenerative arthritis in the upper cervical spine. Injection of the atlanto-occipital and atlantoaxial joints results in a reproducible pain pattern in this region, with the atlanto-occipital joints showing the capacity to generate intense and diffuse pain.¹⁶ Wächli and colleagues¹⁷ reported unilateral headaches and atypical facial pain as a result of degenerative changes at the C2-3 level. Some patients with suboccipital headaches presumably have irritation of the greater occipital nerve, which originates from the posterior rami of C2, C3, and C4.¹⁸ The sinuvertebral nerves from C2 and C3 exist as another potential source of suboccipital pain, ascending proximally to innervate the atlantoaxial ligaments, tectorial membrane, and dura mater of the upper cervical cord and posterior cranial fossa.¹⁰

Pathophysiology of Radiculopathy

Radicular findings in the arm originate from the cervical nerve roots at some point between their origins as nerve rootlets from the spinal cord and their transition into peripheral nerves as they emerge from the neural foramen. Degenerative changes at the cervical motion segment, soft disc herniations, stenosis, intrinsic nerve root pathology, and trauma all can result in these symptoms. Loss of disc height leads to impingement on the nerve root origins from disc bulging, infolding of the facet joint capsule and ligamentum flavum, and osteophyte formation at the disc margins (hard disc formation) and at the uncovertebral and facet joints, all of which result in foraminal stenosis and radiculopathy (Fig. 36–4). Osteophytic spur formation may also compromise the blood supply to the nerve roots. Osteophytes may compress radicular arteries within the dural root sleeves leading to spasm and reduced vascular perfusion. Additionally, blockage of venous outflow may occur, resulting in edema and further compromise of the blood supply of the nerve roots.¹⁹

FIGURE 36–4 Nerve root compression in lateral spinal canal from disc, uncovertebral joint, or facet joint pathology can lead to cervical radiculopathy.

Mechanical deformation of the nerve root may lead to motor weakness or sensory deficits. The exact pathogenesis of radicular pain is unclear, but the general belief exists that in addition to the compression, an inflammatory response must occur for pain to develop. Within the compressed nerve root, intrinsic vessels show increased permeability, secondarily resulting in edema of the nerve root. Chronic edema and fibrosis (scar) within the nerve root play a role in altering the response threshold and heighten the sensitivity of the nerve root to pain.²⁰ Neurogenic chemical pain mediators released from the sensory neuron cell bodies and non-neurogenic mediators released from disc tissue may initiate and perpetuate this inflammatory response (Table 36–1).^21,22

TABLE 36–1 Chemical Mediators of Spinal Pain

diHETE, dihydroxyeicosatetraenoic acid

From Chabot MC, Montgomery DM: The pathophysiology of axial and radicular neck pain. Semin Spine Surg 7:2-8, 1995.

Dynamic factors in the cervical spinal column affect the amount of nerve root compression. Flexion of the cervical spine lengthens the cervical neural foramina 18% to 31%, whereas extension shortens the foramina 16% to 22%.²³ Rotation to the ipsilateral side narrows the foramen, whereas rotation to the contralateral side widens the foramen. The facet joint capsule and ligamentum flavum buckle with extension, narrowing the foraminal dimensions further. Translation or angulation between vertebral bodies in flexion or extension may result in increased stretch on the nerve root and predispose the individual to radicular symptoms. Patients who do not have nerve root compression with their necks in a static, neutral position may dynamically compress the nerve root during normal activities, resulting in radicular symptoms.

Changes in intrinsic tension within the nerve root have the ability to alter radicular pain. Davidson and colleagues²⁴ postulated that the decrease in tension within the nerve root caused by a patient resting the hand atop the head—the shoulder abduction sign—relieves radicular pain. These investigators also postulated that this change in arm position lifts the sensory root, or dorsal root ganglion, directly cephalad or lateral to the source of compression and that this position decompresses the epidural veins, augmenting pain relief. Another study suggested that the abducted arm position allows relative laxity in the dural ligaments (of Hoffman), resulting in decreased tension on the nerve root.²⁵

Often, patients present with radicular pain in an atypical distribution.²⁶ An anatomic human cadaveric study confirmed the high incidence of intradural connections among C5, C6, and C7 dorsal rootlets (noted to be anatomic variants because of their high incidence rather than anatomic anomalies) and postulated that these variant intradural connections potentially explain the clinical variation and overlapping sensory symptoms frequently observed with cervical spine nerve root compression.²⁷

