The Epidemiology of Neck Pain

  Donald R. Gore, MD, Medical College of Wisconsin, Milwaukee, Wis.   Abstract Neck pain is a common problem in our society and, at any given time, affects about 10% of the general population. The sources of pain are caused by conditions that compress, destroy, or irritate pain-sensitive structures such as the annulus fibrosus, posterior longitudinal ligament, and the capsule of the zygapophyseal joints. Involvement of the cervical nerve roots usually results in pain and neurologic findings in the distribution of the nerve. Referred pain from visceral disease may cause neck pain and may also be confused with primary shoulder disease and peripheral nerve entrapments. Common conditions thought to cause neck pain are degenerative disc disease, with or without disc herniation, and degenerative arthritis of the zygapophyseal joints. Aside from patients with disc herniations demonstrated on imaging studies and pain in a specific nerve root distribution, the relationship with degenerative changes is not always clear. This is because degenerative conditions are common with aging and many times are incidental findings in asymptomatic people. Specific conditions that have been studied but also are not well understood are post-traumatic neck pain syndrome, commonly known as whiplash injuries, and pain following repetitive activities in an occupational setting. Although causes of neck pain are not well understood, outcome studies have shown that it frequently is not a self-limiting condition and can be a long-term problem. [ 1998 Medscape, Inc.]

   Introduction Epidemiology is the branch of medical science that studies the causes, incidence, prevalence, and control of a disease in a defined population. Although there are numerous epidemiologic studies of low-back pain, relatively few investigations of neck pain have been conducted. There are several reasons for this, the most important being that neck pain is not as common as low-back pain and, when present, is not as disabling; therefore, it doesn't have the same economic impact on society as does low-back pain.  Neck pain is a symptom of a disease process. Knowing the etiology of neck pain aids in understanding its epidemiology.

Sources of Neck Pain

The human neck is a complex structure that contains the extension of a number of vital visceral structures, including the trachea, esophagus, and the carotid and vertebral arteries, and a musculoskeletal system that provides for support and motion of the head. The cervical spine itself is a series of seven separate bone elements, all with intricate articulations and an elaborate system of ligaments and associated muscles. The first and second cervical vertebrae are different in size and shape from each other and the remaining five vertebrae. However, all of the segments have true synovial joints. The anterior articulations of the vertebrae below C2 occur via intervertebral discs. Both the anterior and posterior joints are surrounded by a fibrous capsule and supported by ligaments and muscles. These joints both allow and limit neck motion. The capsule, ligament, and muscles all contain an abundance of free nerve endings which are capable of transmitting pain impulses. Irritation or damage to these structures causes primary neck pain.

The cervical vertebrae also protect and allow passage of the spinal cord and cervical nerve roots. Pathologic processes such as compression, especially of the nerve roots, are a frequent source of neck pain and referred pain from the neck. Cervical nerves are both sensory and motor so that damage, in addition to pain, may cause numbness, tingling, muscle weakness, and reflex deficits in a specific location. Signs and symptoms along the distribution of a cervical nerve root are called cervical radiculopathy.

The cervical nerve roots C5, C6, and C7 are the most commonly involved and result in characteristic signs and symptoms in the upper extremities. Because the distal-most innervation of C4 is to the top of the shoulder, compression of the C4 nerve root does not produce symptoms below the level of the shoulder, and usually there is no demonstrable muscle weakness or any reflex abnormalities. Damage or irritation of C1, C2, and C3 does not result in reflex or motor deficits but can result in pain in the back of the neck extending along the back of the head. Pain from neck sources other than cervical nerve roots does not result in sensory, motor, or reflex deficits and the pain patterns are not as well defined. Pain reproduction studies have investigated patients with neck pain but without evidence of specific nerve root involvement. Discography and zygapophyseal joint injections[1] were used, indicating that there are a variety of etiologies for neck pain. Other possible sources of neck pain, whose importance has not been established, are the cervical sympathetic nerves and the innervation present in the anterior surface of the dura.

Causes of Neck Pain

Pain originating in and confined to the neck may arise from infections, tumors, and degenerative changes of the zygapophyseal joints and intervertebral discs. Cervical radicular pain is pain in the distribution of a cervical nerve root. This can be caused by any process that compresses or irritates the nerve, the most common being herniated intervertebral discs (Figure 1a,b) and osteophytes which narrow the neuroforamen (Figure 2a,b,c). Disc protrusion and osteophytes can also narrow the spinal canal, causing pressure on the cervical cord and resulting in a myelopathy (Figure 3).

