Cervical Sprain and Strain

Updated: Apr 09, 2021
Author: Michael D Freeman, MedDr, PhD, MScFMS, MPH, MFFLM, DLM, FACE; Chief Editor: Consuelo T Lorenzo, MD 


Practice Essentials

Cervical strain is one of the most common musculoskeletal problems encountered by generalists and neuromusculoskeletal specialists in the clinical setting. The predominant cause of cervical strain injury is traffic crashes, which produce indirect trauma to the neck via acceleration-deceleration, a mechanism in which there is a back and forth whipping motion of the head. The term "whiplash" is used generically to denote both the injury mechanism that produces neck injury in crashes, as well as the injury itself. Radiography is useful in the evaluation of cervical sprain and strain. Early rehabilitation helps to prevent chronic pain and disability.

Normal and straightened lordotic lateral cervical curves are shown in the images below.

Radiograph of the lateral cervical spine shows a n Radiograph of the lateral cervical spine shows a normal lordotic curve.
Radiograph of the lateral cervical spine shows str Radiograph of the lateral cervical spine shows straightening of the lordotic curve.

Neck injury following whiplash trauma is the most common musculoskeletal injury seen in traffic crashes, and yet it is one of the more poorly understood disorders of the spine. One reason for this contradiction is the lack of correlation between the severity of the crash and the nature of the resulting clinical problems,[1]  and another is the surprisingly high prevalence of chronic pain that results from such injuries, as demonstrated by dozens of prognostic studies.[2] There are a multitude of factors that contribute to a poor outcome; some relate to the fragility of the patient (ie, a history of neck injury is a significant risk factor for chronic neck pain after acute injury),[3]  some relate to patient factors at the time of the crash (ie, a rotated head position at the time of the crash can increase the strain on the facet capsules, resulting in increased injury risk),[4]  and some relate to the vehicle environment (ie, poor head restraint geometry increases injury risk).[5]

While some authors have attempted to classify whiplash injuries by ranked categorization of neck-related symptoms,[6]  since the early 2000s, a more sophisticated understanding of the biomechanics, pathology, and neurologic mechanisms of whiplash injuries has revealed a complex syndromic condition that defies such simple descriptions.[7, 8]

Signs and symptoms

The most common symptoms of cervical disorders are suboccipital cervicogenic headache and/or ongoing or motion-induced neck pain. Other signs and symptoms associated with cervical strain include the following:

  • Neck pain
  • Headache
  • Shoulder, scapular, and/or arm pain
  • Visual disturbances (eg, blurred vision, diplopia)
  • Tinnitus
  • Dizziness
  • Concussion
  • Neurologic symptoms
  • Difficulty sleeping due to pain
  • Disturbed concentration and memory

Workup in cervical sprain and strain

Radiography is useful in the evaluation of cervical sprain and strain. Only lateral views are needed for the initial screening of stability. Three views are obtained for the basic evaluation: anteroposterior (AP), lateral, and odontoid. Five views, including the three basic views plus bilateral oblique views, are used to evaluate the intervertebral foramen.

Overall, magnetic resonance imaging (MRI) is the best noninvasive and detailed imaging study for evaluating the status of the discs and spinal cord.

Computed tomography (CT) scanning may be performed if detailed bony imaging is indicated, such as when a fracture or instability is a concern.

Electrodiagnostic studies may show nerve injury, while electromyographic studies can be used to determine if radiculopathy is a factor in the patient's symptoms.

Nerve conduction studies (NCSs) are indicated if concomitant peripheral nerve involvement is suspected and needs to be evaluated.


Passive modalities in physical therapy for cervical sprain and strain include the application of heat, ice, electrical stimulation, massage, myofascial release, and cervical traction.

Active treatment involves therapeutic exercises that are aimed at improving the patient's strength, endurance, flexibility, posture, and body mechanics.

Specific neck exercises for the management of chronic neck pain, including active activation of the deep neck muscles and dynamic strengthening, may significantly improve disability scores.[9]

Occupational therapy may be indicated unless a concurrent problem involves a distal upper-extremity function or ergonomic factors in causation.

Cervical myeloradiculopathy or instability, a possible complication of cervical strain, may require surgical intervention (eg, discectomy/fusion).

Severe sprains of the cervical spine may result in a traumatic rupture of the intervertebral disc and ligaments, which, if not surgically treated, can lead to a significant kyphotic deformity.[10]


Relevant anatomy and physiology

Consistent with known biologic models, injuries to bony, articular (discs and facets), nerve (including root and spinal cord), and soft (ligament, tendon, muscle) tissues of the cervical spine are the most likely sources of dysfunction and pain. Cervical strain is produced by an overload injury to the muscle-tendon unit because of excessive forces on the cervical spine. The cause is thought to be the elongation and tearing of muscles or ligaments. Secondary edema, hemorrhage, and inflammation may occur. 

A major advance in the understanding of chronic pain following whiplash injury over the past two decades has been the discovery that central sensitization plays an important role in symptom perpetuation.[11] There is strong evidence that central sensitization starts shortly after the acute injury and that chronically tender points play a role in mediating the severity of symptoms.[12]

Many cervical muscles do not terminate in tendons but attach directly to the periosteum. Muscles respond to injury by contracting, with surrounding muscles recruited in an attempt to splint the injured muscle. Myofascial pain syndrome, which is thought to be the resultant clinical picture, may be a secondary tissue response to disc or facet-joint injury.