Pathophysiology of Myelopathy

Although it is generally agreed that mechanical compression of the spinal cord is the primary pathophysiologic mechanism resulting in myelopathy, in many patients a combination of this static compression with dynamic factors secondary to motion between the vertebral bodies, a congenitally stenotic canal, changes in the intrinsic morphology of the spinal cord, and vascular factors contributes to the development of myelopathy. A developmentally narrow spinal canal in the anteroposterior plane can contribute to the development of cervical myelopathy. The normal anteroposterior diameter of the cervical spine measures 17 to 18 mm in adults, and the anteroposterior diameter of the spinal cord in the cervical region measures approximately 10 mm. An anteroposterior diameter of the spinal canal less than 13 mm defines congenital cervical stenosis, whereas a diameter greater than 16 mm suggests a relatively low risk of myelopathy (Fig. 36–5A).^28,29 A congenitally narrow spinal canal lowers the threshold at which the cumulative effects of various degenerative structures encroaching on the spinal cord cause signs and symptoms of myelopathy.³⁰

FIGURE 36–5 Radiographic criteria important in pathogenesis of cervical spondylotic myelopathy. A, Mid-sagittal diameter of spinal canal is measured as distance from middle of dorsal surface of vertebral body to nearest point on spinolaminar line. Patients in whom osseous canal measures less than 13 mm are considered developmentally stenotic. B, Distance of less than 12 mm from posteroinferior corner of vertebral body to anterosuperior edge of lamina of immediately caudal vertebra with neck in extension is suggestive of dynamic stenosis. C, Olisthesis (retrolisthesis or anterolisthesis) of greater than 3.5 mm is measure of excessive translation between vertebral bodies. Signal changes within substance of spinal cord, noted on T1-weighted and T2-weighted MRI in some patients, are represented diagrammatically with gray lines.

(From Rao RD, Gourab K, David KS: Operative treatment of cervical spondylotic myelopathy. J Bone Joint Surg Am 88:1619-1640, 2006.)

A strong association exists between flattening of the cord within the narrowed spinal canal and the development of cervical myelopathy. Penning and colleagues³¹ believed that symptoms of cord compression occurred when cross-sectional area of the cord had been reduced by a critical amount (30%) and the remaining transverse area of the cord was less than 60 mm². Houser and colleagues³² contended that the extent and shape of flattening of the spinal cord serve as an indicator of neurologic deficit: 98% of their patients with severe stenosis manifested by a banana-shaped spinal cord had clinical evidence of myelopathy. Ono and colleagues³³ described an anteroposterior cord compression ratio calculated by dividing the anteroposterior diameter of the cord by the transverse diameter of the cord. A lower anteroposterior compression ratio (<0.40) correlated well with the areas of most severe injury of the cord histologically. The Pavlov ratio, which is the anteroposterior diameter of the spinal canal divided by the anteroposterior diameter of the vertebral body at the same level, as measured on a lateral radiograph, also indicates static compression; a value of 0.8 or less indicates a developmentally narrow cervical canal and stenosis of the canal.^30,34

Segmental motion of the cervical spinal column affects the development of cervical myelopathy. Hyperextension of the neck narrows the spinal canal by shingling the laminae and buckling the ligamentum flavum ventrally into the canal. Extension and flexion of the neck may alter the diameter of the canal by 2 mm.³⁵ Angulation or translation between vertebral bodies in flexion or extension may result in narrowing of the space available for the cord (Fig. 36–5B). Particularly during extension, retrolisthesis of a vertebral body can pinch the spinal cord between the inferoposterior margin of a vertebral body and the superior edge of the lamina caudad to it. Forward slippage of a vertebral body may compress the spinal cord between the superoposterior margin of the vertebral body below and the lamina above.³⁰ Flexion of the spinal column aggravates this forward slippage. Retrolisthesis and anterolisthesis often cause myelopathy in elderly (≥70 years old) patients (Fig. 36–5C).^28,36 Additionally, hypermobility at the third and fourth cervical levels cephalad to a degenerated and stiffened C4-5 segment commonly exists in elderly individuals, potentially resulting in myelopathy at the hypermobile C3-4 level.³⁷ Research using a spinal cord model showed that the cord is more vulnerable to dynamic, repeated minor loading compared with severe static loading.³⁸