Referred neck pain is generated by disease in an anatomic structure other than the neck. Examples of this are visceral diseases such as angina, apical lung tumors, and subdiaphragmatic irritation as in a subdiaphragmatic abscess. The most common conditions that may be confused with neck problems are intrinsic shoulder diseases such as impingement, rotator cuff tears, and adhesive capsulitis. Peripheral nerve entrapment occurring in thoracic outlet syndrome, ulnar cubital tunnel syndrome, and carpal tunnel syndrome can simulate cervical nerve root compression. Systemic diseases such as rheumatoid arthritis, spondyloarthropathies, fibromyalgia, and herpes zoster may also cause neck pain. However, in these conditions it is unusual for the only symptom to be in the neck.

Incidence and Prevalence of Neck Pain

Neck pain has most frequently been studied in five different populations

Incidence is the number of new cases of a disease which occur during a specified period of time, whereas prevalence is the number of cases present at any one time. Most reports in the medical literature are crude prevalence studies. Since neck pain has many causes, and a number of factors such as age, sex, occupation, and cigarette smoking effect its occurrence,[2] it is difficult to compare the results obtained from research done on differing study populations. In addition, most reports are based on questionnaires, so the cause of the pain cannot be validated; also, neck, shoulder, and upper-extremity pain are frequently considered together.


General Population Even with the limitations mentioned above, some information -- mostly from Scandinavian countries -- is available. Neck pain occurs half as often as low-back pain[3] and is slightly more common in women. In Norway, Bovim and colleagues,[4] in a random sample of 10,000 persons ages 18-67 years, found a prevalence of 13.8%. In a similar study in Finland, Makela and associates[2] discovered neck pain in 9.5% of males and 13.5% of females. The United States' National Center for Health Statistics reported 7.0% of men and 9.4% of women had neck pain in the period between 1976-1980.[3] In addition to neck pain being more common in women, Makela[2] also found that older patients, those involved in both mentally and physically stressful jobs, and current smokers were more likely to have neck pain.

Auto Accident

Post-Traumatic Pain

The most common post-traumatic neck pain syndrome is a whiplash injury and follows an automobile accident. The term was first used by Crowe[5] in 1928 in an unpublished report, then in an article by Davis[6] in 1945, and later by Gay and Abbott[7] in 1953. The original descriptions were of a mechanism of injury rather than a disease process. Although many now object to its use, the term "whiplash" is routinely used by laymen, lawyers, and medical professionals in reference to a patient with neck pain after an automobile accident in which a more specific diagnosis cannot be made.

The most frequent scenario is a patient whose vehicle is struck from behind causing a hyperextension motion of the neck. The combination of seat belts and properly adjusted head restraints reduces the likelihood of neck injuries.[8]

Recently Grauer and colleagues[9] have shown with cadaver studies that in a simulated whiplash injury the neck forms an S-shaped curve with initial hyperextension of the lower cervical spine and upper-level flexion, followed by extension of the entire cervical spine. It would be expected that if physiologic limits of motion are exceeded, than injury would occur. This physiologic limit of motion was reached in the lower cervical spine in their studies.

Hyperextension injuries of the neck can damage a number of structures, including the anterior muscles and ligaments, the disc, and zygapophyseal joints. These injuries have been demonstrated on cadavers and experimental animals and found in human autopsy studies of victims of motor vehicle accidents.[10]

Recently Jonsson and coworkers[11] reported on 50 consecutive patients with whiplash-type cervical spine distortions in automobile accidents. At 6 weeks, 24 had persistent neck pain and underwent MRI imaging. Of these, 8 were found to have large cervical disc protrusions and had surgery. Two patients had posterior fusions for instability based on lateral flexion and extension films. This report is in contrast to our own experience and that of others' where, despite careful evaluation of whiplash patients, conclusive objective pathology is rarely found.

Borchgrevink and associates[12] studied 201 patients with neck pain following automobile accidents. The patients were randomly divided into two treatment groups. In one group, immobilization by means of a cervical collar and sick leave from work was provided. In the other, no immobilization was used, no sick leave was given, and the patients were instructed to act as usual. At 6 months, the "act-as-usual" group showed more overall progress, as measured by subjective symptoms ratings. The researchers found, however, that 10% of this group still had severe symptoms at 6 months, which emphasizes that neck pain following an automobile accident in many patients is not a self-limited condition.