Facet capsular ligaments have been shown to contain free (nociceptive) nerve endings, and distending these ligaments by administering facet joint injections has produced whiplash-like pain patterns in healthy individuals. The cervical facet capsular ligaments may be injured under whiplashlike loads of combined shear, bending, and compression forces; this mechanism provides a mechanical basis for injury caused by whiplash loading.[13]

Chronic pain associated with cervical strains is most likely to affect the zygapophysial (facet) joints, intervertebral discs, and upper cervical ligaments. The C2-3 facet joint is the most common source of referred pain in patients with a dominant complaint of occipital headache (60%). The C5-6 region is the most common source of cervical, axial, and referred arm pain. Cervical facet joint pain is typically a unilateral, dull, and aching neck pain with occasional referral into the occiput or interscapular regions. The cervical facet joints can be responsible for a substantial portion of chronic neck pain. The cervical facet joints refer pain overlapping with both myofascial and discogenic pain patterns.

Neuroanatomic studies reveal that the facet joint is richly innervated and contains free and encapsulated nerve endings. The facet capsule is richly innervated with C fibers and A-delta fibers. Many of these nerves are at a high threshold and likely to indicate pain. Local pressure and capsular stretch can mechanically activate these nerves. These neurons can be sensitized or excited by naturally occurring inflammatory agents, including substance P and phospholipase A.[14]

Cervical extensor muscle function was studied in 15 individuals using muscle functional magnetic resonance imaging (mfMRI) during neck exercises, with and without experimentally induced pain. Function of the cervical extensor muscles was recorded at rest and after the performance of a cervical extension exercise. The authors reported instantaneous decrease in function of the deep and superficial cervical extensor muscle layers following a saline injection into the upper trapezius muscle. The authors conclude that early evaluation of cervical extensor muscle function is appropriate for patients with painful cervical spine injuries.[15]

Physiologic changes in the spinal cord, particularly the pain complexes of the dorsal horn, implicate excitatory amino acids, such as substance P, glutamate, gamma-aminobutyric acid (GABA), and N -methyl-D-aspartate (NMDA), as well as other factors that sensitize the dorsal horn in chronic pain. The mechanism is massive input of noxious stimuli from cervical spine injury.[16]

In lumbar spine studies, inflammatory cytokines are found at high levels in facet joint tissue when a degenerative disorder is present. Facet joints are covered by hyaline cartilage and enclosed with synovium and joint capsules. This basic structure is found throughout the spine and in the joints of the arms and the legs.[17]

According to Bogduk, results of postmortem studies, biomechanical studies, and clinical studies converge to suggest that the zygapophysial joints are injured in cases of whiplash. Clinical studies have shown that pain in the zygapophysial joint is common in patients with chronic neck pain after whiplash injury.[18] Injury was sustained to cervical facet capsular ligaments as a result of the combined shear, bending, and compression load levels that occur in rear-end impacts.[19]

An overload injury to the muscle-tendon unit produces cervical strain because of excessive forces on the cervical spine. This injury is accompanied by elongation and tearing of muscles or ligaments, secondary edema, hemorrhage, and inflammation. Many cervical muscles attach directly to bone (periosteum), and the muscle response to injury is contraction, with surrounding muscles recruited to splint the injured muscle.

Classic mechanism of whiplash injury

A collision in any direction can cause chronic whiplash.[20]

In a clinical review, Barnsley and colleagues described the classic whiplash scenario in which the patient's car has been struck from the rear.[21] This type of crash typically occurs in the following manner:

  • At the time of impact, the vehicle suddenly accelerates forward. About 100 ms later, the patient's trunk and shoulders follow, induced by a similar acceleration of the car seat.

  • The patient's head, with no force acting on it, remains static in space. The result is forced extension of the neck, as the shoulders travel anteriorly under the head. With this extension, the inertia of the head is overcome, and the head accelerates forward.

  • The neck then acts as a lever to increase forward acceleration of the head, forcing the neck into flexion.

Frontal impact causes middle C2-3 to C4-5 and lower C6-7 and C7-T1 injury.[22] Direct facial impact has shown a flexion motion of the upper or middle cervical spine, with extension of the lower cervical spine.[23]

The forces involved in a rear-impact collision of only 5-10 mph (8-16 km/h) can result in peak head accelerations of more than 15 G, sufficient to result in angular accelerations associated with concussion.[24] If the head is in slight rotation, a rear impact forces the head into further rotation before extension, prestressing various cervical structures, such as the capsules of the zygapophysial joints, intervertebral discs, and the alar ligament complex. These structures are thus rendered susceptible to injury. Muscle injury may be less likely after low-velocity impacts with head rotation at the time of impact than they are in other mechanisms.[25, 26, 27, 28, 29]

When a rear impact is offset to the subject's left, it not only results in increased electromyographic activity in both sternocleidomastoids, it also the causes the splenius capitis contralateral to the direction of impact to bear part of the force, thus causing injury. Which muscle responds most to a whiplash-type injury is determined by the direction of head rotation. The sternocleidomastoid on the right responds most with the head rotated to the left, and vice versa. Measures to prevent whiplash injury need to account for the symmetric muscle response caused by victims looking to the right or left at the time of collision.