Cervical spine flexion and extension cause morphologic changes within the spinal cord itself. Breig and colleagues³⁹ showed that the spinal cord thickens and shortens with extension, which renders it more susceptible to pressure from the infolded ligamentum flavum or lamina. The spinal cord stretches with flexion, which may subject the cord to higher intrinsic pressure if it presses against a disc or a vertebral body anteriorly. Flexion of the cervical spine may cause stretch (strain) injury to the axons through tensile loading, resulting in increased permeability and myelin injury, rendering these already injured axons more susceptible to secondary injury from other processes, including ischemia.⁴⁰

Barre⁴¹ first proposed in 1924 the possibility that vascular factors play a significant role in the development of cervical myelopathy. The acute development or progression of findings suggests vascular involvement. In two separate canine experiments, cervical cord ischemia superimposed on compression of the cord resulted in a dramatic increase in neurologic findings.^42,43 The effects of compression and ischemia were additive and responsible for the clinical manifestations of myelopathy. These investigations also led to the proposal that ischemia may play an important role in the irreversibility of spinal compression.⁴² In a separate dog study, obstruction of the peripheral arterial plexus caused structural changes within the spinal cord.⁴⁴

The classic study by Breig and colleagues³⁹ established that blood flow through the anterior spinal artery and anterior radicular arteries diminishes when those vessels are tented over a disc or a vertebral body, but that this position does not have a substantial impact on flow through the tortuous posterior spinal arteries. Vessels considered most vulnerable to reduced blood flow include the transverse intramedullary arterioles, arising from the anterior sulcal arteries. These vessels perfuse the gray matter and adjacent lateral columns.⁴⁵ Ischemia may also occur from venous congestion.⁴⁶ One cell type known to be particularly sensitive to ischemic injury, the oligodendrocyte, plays a principal role in insulating axons with a myelin sheath. Oligodendrocyte death caused by ischemic insult, likely through the mechanism of oligodendrocyte apoptosis, may explain the demyelination and subsequent irreversible neurologic deficit associated with chronic cervical myelopathy.^40,47

Severe compression results in pathologic changes within the spinal cord. The central gray matter and the lateral columns show the most changes, with cystic cavitation, gliosis, and demyelination most pronounced caudad to the compression site. The posterior columns and posterolateral tracts show wallerian degeneration cephalad to the site of compression. The irreversibility of these changes may explain why some patients fail to recover after decompressive surgery. The anterior white columns are relatively resistant to infarction, even in cases of severe compression.⁴⁸

Axial Neck Pain

Neck pain commonly affects adults of all ages and both sexes almost equally. Few population-based studies exist on the prevalence of neck pain. A study of the Saskatchewan adult population showed that neck pain is more prevalent than commonly thought, with 66% of adults experiencing neck pain during their lifetime and 5% highly disabled by it.⁴⁹ Another study showed a 9% point prevalence of neck and shoulder pain.⁵⁰ The prevalence of neck pain increases in highly educated individuals and in individuals with a history of injury, headaches, low back pain, or medical comorbidities such as cardiovascular and digestive disorders.⁵¹

No true natural history studies of axial neck pain exist; all published studies involve some form of treatment in most patients. DePalma and Subin⁵² found that most patients with axial symptoms from cervical spondylosis respond favorably to nonoperative treatment. After 3 months of nonoperative treatment, 29% of their patients had total relief of symptoms, 49% improved, and 22% did not improve. Rothman and Rashbaum⁵³ reported on the 5-year outcome of patients with “predominantly” axial neck pain treated conservatively. They found that 23% of these patients remained partially or totally disabled from their symptoms. At the 5-year follow-up, Rothman and Rashbaum⁵³ found no significant difference between this group and another similar group of patients who underwent surgery and recommended nonoperative management for “non-neurogenic” axial neck pain symptoms.

Generally, most patients who present early with a single episode of axial neck pain may be reassured that their symptoms will resolve spontaneously. Patients who have persistent or recurrent symptoms that require continued treatment likely fall into a separate group, with approximately one quarter of these patients going on to residual moderate to severe pain. This group should be evaluated more carefully to rule out underlying discogenic or other pathology that may be responsible for their continued symptoms.

