Neck pain is a common complaint. The prevalence is approximately between 75% and 80% in the U.S. population. Fortunately, acute neck pain has a very favorable prognosis, with 80% of cases resolved within 2 years.¹ But 20% of cases are estimated not to improve and of these, 5% are characterized by severe disabling chronic neck pain.² The International Association for the Study of Pain (IASP) describes chronic cervical spine pain as follows: Pain perceived as arising from anywhere within the region bounded superiorly by the superior nuchal line, inferiorly by an imaginary transverse line through the tip of the first thoracic spinous process, and laterally by sagittal planes tangential to the lateral borders of the neck.³ The potential sources of neck pain are derived from those structures that have abundant nociceptive innervation, which include the cervical zygapophysial (facet) joints (including atlantoaxial and atlanto-occipital), posterior neck muscles, cervical intervertebral discs, vertebral bodies, anterior and posterior ligaments, dura mater of cervical spine, prevertebral muscles, carotid and vertebral arteries, and the transverse ligament.⁴ The paucity of nociceptors in ligamentous structures makes them less likely to cause pain. The neck is a very mobile structure and is, therefore, susceptible to trauma in addition to wear and tear. It is further burdened by the weight of the head and rests on a relatively fixed thorax.

The evaluation of neck pain is based upon history, physical examination, radiologic, and laboratory tests. In the assessment of acute pain, history is of paramount importance in that it offers clues to potentially rare but serious disorders (Table 37-1).

HISTORY

The key elements of history include elucidation of the onset, mechanism, neurological symptoms, and psychosocial setting. Therefore, these features include:

1. 
   

   Precipitating and associated events (trauma, infection, emotional stress).

   
   
2. 
   

   Duration (acute versus chronic).

   
   
3. 
   

   Characteristics of pain (sharp, burning, dull, throbbing).

   
   
4. 
   

   Point of origin (axial neck with or without appendicular radiation).

   
   
5. 
   

   Aggravating and alleviating factors.

   
   
6. 
   

   Topographical regions of maximal pain.

   
   
7. 
   

   Co-existing neurologic symptoms (weakness, numbness, clumsiness, bowel and bladder dysfunction, and disturbances of balance).

   
   
8. 
   

   Associated medical symptoms and conditions (fever, night sweats, weight loss, dysphagia, immunosuppression, illicit drug use, infections).

   
   
9. 
   

   Previous treatment (surgery, manipulation).

   
   
10. 
    

    Pending litigation or workers’ compensation.

Acute neck pain as defined by neck pain of less than 3 months is often in the setting of trauma. The main concern is cervical spine instability that can compromise the long tracts of the spinal cord. Progressive weakness of the upper extremity, lower extremities, or bowel and/or bladder dysfunction warrants radiographic evaluation and spine surgical referral. Additionally, undiagnosed tumors, infections, epidural hematomas, and autoimmune disorders (e.g., rheumatoid arthritis) are rare causes with a prevalence of less than 0.4%.⁴

The risk factors for developing neck pain commonly seen in clinical practice are not structural as would be expected. Degenerative intervertebral discs as well as zygapophysial joints do not seem to imply that a patient is at risk for neck pain.¹² Interestingly, educational level, previous injuries, motor vehicle accident that causes whiplash, and occupation factors are presently the key risk factors.^13,14 While operating machinery is linked to the development of neck pain, there has been no clear ergonometric pattern of work-related physical stress that can be modified in a positive manner.¹⁵ Higher levels of education and the lack of previous injuries to the neck decrease the probability of developing neck pain. While there are no apparent psychological factors contributing to the onset of neck pain, psychosocial stress in the work place is felt play a role in symptom complaint.¹⁶ As expected, high work demands, time pressure, and lack of support are at the root of an unfavorable work environment that may precipitate pain in the neck region.

While there have been risk factors identified for the development of neck pain, there is very little the literature offers to the clinician to aid in prognosticating long-term outcome. Aside from most acute neck pain improving as already discussed, there are no validated prognostic risk factors for neck pain—with the exception of whiplash. Patient with complaints of a high level of pain and disability following a whiplash injury carry a long-term unfavorable probability of recovery.¹⁷ These patients are characterized by diffuse hyperalgesia, greater work interference by pain, and reduced activity.¹⁸ The additional factor of litigation is weaker but seems to be a definite factor in trending toward poor recovery. Taken together, our understanding of neck pain in the acute setting will improve, but it is unclear as to why it has such a favorable outcome.