Lower cervical facet joints respond with a shear plus distraction mechanism in the front and shear plus compression in the back. In studies, females were more likely to be injured than were males, possibly owing to sex-related genetic, hormonal, structural, or tolerance differences.[30]

Head-turned rear impact also causes significantly greater injury at C0-1 and C5-6 as compared with head-forward rear and frontal impacts. Multiplanar injury that occurs at C5-6 and C6-7 has also been found to occur with head-turned impact.[31] Head-turned rear impacts up to 8 G do not typically injure the alar, transverse, and apical ligaments.[32]

Head-turned impact also causes dynamic cervical intervertebral narrowing, indicating potential ganglion compression even in patients with a nonstenotic foramen at C5-6 and C6-7. In patients with a stenotic foramen, the risk greatly increases to include C3-4 through C6-7.[33]

A rear-end collision is most likely to injure the lower cervical spine, with intervertebral hyperextension at a peak vehicle acceleration of 5 G and above.[34, 35] The first substantial increase in intervertebral flexibility occurs at C56 following 5-G acceleration. At accelerations faster than this, the injuries spread to the surrounding levels (C4-5 to C4-T1). The 2 injury phases during whiplash are (1) hyperextension at C5-6 and C6-7 and mild flexion at C0-4 and (2) hyperextension of the entire cervical spine.[36]

An instantaneous change occurs in the pivot point at C5-6, causing a jamming effect of the inferior facet of C5 on the superior facet of C6.[16] The nonphysiologic kinematic responses that occur during a whiplash impact may induce stresses in upper cervical neural structures or in lower facet joints. The result may be compromise sufficient to elicit neuropathic or nociceptive pain.[37]

The muscular component of the head-neck complex plays a central role in the abatement of higher acceleration levels; it may be a primary site of injury in the whiplash phenomenon. Muscle responses are greater with faster accelerations than with slower ones.[38] Cervical muscle strains induced during a rear-end impact are greater than the injury threshold that had previously been reported for a single stretch of active muscle, with larger strains in the extensor muscles being consistent with clinical reports of pain in the posterior cervical region after the occurrence of a rear-end impact.[39]

The risk of whiplash injury in motor vehicle collisions increases when subjects are surprised and unprepared for the impact.[40]

One of the most important studies of cervical spine injury is of a case series of roller coaster injuries. The roller coaster studies have shown, over approximately 100 ms, a peak of 4.5-5 G of vertical or axial acceleration and 1.5 G of lateral acceleration. During the 19-month study period, 656 neck and back injuries were studied. The injuries included disc herniations, bulges, and compression fractures. The results of the study suggested that a minimum threshold of significant spine injury is not established. The greatest explanation for injury from traumatic loading of the spine was thought to be individual susceptibility to injury, which is an unpredictable variable.[41]


Cervical myeloradiculopathy is a complication of flexion/extension injuries in patients with underlying spondylosis. Cervical discs may become painful as part of the degenerative process, because of repetitive microtrauma or a single excessive load. Pain due to a disc injury may result from annular tears with inflammation or compression of the local nervous or vascular tissue.

Spinal cord compression after whiplash due to physiologic extension loading is not likely. However, individuals with a narrow spinal canal, most commonly due to degenerative spinal stenosis, have an increased risk of quadriparesis secondary to the spinal cord compression.[35]

Postmortem studies have shown that ligamentous injuries are common after whiplash injuries, but disc herniation is a rare event.[42]

In one study, 33% of patients with whiplash injury had disc herniations with medullary or dura impingement over 2-year follow-up after injury.[43]

In another study, whiplash-type distortions were associated with a 16% incidence of discoligamentous injuries. On magnetic resonance imaging (MRI), most patients with severe, persisting, radiating pain had large disc protrusions that were confirmed as herniations at surgery. Neck and radiating pain were alleviated with early disc excision and fusion.[44]

Strain or tears of the anterior annulus and the alar portions of the posterior longitudinal ligament (when stretched by a bulging disc) are possible causes for discogenic pain after whiplash injury. Injuries of the zygapophysial joint found in clinical and cadaveric studies include fracture, bleeding, rupture or tear of the joint capsule, fracture of the subchondral plate, contusion of the intra-articular meniscus, and fracture of the articular surface.[45]

Upper cervical disc protrusions as a result of cervical strain injury may result in nonspecific and shoulder pain. Motor weakness or reflex or sensory abnormalities may be limited or nonspecific. Cervical radiculopathy is more likely than are pathologic signs of upper motor neuron or spinal cord myelopathy.

MRI or computed tomography (CT) myelography are necessary for the diagnosis.[46]



United States

Almost 85% of all neck pain is thought to result from acute or repetitive neck injuries or from chronic stresses and strain. Dreyer and Boden showed that, in the general population, the 1-year prevalence of neck and shoulder pain is 16-18%.[47]

Estimates indicate that more than 1 million whiplash injuries occur each year due to automobile accidents. Barnsley and colleagues estimated that the annual incidence of symptoms due to whiplash injury is 3.8 cases per 1000 population.[45] Freeman and co-investigators cautiously estimated that 6.2% of the US population, or 15.5 million individuals, have late whiplash syndrome.[48]


The annual incidence in Switzerland is 0.44 cases per 1000 population. In Norway, a rate of 2 cases per 1000 population has been reported. The approximate annual incidence in Western countries is 1 case per 1000 population.

A study by Kumagai et all of 1140 members of a community in Japan found that 7.7% and 9.6% of men and women, respectively, had experienced whiplash injury.[49]


Mortality is rare unless severe trauma causes the cervical strain, with associated brain or spinal cord trauma, respiratory compromise, or vascular injury.

Morbidity includes cervical pain syndromes with associated symptoms. Disability in acute or chronic cervical strains is responsible for significant socioeconomic costs.

Low-energy collisions occurring at less than 6-9 mph (9.7-14.5 km/h) are thought to be unlikely to produce significant neck trauma.


Chronic neck pain, regardless of its cause, is identified in 9.5% of men and in 13.5% of women.


On average, patients with a whiplash injury are in their late fourth decade.




The most common symptoms of cervical disorders are suboccipital cervicogenic headache and/or ongoing or motion-induced neck pain. Other signs and symptoms associated with cervical strain include the following:

  • Neck pain

    • At the time of accident, neck pain may be minimal, with an onset of symptoms occurring during the subsequent 12-72 hours.