Cervical Radiculopathy

In a study of a Midwestern U.S. population, the annual incidence of cervical radiculopathy was found to be 83 per 100,000 population, with a peak incidence in the 6th decade of life.⁵⁴ The point prevalence of cervical radiculopathy was found to be 3.5 per 1000 population.⁵⁵ As with the natural history of neck pain, no studies on the true natural history of radiculopathy exist, with some form of treatment being provided in most patients. With varying degrees of nonoperative management, 45% of patients with cervical radiculopathy have good resolution of symptoms within 6 weeks of onset; the remaining 55% continue to have a minor to moderate degree of long-term morbidity.

The reported outcomes of cervical radiculopathy vary depending on the study population. Population-based and primary care–based studies suggest a benign natural or nonoperative history of cervical radiculopathy. Good outcomes occur in 71% to 92% of patients after nonoperative measures such as medications, exercise or physical therapy, and traction.^56–59 A population-based study in Rochester, Minnesota, reported that 90% of patients initially diagnosed with cervical radiculopathy were asymptomatic or minimally affected by their condition at 5.9 years of follow-up. Surgery was performed in 26% of this group, but the effects of intervention were not independently analyzed.⁵⁴ Studies originating from tertiary referral centers or surgical practices show persistent symptoms and disability in a significant percentage of patients with cervical radiculopathy.

The 1963 study by Lees and Turner⁶⁰ on the “natural history” of cervical spondylosis showed the natural history and prognosis to be generally favorable. At long-term follow-up (2 to 19 years) of 51 patients with radiculopathy, 45% had only a single episode of pain without recurrence, 30% had mild continuing symptoms, and 25% had persistent or worsening symptoms. Lees and Turner⁶⁰ found that nonoperative treatment helped improve initial symptoms but did not affect end results. Of the patients followed for cervical radiculopathy, none had evidence of myelopathy on follow-up.

Cervical Myelopathy

The true incidence of cervical myelopathy is difficult to ascertain because of the subtle findings in its early stages and the fact that many of the clinical findings of myelopathy are attributed to old age. Similarly, no modern studies on the true natural history of spondylotic myelopathy exist because surgical intervention is so commonly part of the treatment.⁶¹ In 1963, Lees and Turner⁶⁰ reported on 44 patients with radiologic and myelographic evidence of myelopathy followed for 3 to 40 years (22 patients for >10 years and 22 additional patients for <10 years). The authors concluded that cervical spondylotic myelopathy follows a protracted clinical course consisting of long periods of relatively stable symptoms punctuated by exacerbations of variable duration. Clark and Robinson⁶² showed in a study of 120 patients that the natural history of cervical spondylotic myelopathy consists of progressive deterioration of motor symptoms, with 75% of patients deteriorating stepwise with intervening variable periods of stable disease, 20% deteriorating gradually and steadily, and 5% experiencing a rapid onset of symptoms followed by a lengthy period of quiescence. None of the 120 patients had a return to a normal neurologic state or reversal of symptoms. Nurick⁶³ retrospectively assessed 37 patients, noting that the neurologic disability manifests early in the course of the disease and subsequently consists of static periods lasting many years. He noted that the prognosis improved for patients presenting with mild disease and that the disability tended to progress in patients older than 60 years. Nurick⁶³ concluded that spondylotic myelopathy is a benign condition with minimal risk of future neurologic deterioration. Finally, Symon and Lavender⁶⁴ argued against the idea that spondylotic myelopathy constitutes a benign disease process and showed in their review that 67% of patients underwent relentless neurologic deterioration without periods of clinical stability. Their analysis of Lees and Turner’s data showed that when disability was used as a criterion, only 18% of patients showed improvement.

Axial Neck Pain

Pain along the posterior neck and trapezius muscles without radiation into the upper extremity is an extremely common, but nonspecific presenting symptom. Patients usually localize the pain to the posterior paraspinal musculature of the neck, with radiation toward the occiput or into the shoulder and periscapular regions. Patients may report stiffness in one or more directions and commonly complain of headaches.⁶⁵ Radiating “referred” pain without a dermatomal distribution in the shoulder or arm may accompany the neck pain. Referred pain may be associated with a sensation of warmth or tingling and autonomic phenomena such as piloerection and sweating. Areas of localized pain and tenderness in the posterior muscles of the neck suggest a muscle sprain or a soft tissue injury. Deep palpation of these trigger points produces referred patterns of pain along the course of the myofascial structures.