The symptom complex most frequently seen is neck pain that may not be present immediately after the accident but begins in most patients within 24 hours.[13] Other frequent complaints are headache, dizziness, paresthesia, and cognitive somatic and psychological sequelae.

This unrelated constellation of symptoms without objective evidence of structural injury has led to speculation that the condition is an emotional rather than a physical problem. Since the neck pain patient's vehicle has been struck from behind, causation and therefore liability usually rest with the other driver. Our current tort system favors documentation which encourages frequent physician visits, exaggeration of complaints, expensive testing, and extensive symptomatic treatment, most of which have no proven value in altering the natural history of the patient's symptoms.

Occupational Neck Pain

Occupational neck pain can be divided into two categories -- those patients who have had specific injuries and those in whom the onset of neck pain seems to be related to normal work activity.

Specific injuries that may occur in the workplace include motor vehicle accidents, falling from a height, and being struck on the head. In these instances, causation is not hard to determine; neck pain that begins during normal work activities, however, is more difficult to assess.

Employees in occupations which require repetitive use of the upper extremities such as machine operators, carpenters, and office workers are more likely to have neck complaints.[14] If work activity is truly the cause the of the patient's complaints then a strong relationship with the activity and the onset and persistence of the symptoms should be evident. For instance, it must be established that the symptoms began after performing the activity and the complaints improve or completely subside if that activity is eliminated. Usually the distinction between work causation and other factors is not clear because preexisting disease and activities that are not involved with work cloud the picture. In addition, there is no conclusive evidence in the medical literature that overuse results in structural damage. There is, however, a segment of the population with permanent symptoms after a period of overactivity at a specific task. In these situations, evaluation and treatment proceeds as with any other group of patients but causation usually cannot be established.

Herniated Intervertebral Cervical Discs

In contrast to studies of patients with neck pain as a syndrome, a herniated cervical disc is a specific diagnosis. The only published study that provides an incidence rate was done by Kondo and colleagues.[15] They analyzed residents of Rochester, Minn, from 1950 to 1974 and found an annual herniated disc incidence of 5.5/100,000 people. The most frequent level involved was C5-6, followed by C4-5 and C6-7. In reviews of surgically-treated patients, these are also the most frequent levels involved.

Kelsey and associates[16] reported on 88 people with cervical disc protrusions living in New Haven and Hartford, Conn. Forty were surgically treated after the diagnosis of herniated cervical disc was made. Based on their clinical appearance, 20 were listed as probable and 28 as possible disc protrusions. Fifty-two patients were men and 36 were women, and most patients were in their 40s and 50s. The researchers compared cervical disc protrusion patients with age- and sex-matched controls. A strong association was found between protrusion and recurrent lifting of heavy objects on the job, cigarette smoking, and frequent diving from a board. Driving vibrating equipment and time spent in motor vehicles were weakly associated. Frequent twisting of the neck on the job and sitting on the job were not associated with the clinical diagnosis of herniated disc.

The association of lifting heavy objects and driving vibrating equipment with prolapsed disc is not surprising, but the relationship with smoking is not as easily explained. Cigarette smoking has been implicated in impeding bone metabolism and in interfering with fracture repair, in nonunions in fractures, in arthrodesing procedures, and in increasing the rate of postoperative wound infections.[17] A number of studies have identified smoking as a risk factor for low-back pain, and although several explanations have been proposed, the mechanism has not been elucidated.

 Degenerative Changes

Degenerative changes of the intervertebral discs cause disc-space narrowing, osteophyte formation, and sclerosis of the vertebral body end plates (Figure 4). These changes are easily seen on lateral roentgenograms but are the response of the vertebrae to disc degeneration and so appear after the process is well developed. Therefore, any study based on plain roentgenograms underestimates the prevalence of disc degeneration. Degenerative changes in the zygapophyseal joints include joint-space narrowing, sclerosis, and osteophyte formation; but the changes are not as easily seen or quantified on plain roentgenograms (Figure 5). The joints are paired and located behind the vertebral bodies, so they can only be isolated by oblique views; and even then, one oblique view usually does not show all the joints. For these reasons, little information is available on the frequency of degenerative changes in these joints.