PHYSICAL EXAMINATION

The examination of the neck has several overall elements as listed:

• 
  

  Anterior and posterior inspection and palpation.

  
  
• 
  

  Range of motion.

  
  
• 
  

  Neurological examination.

Inspection of the neck begins when first encountering the patient and during the interview process. A clinician can gain insight into the range of motion and usual posture. The general medical exam includes inspection for masses, muscular asymmetries, scars, discolorations, and cutaneous lesions. The thyroid gland should be assessed for tenderness, enlargement, and nodules. The presence of cervical lymphadenopathy may signify the presence of malignancy or infection. Lymphadenitis may present as torticollis. Similarly the supraclavicular fossa must be assessed for masses that could be related to lymphadenopathy, aneurysm of the subclavian artery, or an outflow obstruction from a superior vena cava syndrome. Tenderness over the bifurcation of the carotid artery is the hallmark of carotidynia. Horner’s syndrome raises concern for carotid artery dissection. Finally, in an ill-appearing patient with severe headache and neck pain, passive forward flexion of the neck triggers significant pain (Kernig’s sign) secondary to meningeal inflammation. Unfortunately, with respect to diagnosing the musculoskeletal disorder responsible for a patient’s neck pain (whether acute or chronic), the physical exam has limited utility. Documentation of the range of motion is important to gage the benefit of future therapies, but this does not give insight as to the cause of pain. Palpation of the base of the occiput may reveal tenderness in the territory of the greater occipital nerves but is a nonspecific finding as this can be seen in primary headache disorders such as migraine in addition to occipital nerve entrapment. Tenderness of the muscles overlying the cervical zygapophysial joints raises suspicion for facetogenic pain. But, again, sensitivity over the cervical facets is not diagnostic of the cause of pain. Finally, tenderness over a taut band of muscle that causes referred pain may signify the presence of trigger points. Muscles such as the trapezius and semispinalis cervicis may have such entities and can be a primary or a secondary (e.g., underlying facetogenic pain) myofascial pain syndrome.

The neurological examination serves as a screen for potential nerve root involvement but does not diagnose the cause of a patient’s neck pain. The extent of neurological deficit (motor weakness, hyporeflexia, and sensory loss) of the upper extremities is of significant importance and can be assessed via the information in Table 37-2 and Figure 37-1. The lower extremities should be screened for myelopathy, which can present with sensory loss, spastic weakness, clonus, or impaired vibratory or position sense. Other specialized examination maneuvers for provoking symptoms of cervical radiculopathy are summarized in Table 37-3. The basic trend in the literature suggests these tests have a low sensitivity, high specificity, and reasonable inter-examiner reliability.

WHIPLASH-ASSOCIATED DISORDERS

Neck pain from a traumatic origin includes many injuries ranging from self-limited acute cervical strain to cervical fracture with paralysis. The Quebec Task Force proposed a theoretical classification of whiplash-associated disorders (WADs) in order to allow comparative research on an international basis.^21,22 The following grading system is presently in use:

• 
  

  Grade 0: No complaints in the neck. No physical signs.

  
  
• 
  

  Grade I: Neck pain without symptoms indicating serious pathology and minimal influence on daily activities.

  
  
• 
  

  Grade II: Neck pain without symptoms indicating serious pathology but having an impact on activities of daily living.

  
  
• 
  

  Grade III: Neck pain with no symptoms indicating serious pathology but with the presence of neurologic dysfunction that includes weakness, sensory loss, or decreased reflexes.

  
  
• 
  

  Grade IV: Neck pain that involves serious underlying pathology, which may include fracture, myelopathy, hemorrhage, or neoplasm.