Determining a position of maximal discomfort may also provide a clue to the underlying pathologic etiology. Anterior neck pain along the sternocleidomastoid muscle belly exacerbated by rotation of the head to the contralateral side most often results from muscular strain. Pain in the posterior neck muscles that worsens with flexion of the head suggests a myofascial etiology. Pain in the posterior aspect of the neck aggravated by extension and especially by rotation of the head to one side may suggest a discogenic component. Suboccipital pain radiating to the back of the ear, occiput, or neck raises the question of pathologic involvement of the upper cervical spine. Limited rotation of the head to one side suggests involvement of the ipsilateral atlantoaxial articulation.

Postural adaptations to pain initiated elsewhere in the body may generate secondary pain in the neck and shoulder girdle. The adaptations and compensatory overuse of normal tissues in the neck and shoulder girdle generate new pain patterns that may remain even after the initial source of pain has resolved. This situation underscores the need to obtain an accurate history on how the neck pain initially presented and how it has evolved over time.

Pathologic processes in the shoulder may manifest with localized pain or referred pain to the neck, which may radiate down the anterior or lateral aspect of the arm. A thorough shoulder examination helps differentiate shoulder pathology from neck pathology. Pain in the neck and shoulder girdle can also be referred from pathologic processes in the heart, lungs, viscera, and temporomandibular joint. Fever, unintended weight loss, and nonmechanical neck pain, especially when worse at night, point to an infectious or neoplastic etiology. Morning stiffness, polyarticular involvement, rigidity, and cutaneous manifestations suggest an inflammatory arthritic element.

Cervical Radiculopathy

Cervical radiculopathy refers to symptoms in a specific dermatomal distribution in the upper extremity. Patients describe sharp pain, tingling, or burning sensations in the involved area. There may be sensory or motor loss corresponding to the nerve root involved, and reflex activity may be diminished.

Patients typically have severe neck and arm pain (frequently unilateral) that precludes them from finding a comfortable position. They may present with the head cocked to the side opposite to their arm pain and sometimes hold the arm over the head, typically resting the wrist or forearm on top of the head—the shoulder abduction sign.²⁴ The Valsalva maneuver typically exacerbates patients’ pain complaints.⁶⁶ Extension and lateral rotation of the head to the side of the pain usually aggravate the symptoms—the Spurling maneuver. Aggravation of the symptoms by neck extension often helps differentiate a radicular etiology from muscular neck pain or a shoulder pathologic process with secondary muscle pain in the neck. The Spurling maneuver is particularly useful in differentiating cervical radiculopathy from other upper extremity neck pain etiologies, such as peripheral nerve entrapment, because it stresses only structures located within the cervical spine by decreasing the size of the intervertebral foramen and impinging further on the involved nerve root.^66,67

Multiple sources of pain in the neck and upper extremity commonly coexist, and the structures may be compressed at more than one site.⁶⁸ Patients with metabolic disorders such as diabetes who have accompanying neuropathy may be more susceptible to radiculopathy and compressive neuropathy. Adaptations to an initial presentation of radiculopathy may result in secondary shoulder pathology, carpal tunnel syndrome, or ulnar nerve irritation persisting long after the initial radicular pain resolves (Table 36–2).

TABLE 36–2 Differential Diagnoses of Radiculopathy

From Rao R: Neck pain, cervical radiculopathy, and cervical myelopathy: Pathophysiology, natural history and clinical evaluation. J Bone Joint Surg Am 84:1872-1881, 2002.

Henderson and colleagues²⁹ reviewed clinical presentations in 736 patients with cervical radiculopathy: 99.4% had arm pain, 85.2% had sensory deficits, 79.7% had neck pain, 71.2% had reflex deficits, 68% had motor deficits, 52.5% had scapular pain, 17.8% had anterior chest pain, 9.7% had headaches, 5.9% had anterior chest and arm pain, and 1.3% had left-sided chest and arm pain, known as cervical angina. Neurologic deficits corresponded with the offending disc level in approximately 80% of patients with radiculopathy. Another study of 275 patients with cervical radiculopathy noted that 59% of these patients reported headache, frequently occurring ipsilateral to the radicular symptoms.¹⁸