    • Nonspecific neck and shoulder pain (a variety of cervical radiculopathies) may indicate an injury to a disc in the upper cervical spine.[46]

  • Headache

    • Headache is a frequent symptom of cervical strain.[50]

    • Neck structures play a role in the pathophysiology of some headaches, but the clinical patterns have not been defined adequately.

    • Increased muscle hardness (determined by palpation) is significantly increased in patients with chronic tension-type headaches.

    • Facet joints and intervertebral disc damage have been implicated in the pathology of headaches due to neck injury.[16]

    • No specific pathology on imaging or diagnostic studies has been correlated with cervicogenic headaches.

  • Shoulder, scapular, and/or arm pain

  • Visual disturbances (eg, blurred vision, diplopia)

  • Tinnitus

  • Dizziness - This may result from injury to facet joints that are supplied with proprioceptive fibers; when injured, these fibers can cause confused vestibular and visual input to the brain.[16]

  • Concussion

  • Neurologic symptoms - These may include weakness or heaviness in the arms, numbness, and paresthesia.

  • Difficulty sleeping due to pain

  • Disturbed concentration and memory

    • Late whiplash syndrome includes symptoms such as headache, vertigo, disturbances in concentration and memory, difficulty swallowing, and impaired vision. These cognitive impairments remain poorly understood.

    • Many patients with these changes have abnormal results on single-photon emission CT (SPECT) scans or P300 event-related potentials.[51]

    • Bladder or bowel dysfunction - These may be symptoms of complication of myelopathy (spinal cord involvement).


The physical examination is a vital part of the diagnosis of cervical stress and strain injuries. Various signs and symptoms may be noted during the physical examination. Observation of the patient's general appearance may yield information about pain behavior, verbal or nonverbal.

Spinal examination

During the postural assessment, the clinician may note the following findings: stiffness of the neck, forward head, flexed neck, rounded shoulders, asymmetry of the neck or shoulders, neck tilt or rotation, and one shoulder higher or tighter than the other.

Palpation may reveal rigidity (loss of motion or postural abnormality), spasm tightness, muscle hardness, crepitation, swelling, enlargement of joints, tenderness, tender points, and trigger points.[52, 53] Palpation of the zygapophysial joints may be helpful in determining the painful joints, because of osteoarthritis or posttraumatic irritation of the joint capsule. Painful cervical facet joint – loading maneuvers confirm the clinical diagnosis of cervical facet syndrome following a whiplash injury.

Decreased active and passive ROM may be noted. Impaired cervical ROM (particularly in the sagittal plane) is useful in distinguishing between asymptomatic persons and those with persistent whiplash-associated disorders.[54] Special methodology for measuring cervical ROM compared healthy persons with individuals suffering from chronic whiplash. Using mean coefficient of variation (MCV) and total cervical range of motion (TCROM), the TCROM was significantly lower and the MCV was significantly higher in injured patients as compared with healthy individuals.[55]

After acute whiplash injury, neck mobility is significantly reduced. After 3 months, however, mobility has been found to be similar between control subjects and patients with whiplash injury.[56]

Cervical neurocompression by way of cervical extension may cause parascapular or arm pain by narrowing the neural foramen (causing nerve root compression) or by causing pressure on the facet joints.

Neurologic examination

This includes the following:

  • Mental status: Mood disturbance, such as anxiety or depressive affect, may be noted

  • Motor function: If cervical radiculopathy is present, the strength or bulk of the involved upper extremity may be decreased in a myotomal distribution; if myelopathy is present, weakness of upper and lower extremities may be noted

  • Circumference: The dominant arm and forearm are usually slightly larger than are those of the nondominant side

  • Reflexes in cervical radiculopathy: In cervical radiculopathy, muscle stretch reflexes (MSRs) may be decreased in a myotomal pattern in the affected upper limb; however, they should remain normal in the lower limbs

  • Reflexes in cervical myelopathy: In cervical myelopathy (cervical spinal cord involvement), the MSRs arising from a given level of the cord may be decreased in the upper limbs; however, MSRs in the lower limbs may be increased, with spasticity of the lower extremities, a positive Babinski sign, and a positive Hoffman sign

  • Sensation: If cervical radiculopathy is present, pain or 2-point discrimination of light touch may be reduced in a radicular dermatomal pattern in the involved upper extremity

  • Coordination: With radiculopathy or myelopathy, coordination may be decreased in the involved upper extremity

  • Gait: In cases of cervical myelopathy, the patient's gait pattern may be abnormal as a result of spasticity; the presence of spasticity implies an upper motor neuron dysfunction, in contrast with injury to the peripheral nerves

  • Provocative maneuvers: The Spurling test uses cervical extension and lateral bending while the examiner applies a downward axial load; this test may provoke (reduce) radicular symptoms in a patient with cervical radiculopathy


Common traumatic events or factors that may lead to cervical strain/sprain injuries include motor vehicle accidents, lifting or pulling heavy objects, awkward sleeping positions, unusual upper-extremity work, and prolonged static positions.

Flexion/extension injuries may precipitate a myeloradiculopathic presentation in a patient with cervical spondylosis. Nerve root or spinal cord compression may occur from neural ischemia due to the preexisting stenosis that accompanies cervical spondylosis. Flexion/extension injuries, blows to the head, or neck injury while lifting heavy objects may precipitate an acute exacerbation of cervical spondylosis.

Repetitive or abnormal postures may contribute to cervical sprains and strains.