The patients typically presenting in the outpatient setting fall into WAD I and II, and, therefore, these categories will be discussed. Reports indicate that 85% of neck disorders result from acute or repetitive neck injuries or chronic stresses and strain.²³ Minor trauma resulting in acute cervical pain is often secondary to musculoskeletal injury and, most frequently, is self-limited using conservative treatment. Indeed the prognosis for WAD I remains favorable, with 85% returning to baseline activities within 6 months post-accident while at least 15% to 26% develop chronic symptoms.^21,24

MECHANISMS OF INJURY

The term whiplash classically describes the resultant injury caused by an abrupt hyperextension of the neck from an indirect force. When forward flexion of the neck is produced by acceleration or deceleration, the forward flexion of the head is limited by the chin touching the chest.²⁵ Lateral flexion movement stops when the ear hits the shoulder. These movements are within the physiologic range of motion of the cervical spine. By contrast, backward extension of the head stops when the occiput hits the posterior thorax. This is beyond the physiologic range of motion. In a rear-end collision, the body is propelled in a linear horizontal direction.²⁶ The head abruptly moves backward, necessitating acute hyperextension of the cervical spine. This is followed by recoil of the head with severe cervical neck flexion and, finally, a return to the neutral position. The opposite sequence occurs in head-on collisions.

Modern studies have recently begun to refute the flexion-extension injury or acceleration-deceleration injury model. High-speed photography has allowed researchers to determine that the trunk is forced upward into the cervical spine, causing compression from below.²⁷ The cervical spine is forced into a sigmoid deformation, during which the posterior neck structures are impacted while the anterior elements are distracted.²⁸ To be specific, the cervical zygapophysial joints are found to have intra-articular hemorrhages, meniscoid contusions, articular subchondral fracture, and articular pillar fracture, while the cervical discs have annular tears.²⁹ Chronic pain in WAD I or II is thought to be a result of traumatic arthritis to the cervical zygapophysial joints and/or annular tears of the cervical discs. While alar ligaments can also be damaged by whiplash trauma, the contributions of these structures to chronic pain are uncertain.³⁰

SYMPTOM COMPLEX

It is important to note that symptoms may not occur for 12 to 24 hours after a whiplash injury because muscular hemorrhage and edema may need to evolve prior to inciting a nociceptive response. The cervical flexor muscles—specifically, the sternocleidomastoid, the scalene muscles, and the longus colli—undergo an acute stretch reflex, which can disrupt muscle fibers.³¹ One study reported characteristic symptoms of patients after a motor vehicle accident.³² This author followed 146 walk-in patients for 5 years after motor vehicle accidents that caused soft-tissue neck injury without fractures or dislocations. Seventy percent of these accidents were rear-end collisions. Loss of consciousness occurred in 10% of patients. Almost all patients complained of neck pain and stiffness. Two-thirds of patients had headaches, and one-third had shoulder or intrascapular pain. Ten percent had arm and hand pain or arm and hand numbness. Only 3% had a focal neurologic deficit.

The primary complaint of WAD is pain typically perceived on the back of the neck that is dull and/or achy accompanied by exacerbations on movement. Persistent suboccipital pain does not necessarily involve a local lesion at the atlantoaxial region but may be referred pain from a damaged cervical segment.³³ In specific, the C2-3 facet joint may account for up to 53% of cervicogenic headache post-whiplash.³⁴ As indicated earlier, transverse and alar ligaments and the atlantoaxial joint may produce cervical pain with headache, but the contribution and confirmation remains to be determined. Although pain and numbness radiating down the arm are prognostic indicators of chronicity of symptoms, they do not necessarily indicate nerve root pressure.³⁵ Non-neurogenic radiation of pain and numbness may be caused by chronic irritation of the musculoligamentous joint and intervertebral disk rather than by organic nerve pressure. These radicular symptoms are non-neurogenic; therefore, they follow no specific nerve pathway. They are not well defined by the patient in contradistinction to the well-defined dermatomal pattern of neurogenic symptoms. Subjective numbness in the ulnar distribution may represent anterior scalenus spasm and entrapment of the brachial plexus; this scenario is amenable to injection of the muscle with a local anesthetic and corticosteroid (see “Thoracic Outlet Syndrome”). Radicular-type symptoms (across the back, shoulders, and into the arms) may be caused by damage to the posterior scapular muscles.³⁶ History taking usually allows the provider to rule out WAD III and IV.