Occasionally, patients with nerve root compression present with “referred” upper trapezial or interscapular pain without radiating arm pain. The absence of radiating symptoms in a dermatomal fashion does not rule out symptomatic nerve root compression. The clinician should perform a careful physical examination to identify any involved nerve roots, keeping in mind that crossover between myotomes and dermatomes may be present.⁶⁷

C3 radiculopathy results from disc pathology at C2-3 and is unusual. The posterior ramus of C3 innervates the suboccipital region, and involvement of this nerve manifests with pain in this region, often extending to the occiput and back of the ear. No specific neurologic deficits help identify radicular involvement of the C3 nerve root. These patients are difficult to distinguish from patients with other sources of axial neck pain. Unilateral pain, worsening of pain with extension and rotation, and concordant imaging findings may indicate radicular involvement.

C4 radiculopathy may also be a source of unexplained neck and shoulder pain. Patients occasionally have paresthesias or numbness in the lower neck extending laterally to the superior aspect of the shoulder. Diaphragmatic involvement may result from involvement of C3-5 nerve roots.^69,70 Motor deficits in the diaphragm manifest as paradoxical respiration and can be confirmed by fluoroscopic evaluation of the diaphragm during respiration. With paradoxical respiration, the unaffected hemidiaphragm contracts and descends during inspiration; this downward excursion transmits pressure to the abdominal cavity, resulting in upward passive movement of the paralyzed side. A “sniff test,” done under fluoroscopy, detects paradoxical movement: Rapidly repeated inspirations through the nostrils normally result in the descent of both hemidiaphragms, but with unilateral diaphragmatic paralysis, there is paradoxical upward motion of the paralyzed side.⁷¹

C5 radiculopathy classically manifests with pain or paresthesias in an “epaulet” distribution, from the superior aspect of the shoulder extending laterally to the mid-arm. The C5 nerve solely innervates the deltoid muscle, and involvement of C5 can result in profound deltoid weakness. Subtle weakness may also exist in external rotation of the shoulder (supraspinatus and infraspinatus) and elbow flexion (biceps brachialis). The biceps reflex primarily indicates neurologic integrity of C6 but also has a C5 component. Rotator cuff injury and other shoulder pathology manifest in a similar fashion and may coexist with cervical radiculopathy; the shoulder joint must be thoroughly examined in all patients with suspected cervical radiculopathy. Painless shoulder range of motion with good strength in the rotator cuff muscles helps rule out shoulder pathology.

C6 radiculopathy manifests as pain radiating from the base of the neck to the lateral aspect of the elbow, into the radial forearm and radial digits, more commonly involving the thumb. Numbness or paresthesias may exist in the same distribution. Motor deficits may be elicited in the wrist extensors, elbow flexion, and forearm supination. C6 compression most directly affects the brachioradialis reflex; however, subtle changes in the biceps reflex may exist as well.⁶⁶ The sensory symptoms may mimic symptoms of carpal tunnel syndrome, which typically involves the radial three and a half digits and causes weakness in the thenar musculature.

C7 is the most frequently involved nerve root in cervical radiculopathy and results from C6-7 disc space pathology. Patients report pain radiating from the neck to the shoulder, down along the triceps, then along the dorsum of the forearm onto the dorsum of the middle finger. Patients usually pronate the forearm while trying to describe the radiation of their symptoms into the dorsum of the hand or long finger, a useful observation when attempting to differentiate the hand symptoms from carpal tunnel syndrome or C6 radiculopathy.⁵ Chronic breast pain also has been associated with C7 radiculopathy.⁷² Motor weakness exists in the triceps, wrist flexors, and finger extensors with C7 radiculopathy. The triceps reflex may be absent or diminished.

C8 radiculopathy occasionally results from disc herniation or spondylosis at the C7-T1 level. Patients present with paresthesias or pain in a dermatomal distribution along the ulnar border of the arm and forearm, radiating into the ulnar aspect of the hand to the small finger and the ring finger. Numbness usually involves the dorsal and volar aspects of the ulnar two digits and hand. The small muscles of the hand exhibit profound weakness, and patients report difficulty using their hands for routine daily activities. The clinician must differentiate between C8 radiculopathy and ulnar nerve entrapment. C8 radiculopathy may affect function of the flexor digitorum profundus in the index and long fingers and function of the flexor pollicis longus in the thumb, but ulnar nerve entrapment has no effect on these muscles. Ulnar nerve involvement spares all of the short thenar muscles except the adductor pollicis, whereas C8 radiculopathy affects these muscles (Fig. 36–6).