In a study by Giannoudis and colleagues, no dose-response association between the magnitude of trauma severity and the incidence of whiplash injury was found.[57]



Diagnostic Considerations

These include the following:

  • Cervical herniated disc

  • Cervical myelopathy

  • Cervical osteoarthritis

  • Infection or osteomyelitis

  • Inflammatory rheumatologic disease

  • Malingering

  • Psychogenic pain disorder

  • Referred pain from cardiothoracic structures

  • Tumor or malignancy of cervical spine

  • Vascular abnormality of cervical structures

Differential Diagnoses



Laboratory Studies

See the list below:

  • Complete blood count (CBC) with differential, if infection or tumor is a concern

  • An arthritis profile, including a determination of the erythrocyte sedimentation rate (ESR), if inflammatory arthritis or polymyalgia rheumatica is suggested

Imaging Studies

See the list below:

  • Although not pathognomonic for sprain/strain, imaging results are important for excluding other diagnoses and more extensive injuries.

    • Motor vehicle crashes causing fatalities may also result in occult pathoanatomic lesions in the cervical intervertebral disc and zygapophysial joints. Present imaging methods do not depict these subtle lesions; hence, underreporting of pathoanatomic lesions during standard autopsy is probably common.

    • These findings may have clinical relevance in the management of road traffic trauma survivors with potentially similar pathoanatomy.[58]

  • Radiography is useful in the evaluation of cervical sprain and strain.

    • Only lateral views are needed for the initial screening of stability. Three views are obtained for the basic evaluation: anteroposterior (AP), lateral, and odontoid. Five views, including the 3 basic views plus bilateral oblique views, are used to evaluate the intervertebral foramen.

    • Flexion/extension views may be obtained if instability is suggested. Hypermobility in the lower cervical segments in 12 out of 34 patients with chronic whiplash-associated disorders were identified by a new measurement protocol determining rotational and translational motions of segments C3-4 and C5-6.[59]

    • Order radiographic studies early in any of the following cases: when significant trauma, pain, or dysfunction develops; when a chronic condition develops; or when documentation of the patient's condition is required (in instances when litigation is anticipated).

    • Radiographs of the lateral cervical spine may show straightening or reversal of the normal lordotic curve (see images below). This finding is thought to represent spasm, guarding, or splinting of the muscles that stabilize the neck. Although these findings may be seen in as many as 20% of healthy control subjects, the rates are higher in the injured population .

      Radiograph of the lateral cervical spine shows a n Radiograph of the lateral cervical spine shows a normal lordotic curve.
      Radiograph of the lateral cervical spine shows str Radiograph of the lateral cervical spine shows straightening of the lordotic curve.
  • Overall, MRI is the best noninvasive and detailed imaging study for evaluating the status of the discs and spinal cord.

    • Order MRI if detailed analysis of spinal structures (eg, spinal cord, disc) is indicated, as in, for example, an evaluation for underlying herniated nucleus pulposus (HNP).

    • A relative number of abnormal findings on cervical spine MRI scans can be found in asymptomatic individuals. According to Matsumoto and colleagues, the most common findings involve disc degeneration, but nearly 10% of patients can have asymptomatic spinal cord compression.[60]

    • Lateral disc protrusions (see image below) are rarely found in asymptomatic patients, who usually present with concordant radiculopathy.

      MRI of the cervical spine shows disc protrusion. MRI of the cervical spine shows disc protrusion.
    • Extruded discs are not seen in asymptomatic patients. When seen in the cervical spine, they are almost invariably associated with the patient's symptoms.

    • A clearly defined extrusion, when arising from a normally hydrated disc with no osseous ridging and when compressing an appropriate nerve root concordant with the patient's symptoms, can be considered with confidence to be acute or subacute.

    • MRI is indicated in patients with persistent arm pain, neurologic deficits, or clinical signs of nerve root compression.

    • MRI is unable to reliably depict sources of cervical discogenic pain, because significant annular tears often escape MRI detection.[16]

  • CT scanning may be performed if detailed bony imaging is indicated, such as when a fracture or instability is a concern. CT scanning may be used as an alternative to MRI in patients with claustrophobia, although disc imaging with CT scanning offers low resolution.

  • CT myelography is an invasive imaging study that may be useful for a detailed analysis if plain CT scanning and MRI do not provide a definitive answer regarding the suspected pathology.

    • The degree of concordance between CT myelography and MRI is only moderately good; discrepancies are noted especially in the differentiation of disc and bony pathology.

    • A disadvantage is that lumbar puncture is required.

  • Bone scanning is indicated if a spinal tumor, infection, or occult fracture is suggested.

  • Videofluoroscopy is a controversial study used to evaluate increased, decreased, or abnormal segmental movement of the cervical spine.

    • In a study by Hino and colleagues, motion patterns were different between normal spines and pathologic spines.[61]

    • Cineradiography allows the identification of soft-tissue injuries and early subluxations of the cervical spine that may not be identified with static radiography or physical examination.[62]

  • Discography is used in the presurgical evaluation, to identify the level on which to operate. Significant tears are often missed with MRI, but provocative discography can reveal a discogenic source of cervical pain. Although MRI can identify most of the painful discs, it has relatively high false-negative and false-positive rates. Discography can direct a surgeon in making critical management decisions.[63]

Other Tests

See the list below:

  • Electrodiagnostic studies

    • These physiologic studies may show nerve injury (as opposed to imaging studies, which may show only structural injury).

    • These studies should be performed and interpreted by an appropriately trained and board certified electromyographer. The American Association of Neuromuscular and Electrodiagnostic Medicine (formerly the American Association of Electrodiagnostic Medicine) is the certifying board.

  • Electromyography (EMG)

    • Electromyographic studies can be used to determine if radiculopathy is a factor in the patient's symptoms.

    • EMG is usually performed after 1-2 weeks (or longer), when the physiologic changes are first found.

    • In patients with acute radiculopathy, electromyographic findings include increased insertional activity, fibrillation potentials, positive sharp waves, and complex repetitive discharges.