In addition to pain, WAD commonly presents with associated symptoms, which include dizziness, paresthesia, tinnitus, weakness, cognitive impairment, visual disturbances, and back pain.³⁷ However, temporomandibular joint abnormalities are not associated with whiplash syndrome.³⁸ None of these lesser symptoms have been adequately studied, but suggested explanations are as follows:

• 
  

  Dizziness: Speculative damage to vestibular apparatus.

  
  
• 
  

  Paresthesia: Proposed myogenic thoracic outlet syndrome.

  
  
• 
  

  Tinnitus: No attractive explanation.

  
  
• 
  

  Cognitive impairment: No conclusive evidence to support traumatic brain damage, though still believed to be the primary mechanism.

  
  
• 
  

  Visual disturbances: Most common report is difficulty focusing thought to relate to disturbances in the spinociliary reflex. Persistent pain in the neck can therefore affect sympathetic outflow to the eye.

  
  
• 
  

  Weakness: Often a global complaint and thought to relate to reflex inhibition of muscle groups secondary to persistent neck pain.

  
  
• 
  

  Back pain: A common report but unclear as to the mechanism or actual prevalence.

Psychosomatic reactions may occur after soft-tissue neck injuries. Psychological factors have not been found to consistently predict the persistence of pain and disability post-whiplash injury. A randomized, double-blind, placebo-controlled trial demonstrated resolution of psychological distress with radiofrequency neurotomy of the nerves to a single cervical zygapophysial joint.³⁹ In addition to WAD being dismissed on a psychological basis, symptoms have also been attributed primarily to ongoing litigation. One study evaluated the effects of pending litigation on patients with persistent symptoms after a motor vehicle accident.⁴⁰ If litigation claims were settled within 6 months, 83% were symptom free at 5 years. However, if litigation settlement did not occur until 18 months after the accident, then follow-up at 5 years revealed that only 38% were symptom free. Two other studies have found persistent symptoms in 12% to 45% of patients after litigation settlements.^41,42 As would be expected from the underlying anatomic pathology, in many cases, patients are not “cured by a verdict,” as is commonly thought.

DIAGNOSIS

The physical examination is first used to confirm the absence of significant neurological deficit. The clinical examination of the neck often reveals localized muscle spasm, tenderness, and reduced range of motion (usually rotation, lateral bending, and extension). No definitive diagnosis is derived from the clinical exam in WAD I and II.

The patient with neck trauma is classically evaluated with a plain-film x-ray study, which includes (1) anteroposterior (AP) view of the atlantoaxial articulation (open mouth), (2) AP view of the lower cervical spine, (3) lateral view, and (4) each oblique view.⁴³ While this approach is used as the initial imaging evaluation for cervical spine instability, there is no evidence of utility in WAD I and II.⁴⁴ Advanced studies with magnetic resonance imaging (MRI), which are agreed upon as a helpful screening tool for occult fractures, infections, and tumors, also fail to determine the cause of WAD I and II. Electrophysiologic studies do not help target the cause or assist in the treatment of WAD I or II. Thus, a clinician is often left short as to the cause of pain in a whiplash case even after careful review of the history, physical exam, and imaging data.

TREATMENT

The initial treatment is conservative and is largely confined to the symptomatic treatment of the pain and range of motion. Most authors recommend a soft cervical collar, nonsteroidal anti-inflammatory agents (NSAIDs), analgesics, and limited bed rest with gradual increase in activity for the first 1 to 2 weeks. Some suggest physical therapy, such as Greenfield isometric neck exercises, heat, and traction.⁴¹ Transcutaneous electrical nerve stimulation (TENS) has been found to be useful for acute cervical train; it hastens pain relief and the return or range of motion.⁴⁰

Despite improvement in most patients’ symptoms, a substantial number of patients with whiplash have chronic symptoms. Forty-three percent of patients assessed 5 years after an automobile accident reported persistent symptoms.⁴⁰ Interventional strategies are often used in the chronic stage, after 3 to 6 months. These have included epidural steroid injections, trigger points, medial branch or facet injections, botulinum toxin intramuscular injections, and radiofrequency neurotomy of medial branches supplying the cervical facet joints. The effectiveness of epidural injections for the axial complaints of WAD I and II categories has not been established. Intra-articular facet injections have not proven effective in whiplash patients.⁴⁵ Trigger-point injections have comparable effects to ultrasound and physical therapy, and the addition of botulinum toxin has not proven to be effective.^46,47