Plain lateral roentgenogram showing end-plate sclerosis, narrowing of the intervertebral disc space, and anterior osteophyte formation.

 5. (click image to zoom) Plain lateral roentgenogram showing sclerosis, narrowing, and osteophyte formation in the C3-4 zygapophyseal joint.                                                                

Degenerative changes of the cervical spine, as seen on plain roentgenograms and more sophisticated imaging studies, are common in both symptomatic and asymptomatic people and are thought to be part of the normal aging process (Figure 6). Degenerative findings are considered to be pathologic when they produce symptoms. However, with the exception of patients with radicular pain, localizing neurologic deficits, and nerve root compression as seen on MRI or CT myelogram studies, the relationship with the patient's neck pain is unclear.


Figure 6. (click image to zoom) A. Normal, plain lateral roentgenogram of 44-year-old, asymptomatic female. B. Plain lateral roentgenogram of 54-year-old female, indicating degenerative changes of zygapophyseal joints most severe at C4-5 and intervertebral disc degenerative changes at C6-7.                                                                                                     

One of the most perplexing clinical challenges is to distinguish the source of a patient's pain when degenerative changes are present. In a review of 200 asymptomatic women, we found that by age 60 to 65, 95% and 70% of women had degenerative changes as seen on plain roentgenograms.[18] Boden found MRI abnormalities of the cervical spine in 19% of 63 asymptomatic volunteers. Fourteen percent occurred in subjects under the age of 40, and 28% in those over 40.[19] Zapletal and colleagues[20] evaluated the atlanto-odontoid joint in 500 consecutive patients who underwent computed tomography of the brain or paranasal sinuses. They found no abnormalities before the fourth decade but thereafter the prevalence increased steadily with age, so that by the ninth decade over 60% had degenerative changes. In a separate article, Zapletal and associates[21] evaluated 355 occipital frontal radiographs of the paranasal sinuses for evidence of osteoarthritis of the lateral C1-C2 joints. Degenerative changes were found ranging from 5.4% in the sixth decade to 18.2% in the ninth. They emphasize that these degenerative changes could be a source of upper neck pain and occipital headaches (Figure 7).

 Plain open-mouth roentgenogram showing unilateral degenerative changes at C1-2.                 


In 1982, Rothman[22] stated, "It does not appear that cervical disc degeneration is a brief self-limited disorder but rather a chronic disease productive of significant pain and incapacity over an extended period of time."

As discussed in the previous sections, degenerative disease of the cervical spine and neck pain are not synonymous. Degenerative changes are often present in asymptomatic people, and in some people with neck pain no structural abnormality can be demonstrated. However, in our experience, Rothman's statement holds true for patients with neck pain with or without degenerative changes.

In 1987, we reported on a review of 205 patients initially seen for neck pain in an office setting.[23] Patients with previous neck surgery, objective neurologic deficits, malignancies, or rheumatoid arthritis were excluded. The patients were re-examined and interviewed an average of 15 years (10 to 25 years) after the onset of their neck problems. In all patients, lateral roentgenograms were available for comparison between the initial visit and the final evaluation.

At follow-up, 79% had a decrease in pain, and of these, 43% were pain-free; however 32% had moderate or severe residual pain. Patients who had been injured and initially had severe pain were most likely to have an unsatisfactory outcome; however, no other clinical features were of value in predicting the final result. Initially, 121 patients had injuries, of which 76 were due to motor vehicle accidents. Sixty-eight were involved in litigation, 58 in personal injury claims, and 10 in workman's compensation claims. At final evaluation, all but 4 claims had been settled, and all of these patients stated their initial pain had decreased in severity. Interestingly, 23 patients were dissatisfied with the outcome of their litigation. However, there was no statistical relationship between their level of satisfaction and the amount of pain or pain relief reported at final interview.

The roentgenographic features measured were degenerative changes at each intervertebral disc space, sagittal diameters of the spinal canal at each disc space, and cervical lordosis. None of the roentgenographic findings present initially or developed in the follow-up period correlated with pain or had any predictive value for pain relief.

Most important, this study emphasizes that neck pain is frequently not a self-limited problem, and that many patients will have long-term symptoms that may be moderately disabling.

Summary Neck pain is a common problem in our society and at any given time affects about 10% of the general population. The actual cause of the problem is frequently difficult to determine. Neck pain in as many as one-third of patients is not self-limiting and may produce moderate long-term disabilities.