    • Chronic radiculopathy findings are noted after approximately 3 months of nerve root involvement; they include polyphasic or broad-duration/large-amplitude motor units, drop out of motor units, decreased recruitment, and an incomplete interference pattern.

    • Findings in the posterior primary division of the nerve root are noted in the cervical paraspinous muscles.

    • The anterior primary division of the nerve root findings is noted in the specific root-innervated muscles (myotome) of the upper extremity.

    • The accessory spinal nerve innervates the trapezius muscle, which is often a source of chronic neck pain due to spasm. Contribution from the C2-C4 motor roots is minimal and inconsistent. Electromyographic recordings from the trapezius muscle can show dysfunction of the spinal motor nerve root.[64]

    • When electromyographic findings of radiculopathy are interpreted, the duration of the symptoms should not influence the diagnosis.[65]

  • Nerve conduction studies

    • In some cases, a nerve conduction study (NCS) may be performed by an appropriately trained and supervised technician.

    • These tests should be interpreted by a board certified electrodiagnostic medicine specialist only with the entire clinical picture in mind.

    • An NCS is indicated if concomitant peripheral nerve involvement is suspected and needs to be evaluated. The study would be performed, for example, when numbness of the radial aspect of the upper extremity is a symptom or when carpal tunnel syndrome versus C6 radiculopathy needs to be identified.



Rehabilitation Program

Physical Therapy

Early rehabilitation helps to prevent chronic pain and disability. Passive modalities include the application of heat, ice, electrical stimulation, massage, myofascial release, and cervical traction. Passive modalities are often used to decrease pain or inflammation and to facilitate participation in an active rehabilitation program, which often involves stretching and strengthening. Extended use of passive modalities without a more active program is generally inappropriate.

Active treatment refers to therapeutic exercises that are aimed at improving the patient's strength, endurance, flexibility, posture, and body mechanics. The goal is to obtain an independent home program or community fitness program at the conclusion of formal physical therapy. The typical therapy prescription is recommended 3 times per week for 4-8 weeks.

Scientific evidence for the physiotherapeutic management of whiplash is sparse. An early, active strategy is recommended to improve functions, increase activity, and prevent chronicity.[66] In patients with whiplash-associated disorders caused by a motor vehicle collision, treatment with frequently repeated active submaximal movements combined with mechanical diagnosis and therapy is more effective in reducing pain than is a standard program of initial rest, use of a soft collar, and gradual self-mobilization.[67]

In patients with whiplash-associated disorders, active intervention is more effective than standard intervention in reducing pain intensity and sick leave, as well as in retaining/regaining total range of motion (ROM). Appropriately trained healthcare professionals can start and support active intervention, that is, frequently repeated, active cervical rotation, which can be followed, if needed, by assessment and intervention according to the McKenzie protocol.[68] Strength and endurance training for 12 months are effective for decreasing pain and disability in women with chronic, nonspecific neck pain. Stretching and fitness training are commonly advised for patients with chronic neck pain, but stretching and aerobic exercising alone are less effective than strength training.[69, 70]

Specific neck exercises for the management of chronic neck pain, including active activation of the deep neck muscles and dynamic strengthening, may significantly improve disability scores.[9] Consistent evidence (from 2 randomized, controlled trials) supports mobilization as an effective, noninvasive intervention for acute whiplash-associated disorders.[71, 72]

A study by Treleaven et al suggested that neck-specific exercise led by a physiotherapist, with a behavioral approach included, is more effective in treating dizziness associated with chronic whiplash than either neck-specific physiotherapist-led exercise without a behavioral approach or general physical activity. The study included 140 patients, who were followed up for 12 months.[73]

Using the same types of exercise as in the Treleaven study, Landén et al found that in terms of pain, self-rated functioning and disability, and self-efficacy, in persons with chronic whiplash, neck-specific exercise with or without a behavioral approach was associated with significantly greater improvement than was general physical activity at 1-year follow-up, but not at 2 years. The study included 216 patients.[74]

In examining the costs and consequences of 2 types of intervention after whiplash trauma in automobile crashes, active intervention using physical therapy was found to be less costly and more effective than short-term immobilization using a cervical collar followed by a gradual self-exercise program taught by a leaflet.[75]

Another study questioned the efficacy of therapeutic interventions. The report found that 1 year after whiplash injury, a strategy employing immobilization, "act-as-usual," or mobilization had a similar effect to the other 2 methods in terms of pain prevention, disability, and work capability.[76]

Occupational Therapy

Occupational therapy may be indicated unless a concurrent problem involves a distal upper-extremity function or ergonomic factors in causation. A workstation ergonomic evaluation may be indicated if biomechanical stresses of work activity are factors in the causation or exacerbation of the condition.

The degree of neck pain or dysfunction can be evaluated by using standardized scales. The choice of a scale should be tailored according to the target population and the purpose of evaluation. The Neck Disability Index is useful for evaluating groups of patients, and the Patient Specific Scale is an effective tool for assessing individual patients.[77]

Medical Issues/Complications

See the list below:

  • Pain complaints may escalate during the rehabilitation program.

  • Pain must be treated aggressively and appropriately.

  • Underlying medical conditions may need to be evaluated and treated to facilitate rehabilitation.

  • The goal of therapy is functional rehabilitation and restoration with an emphasis on improving the patient's strength, endurance, and flexibility.

  • When the patient reaches a plateau, as determined by using objective measurements, therapy progresses to an independent home program or a community fitness program.

  • In a Toronto study, early, aggressive treatment of whiplash injury did not promote faster recovery, and a combination of chiropractic and general practitioner care was found to significantly reduce the patient recovery rate.[78]

Surgical Intervention

See the list below:

  • Cervical strain without myeloradiculopathy or instability is not a condition requiring surgical intervention.