The analgesic effects of radiofrequency treatment of the cervical facet joints are well documented. Both a randomized, double-blind study and a prospective observation study find that between 58% and 70% of patients with WAD thought to stem from cervical facets derived substantial improvement with reduction in neck disability.^48,49 The analgesic effects following this treatment can endure for more than 1 year.⁵⁰ The lack of relief or partial improvement suggests additional pain generators may coexist. Studies have found that it is not always possible to determine the exact source of neck pain and that it is not uncommonly multifactorial.^51,52 Cervical discography has been utilized to assist in the diagnosis of discogenic pain following WAD, and anterior cervical discectomy and fusion have been proposed by some authors as the treatment, though this remains contentious.⁵³

MYOFASCIAL PAIN SYNDROME

One of the most common and frequently overlooked causes of neck pain is the myofascial pain syndrome (MFPS). A myofascial trigger point is a hyperirritable locus that is palpable as an exquisitely tender taut band or knot in a skeletal muscle. Active trigger points are tender, prevent full lengthening of the muscle, weaken the muscle, and can mediate a local twitch response if stimulated adequately. Digital compression causes a characteristic pain reproduction, often with a distal site referral and autonomic phenomena (sweating, vasoconstriction, and pilomotor activity).⁵⁴ The pain pattern may not be limited to a specific dermatome or peripheral nerve segment. Many times, this pattern may superficially mimic other pathology (i.e., herniated nucleus pulposus, radiculopathy), and, therefore, the diagnosis of myofascial pain syndrome is not entertained.

A myofascial pain syndrome may coexist with other cervical disorders. These other pathologic conditions must be evaluated and treated as well. Myofascial pain is often abrupt in onset, and patients may remember a specific precipitating event, often traumatic—for example, a whiplash injury. However, the pain may be more gradual in onset from a chronically overused muscle. Myofascial pain may develop after, or be worsened by, psychogenic stress, viral illness, visceral disease, exposure to cold or damp weather, and strenuous exercise or prolonged tensing of the involved muscle.⁵⁵ The patient often describes pain that is steady, deep, and aching in quality. Although the pain may follow a dermatomal myotomal pattern, it does not follow a characteristic nerve root pattern nor is there usually dysesthesia or paresthesia, which often is present with nerve root irritation.

Diagnosis

There remains a lack of consensus in the literature on the validity and reliability of diagnostic criteria for MFPS with associated trigger points.⁵⁶ However, most would agree that in neck pain of myofascial origin, the muscles of the shoulder and neck are often tense with spasm. Palpation of a taut, bandlike trigger point that reproduces the patient’s pain pattern is pathognomonic for a myofascial pain syndrome. There may be associated weakness but not atrophy of the involved muscles.⁵⁷ Trigger points commonly responsible for pain referred to the cervical area are located in several muscles (Table 37-4). Many patients exhibit a sleep disturbance.

Management

There is considerable clinical overlap among myofascial pain, fibromyalgia, and tension-type headaches, and, as a result, the pharmacological, nonpharmacological, as well as the interventional approaches tend to be similar—even if the evidence is only in one of the three aforementioned syndromes (Table 37-5). Nonsteroidal anti-inflammatory drugs have limited literature supporting their use in MFPS but are considered helpful in fibromyalgia.⁵⁸ The strong evidence supporting the use of tricyclic antidepressants in tension-type headache and dual reuptake inhibitors in the fibromyalgia syndrome have led to their common use in MFPS of the neck.^59–61 The safety and ease of use of the gabapentinoids—especially pregabalin—coupled with its proven efficacy in fibromyalgia has led to its common use in muscle pain.⁶² Lastly, numerous clinical studies demonstrate the effectiveness of skeletal muscle relaxants—particularly cyclobenzaprine and tizanidine—in cervical muscle pain.^63,64