FIGURE 36–6 Neurologic evaluation of a patient with cervical radiculopathy and myelopathy.

(From Rao RD, Currier BL, Albert TJ, et al: Degenerative cervical spondylosis: Clinical syndromes, pathogenesis, and management. J Bone Joint Surg Am 89:1360-1378, 2007.)

These pain distribution patterns represent classic descriptions and should be used as generalized guidelines for evaluation and diagnosis of compressive radicular pathology. Because of anatomic variations, chronic conditions, and involvement of multiple levels, the clinical presentation may be less precise.

Cervical Myelopathy

The subtle nature of the clinical findings of early cervical spondylotic myelopathy makes diagnosis a challenge. The physical findings in cervical spondylotic myelopathy can vary significantly depending on the anatomic portion of the cord primarily involved. Sensory symptoms arise from compression at three discrete anatomic locations: (1) the spinothalamic tract, affecting contralateral pain and temperature sensation with light touch often preserved; (2) posterior columns, affecting ipsilateral position and vibration sense, possibly leading to gait disturbances; and (3) dorsal root compression, leading to decreased dermatomal sensation. The motor and reflex examination typically reveals lower motor neuron signs at the levels of the cervical lesions (hyporeflexia and weakness in the upper extremities) and upper motor neuron signs below the lesions (hyperreflexia and spasticity in the lower extremities).³⁰

Crandall and Batzdorf⁷³ described five general categories of cervical spondylotic myelopathy: (1) In transverse lesion syndrome, the corticospinal, spinothalamic, and posterior cord tracts are essentially equally involved. This myelopathy is associated with the longest duration of symptoms, suggesting this category may represent an end stage of the disease. (2) In motor system syndrome, corticospinal tracts and anterior horn cells are involved, resulting in spasticity. (3) In central cord syndrome, motor and sensory deficits affect the upper extremities more severely than the lower extremities. (4) Brown-Séquard syndrome consists of ipsilateral motor deficits with contralateral sensory deficits and seems to be the least advanced form of the disease. (5) Brachialgia and cord syndrome consists of radicular pain in the upper extremity along with motor or sensory long tract signs.

Ferguson and Caplan⁷⁴ divided cervical spondylotic myelopathy into four syndromes: (1) medial syndrome, consisting primarily of long tract signs; (2) lateral syndrome, consisting primarily of radicular symptoms; (3) combined medial and lateral syndrome, which constitutes the most common presentation and includes aspects of cord and root involvement; and (4) vascular syndrome, which manifests with rapidly progressive myelopathy and likely represents vascular insufficiency of the cervical spinal cord. A clear-cut sensory or motor pattern may not be present with this syndrome because of the variable injury to the cord resulting from vascular ischemia. A fifth clinical presentation, anterior syndrome, has also been described, consisting of painless weakness in the upper extremities without accompanying symptoms in the lower extremities and without radicular or long tract signs.³⁰

The findings in cervical spondylotic myelopathy vary with each patient. Patients may report an insidious onset of clumsiness in the hands or diffuse numbness in the hands resulting in worsening of handwriting or other fine motor skills over the past few months or weeks and difficulty with grasping or holding objects (i.e., trouble with manipulating buttons or zippers).⁷⁵ Patients frequently experience increasing difficulty with balance that they attribute to age or arthritic hips; relatives may note that the patient’s gait has become increasingly clumsy, that the patient holds onto objects to help with balance, and that he or she sustains occasional falls. Nurick⁷⁶ developed a system for grading the disability in cervical spondylotic myelopathy on the basis of gait abnormality. Spasticity, muscle weakness, and wasting in the lower extremities with superimposed loss of proprioception result in an unsteady, broad-based gait. Severely affected individuals can be quadriparetic or quadriplegic when first seen.

Physical examination shows exaggerated deep tendon reflexes, sustained clonus, absent or diminished superficial reflexes, and the presence of pathologic reflexes confirming an upper motor neuron lesion. Myelopathy caused by pathology in the region of the cord cephalad to C3 may result in a hyperactive scapulohumeral reflex (tapping of the spine of the scapula or acromion with a caudally directed force with the seated patient’s arm resting at the side results in brisk scapular elevation or humerus abduction or both). This response represents a stretch reflex of the trapezius muscle.⁷⁷ Superficial reflexes, such as the abdominal or cremasteric reflex, are often diminished or absent in the presence of upper motor neuron lesions. The pathologic reflexes represent abnormal long tract signs and indicate cord compression.