  • Cervical myeloradiculopathy or instability, a possible complication of cervical strain, may require surgical intervention (eg, discectomy/fusion).

  • According to Sampath and colleagues, cervical radiculopathy has a better outcome with surgical intervention than with medical treatment. However, in clinical practice, many physicians believe that most patients respond well to nonsurgical treatment.[79]

  • In one study of patients with cervical spondylotic myeloradiculopathy, the short-term effects of surgery (eg, pain, weakness, sensory loss) were superior. However, at 1 year, no significant differences between surgically and nonsurgically treated groups were found.[80]

  • Severe sprains of the cervical spine may result in a traumatic rupture of the intervertebral disc and ligaments, which, if not surgically treated, can lead to a significant kyphotic deformity.[10]


A board-certified electrodiagnostic medicine specialist may be consulted for EMG and/or an NCS if radiculopathy or peripheral nerve involvement (eg, carpal tunnel syndrome) is suspected. For additional information, contact the American Association of Neuromuscular and Electrodiagnostic Medicine (formerly the American Association of Electrodiagnostic Medicine).

Surgical consultation with a neurosurgeon or orthopedic spinal surgeon may be appropriate if surgical intervention is being considered.

Psychological or psychiatric consultation may be indicated if secondary depression, anxiety, or adjustment disorder needs evaluation and treatment.

  • Patients who achieve complete relief from chronic neck pain resolve all of their psychological distress. Patients with persistent neck pain also have persistent anxiety, depression, and other forms of psychological distress.

  • Findings from a study of patients with whiplash-associated disorders suggested that psychosocial problems of these patients are more pronounced than their physical problems. Coping strategies seem to be a significant predictor of psychological well-being.[81]

A functional capacity evaluation (FCE) may be required if objective evaluation of the level of ability/disability needs to be documented for litigation or for determining the patient's readiness to return to work.

The degree of neck pain or dysfunction can be evaluated by using standardized scales. The choice of scale should be tailored according to the target population and the purpose of evaluation. The Neck Disability Index is useful for evaluating groups of patients, and the Patient Specific Scale is effective for assessing individual patients.[77]

Other Treatment

Upon review of several randomized, controlled trials and epidemiologic studies regarding medical and surgical interventions, published since 1993, moderate evidence exists in support of radiofrequency neurotomy. Evidence for steroid injections, botulinum treatments, and cervical discectomy is conflicting or unclear.[71, 72]

In a review of conservative treatments for whiplash, Verhagen concluded that "the current literature is of poor methodological quality and is insufficiently homogeneous to allow the pooling of results. Therefore, clearly effective treatments are not supported at this time for the treatment of acute, subacute or chronic symptoms of whiplash-associated disorders."[82] The clinician is then left with trying to do the right thing for management of whiplash injury in the face of uncertainty in the scientific community.


Injection may be indicated for patients with chronic, persistent neck pain. Injection is indicated for severe neck pain with functional impairment, particularly cervical radiculopathy. An anesthesiologist, interventional physiatrist, neuroradiologist, or other appropriately trained pain specialist may perform the injection. Types of injection include epidural, selective nerve root, or facet block injections.

Intramuscular injections of lidocaine for chronic mechanical neck disorders (MNDs) and intravenous injections of methylprednisolone for acute whiplash are effective (a single trial). Evidence of the effectiveness of epidural injections of methylprednisolone and lidocaine for chronic MND with radicular findings is limited.[83, 84]

Percutaneous radiofrequency neurotomy

Percutaneous radiofrequency neurotomy of medial branch nerve to facet joint is effective for chronic neck pain due to cervical zygapophysial joint pain.

In one study of the efficacy of radiofrequency medial branch neurotomy to treat cervical zygapophysial joint pain from whiplash injury, the potential for secondary gain did not influence the response to treatment.[85]

Using cervical zygapophysial joint pain as a model of chronic pain, investigators studied the effect of percutaneous radiofrequency neurotomy. In all patients who achieved complete pain relief, their preoperative psychological distress also resolved.[86]

Medical branch blocks of the dorsal rami of the spinal nerves supplying the facet joints are recommended by Schofferman and colleagues. If significant relief occurs on 2 occasions, radiofrequency neurotomy is recommended, providing relief for up to 8-12 months.[87]

Botulinum toxin

Whiplash-associated headache pain may be reduced with the injection of botulinum toxin A in cervical trigger points.[88] Moderate evidence has shown that intramuscular injections of BOTOX ® A for chronic MND were no better than saline injections.


Traction may be helpful. A physical therapist can provide a trial of manual and/or mechanical cervical traction within the clinic. If patients achieve positive results, the physical therapist then may offer instruction in the use of a home overhead cervical traction unit, which must be prescribed by the physician. A home cervical traction unit is most useful for patients with cervical radiculopathy.


Manipulation or manual therapy may offer some benefit in patients with acute or chronic neck pain.[89]

This therapy may be provided by an osteopathic physician (DO), a chiropractic physician (DC), or an allopathic physician (MD) with appropriate training.[89]

According to a study by the RAND Institute, the estimated rate of complication as a result of cervical manipulative procedures is 1 case per 1 million manipulations.[90]


Acupuncture may be beneficial for pain control and should be administered by an appropriately trained and certified provider.


Bracing with a soft cervical collar may provide symptomatic relief. The collar does not immobilize the spine; it only reminds the patient not to move his/her neck. If use of a soft cervical collar is prolonged, it may result in worsening of strength, flexibility, and function.