It is important to note that extensive research has been performed on low impact accidents, and how injuries result to occupants from these accidents.  One such research project was performed by The National Highway Traffic Safety Administration, published by E. Horton, "Why Don't We Buckle Up," Science Digest, Feb. 1985, in which they state, "a ten-mile an hour collision is equivalent to catching a two-hundred pound bag of cement dropped from a second story window.  People don't understand the dynamics of crashes!"  Extrapolate this evidence to a non low impact collision and the potential effects become even more dramatic.


Another research study done by The Engineering Society For Advancing Mobility Land Sea Air and Space, at the University of Texas Health Science Center, page 28, concluded that in rear-end accidents of 2.5 mph, "Despite having experienced no neck excursions beyond their voluntary range limits, three of our four subjects transiently had very mild, but clinical neck discomfort symptoms."  This occurred in healthy individuals that were prepared for a read-end collision of 2.5 mph!  The research was completed in 1993 and published in the SAE Technical Paper Series in March 1-5, 1993 issue. 


Historically, insurance company claims adjusters have assumed that collision injuries correlate to the vehicle external structural damage and the cost of repair of the vehicle. The assumption that injuries relate to the amount of external vehicle damage is in all types of crashes has no scientific basis. (Nordhoff and Emori 1996).


The absence or presence of vehicle damage is not a reliable indicator of injury potential in rear end impacts. Based upon the principle of conservation of energy, any energy, which does not go into damaging the vehicle, must be converted into kinetic energy, which is the source of patient/occupant injury (Smith)


Because of the very large mass of motor vehicles, even the smallest speed collisions generate significant kinetic energy. The kinetic energy is transferred into the struck vehicle. (Kinetic Energy of the striking vehicle is equal to the Kinetic Energy after impact plus the vehicle damage- Newton's 3-rd law of mechanics) The physical facts dictate that the magnitude of passenger injury can not be totally correlated with vehicle damage. In fact, the smaller the vehicle damage the greater the kinetic energy available to cause and injury! This effect is especially relevant in low speed, rear impact collisions (Navin and Romilly, Smith, Nordhoff and Emori).


The development of safety or "no damage" bumpers has been the standard for the last few decades. They are designed specifically to minimize vehicle damage in low impact collisions, and there is clear evidence that insurance property losses have decreased dramatically as a result (Smith). Unfortunately, when vehicle damage energy is reduced, the energy is transferred into kinetic energy that causes patient injury. Current bumper standards have the effect of reducing property damage while subjecting the occupants to a more violent ride and increasing the probability occupant injury. (Navin, Smith). Published experts (Navin and Rommily) in motor vehicle accidents have completed experiments and made observations that degree of patient/passenger injury is not related to the size, speed, or magnitude of damage of the involved vehicles.


The cervical spine is especially vulnerable to trauma because of the physical dynamics involved in the actual force, as well as the inherent weakness of the cervical spine or manner in which the injury occurred. Even a slight impact can produce a large number of pounds of force on the head and neck. For example, a 3500 lb. automobile traveling a mere 10 miles per hour would strike an immovable car with some 25 tons of force. This force on the patients cervical spine is magnified because the base of the neck acts as a fulcrum and the actual neck itself is a lever which propels the head and neck backwards, forwards and side to side.


The cervical spine is the weakest area of the spine and also the most mobile. The bones of the neck are the smallest in the spine, and comprised of over 30 small joints. Each joint about the size of an adult human's smallest finger. Because of the small size and greater mobility, there is greater potential for injury. Adding to the neck's weakness is the fact that the cervical spine is perched on top of a relatively immobile thoracic spine. This situation makes the base of the neck a fulcrum. Much like a bamboo stick, stuck in the ground. If the stick is forced backward, forward, left or right, it will break where it is inserted in the ground. The cervical spine also contains the smallest shock-absorbing disk in the spine, especially between the second and third vertebrae. The cervical spine serves as a support and foundation to the head, which weights from 8-12 lbs. The head is therefore supported on an unstable platform, much like a house being built on quicksand.


In summary:


Motor vehicle collision patient/passenger injury and clinical prognosis for recovery, is not related to the damage of their vehicle. Rather, injury and prognosis are coupled with direction of impact (rear end, awareness, and head/neck rotation or inclination).