Patients with moderate to severe spondylotic myelopathy typically exhibit the following pathologic reflexes to varying degrees: (1) the inverted radial reflex—indicative of cord compression at C6 and present when, during elicitation of a brachioradialis reflex, the brachioradialis is hyporesponsive and the ipsilateral fingers flex briskly at each hammer tap; (2) the Hoffman reflex—present if the ipsilateral interphalangeal joints of the thumb and index finger flex when the volar surface of the distal phalanx of the long finger is flicked into extension and strongly indicative of cord impingement when asymmetric; and (3) the extensor plantar reflex (also called the Babinski sign)—present when rubbing of the lateral sole of the foot from the heel along a curve to the metatarsal pads with a blunt object causes the hallux to dorsiflex and the lesser toes to fan out (see Fig. 36–6).^30,66 Combined cervical and lumbar involvement is present in 13% of patients with spondylosis, resulting in a potentially confusing clinical picture of lower extremity lower motor neuron findings.⁷⁸

Sensory findings in cervical spondylotic myelopathy also vary. Depending on the exact area of compromise of the cord or nerve root, pain, temperature, proprioception, vibratory, and dermatomal sensations all may be diminished. Presenting findings usually do not include sphincter disturbances. Patients may present with urinary complaints: hesitation, frequency, and, rarely, incontinence or retention. In the study by Crandall and Batzdorf⁷³ of 62 patients with cervical spondylotic myelopathy, neck pain was present in less than 50% of the patients, and associated radicular pain was present in 38%. Generalized shocklike sensations in the trunk and upper and lower extremities resulting from quick flexion or extension of the neck—the Lhermitte sign—was present in 27% of patients, and sphincter disturbances were present in 44%.

In the past, hand disturbances were primarily attributed to radicular pathology. Several reports have shown findings specific to “myelopathy hand,” indicating a high cervical myelopathy above the C5 level.^79,80 Diffuse numbness in the hands is extremely common and is often misdiagnosed as carpal tunnel syndrome or peripheral neuropathy. Clumsiness of the hands results in an inability to perform fine motor tasks. Marked wasting of the intrinsic hand muscles is usually present and progresses insidiously with weakness of finger extension and adduction.⁸¹ Ono and colleagues⁸⁰ described two specific signs of myelopathy hand signifying pyramidal tract involvement: (1) the finger-escape sign—when the patient attempts to extend the digits fully with the palm facing down, the ulnar two or three digits tend to drift into abduction and flexion after 30 seconds’ duration; and (2) the grip-and-release test—a decreased ability to open and close the fist rapidly because of weakness and spasticity. Normal is greater than 20 grip-and-release movements in 10 seconds. To distinguish between upper motor neuron signs arising from brain pathology versus signs arising from cervical cord pathology, a jaw jerk test may be performed. Closing of the mouth (upward jerking of the mandible) caused by tapping of the lower jaw at a downward angle with the mouth held slightly open constitutes a positive jaw jerk test. This response signifies that the origin of the upper motor neuron findings may be higher up in the brain rather than in the spinal canal and specifically tests cranial nerve V.⁸²

Many neurologic conditions resemble cervical spondylotic myelopathy. Multiple sclerosis has distinctive plaques that can be seen on magnetic resonance imaging (MRI) of the brain and spinal cord. The disease is a demyelinating disorder of the central nervous system and causes motor and sensory symptoms but typically has remissions and exacerbations and involvement of the cranial nerves. Amyotrophic lateral sclerosis results in upper and lower motor neuron symptoms, without alteration in sensation. Subacute combined degeneration seen with vitamin B₁₂ deficiency causes corticospinal tract and posterior tract symptoms, with greater sensory involvement in the lower extremities. Patients with metabolic or idiopathic peripheral neuropathy have sensory symptoms that may mirror symptoms of myelopathy (Table 36–3).

TABLE 36–3 Differential Diagnoses of Cervical Spondylotic Myelopathy

From Rao R: Neck pain, cervical radiculopathy, and cervical myelopathy: Pathophysiology, natural history and clinical evaluation. J Bone Joint Surg Am 84:1872-1881, 2002.