Moreover, using pooled analysis, a systematic review by Ricciardi et al of randomized, controlled trials indicated that nonrigid cervical collars employed for 1-2 weeks in patients with grade 1 or 2 whiplash-associated disorders offer no benefit over nonimmobilization protocols with regard to pain (as measured using the visual analogue scale score) and range of motion (ROM). The investigators reported, in fact, that nonimmobilization protocols, whether associated with physical therapy or not, appear to provide better pain relief and recovery of neck mobility.[91]



Medication Summary

Early and appropriate treatment with analgesics for pain relief, with anti-inflammatory agents for inflammation, with muscle relaxants for spasms, and with aids for sleep disturbance, are the mainstay pharmaceutical therapies for cervical sprain/strain injuries.

Nonopioid analgesics

Class Summary

Pain control is essential to high-quality patient care. Nonnarcotic analgesics ensure patient comfort and promote pulmonary toilet. These medications have sedating properties, which are beneficial for patients who have traumatic injuries.

Acetaminophen (Tylenol, Panadol, Aspirin-Free Anacin)

DOC for treatment of pain in patients with documented hypersensitivity to aspirin or NSAIDs or in patients with upper GI disease or who are taking oral anticoagulants

Opioid analgesics

Class Summary

These agents are indicated for the medical treatment of moderate to severe pain.

Hydrocodone/acetaminophen (Lortab)

For relief of moderate to severe pain. Dose available with 2.5, 5, 7.5, 10 mg of hydrocodone. Total daily dose of acetaminophen should be considered; not to exceed 4 g/d. Individualize dose from qd to q4h, depending on degree of pain, effect of pain on patient's lifestyle, and need to keep blood levels of analgesic at therapeutic dose consistently or only intermittently.

Cyclooxygenase-2 (COX-2) inhibitors

Class Summary

Although increased cost can be a negative factor, the incidence of costly and potentially fatal GI bleeds is clearly less with COX-2 inhibitors than with traditional nonsteroidal anti-inflammatory drugs (NSAIDs). Ongoing analysis of cost avoidance of GI bleeds will further define the populations for whom COX-2 inhibitors are most beneficial.

Celecoxib (Celebrex)

COX-1 is important for platelet aggregation, regulation of blood flow in the kidney and stomach, and regulation of gastric acid secretion. Inhibition of COX-1 may contribute to NSAID GI toxicity. COX-2 is considered an inducible isoenzyme, being induced during pain and inflammatory stimuli. Celecoxib inhibits primarily COX-2. At therapeutic concentrations, COX-1 isoenzyme is not inhibited; thus, GI toxicity may be decreased. Seek the lowest dose for each patient.

Nonsteroidal anti-inflammatory agents

Class Summary

These agents have analgesic, anti-inflammatory, and antipyretic activities. Their mechanism of action is not known, but they may inhibit cyclooxygenase activity and prostaglandin synthesis. Other mechanisms may exist as well; these include inhibition of leukotriene synthesis, lysosomal enzyme release, lipoxygenase activity, neutrophil aggregation and various cell-membrane functions.

Nabumetone (Relafen)

Nonacidic NSAID rapidly metabolized after absorption to a major active metabolite that inhibits cyclooxygenase enzyme, which in turn inhibits inflammation.

Muscle relaxants

Class Summary

These medications are indicated for the relaxation of increased muscle tone, spasm, and rigidity associated with cervical strain syndromes.

Tizanidine (Zanaflex)

Indicated for treating muscle spasm in patients with cervical strain. Centrally acting muscle relaxant metabolized in the liver and excreted in urine and feces.

Carisoprodol (Soma)

Short-acting medication that may have depressant effects at the spinal cord level.

Cyclobenzaprine (Flexeril)

Skeletal muscle relaxant that acts centrally and reduces motor activity of tonic somatic origins, influencing alpha and gamma motor neurons. Structurally related to tricyclic antidepressants and thus has some of their disadvantages.

Methocarbamol (Robaxin)

Reduces nerve impulse transmission from spinal cord to skeletal muscle.

Tricyclic antidepressants

Class Summary

Disturbed sleep is often a significant symptom with cervical strain. If analgesics and muscle relaxants do not provide enough relief, medications such as low-dose antidepressants can be used. These agents have central and peripheral anticholinergic effects, as well as sedative effects.

Amitriptyline (Elavil)

Analgesic for certain types of chronic and neuropathic pain.


Class Summary

These agents are used for severe inflammation (eg, radiculopathy) caused by the release of inflammatory chemicals from disc injury. These agents have anti-inflammatory properties and cause profound and varied metabolic effects. In addition, they modify the body's immune response to diverse stimuli.

Methylprednisolone (Solu-Medrol, Depo-Medrol)

Indicated for treatment of severe pain and/or radiculopathy if inflammation is suspected.



Further Outpatient Care

Acute medical follow-up is performed at 1- to 2-week intervals.

Subacute medical follow-up is performed at 2- to 4-week intervals.

Long-term medical follow-up is performed at 1- to 12-month intervals.

The type of medication prescribed for pain may influence the frequency of follow-up visits. For example, patients taking schedule II opiates require monthly follow-up visits.

Inpatient & Outpatient Medications

Chronic cervical strain management requires an individually tailored medication regimen, which could require a combination of the following:

  • Analgesics

    • Acetaminophen (Tylenol)

    • Opiates (Consider applicable medical practice guidelines for their appropriate use in chronic benign pain syndromes.)

  • Muscle relaxants

    • Soma

    • Robaxin

    • Skelaxin

    • Flexeril

    • Zanaflex

    • Parafon-Forte

  • Low doses of sleep disturbance aids

    • Elavil

    • Pamelor

    • Desyrel


Neuromusculoskeletal specialists, such as physiatrists, often perform follow-up evaluations in patients with cervical sprains or strains.

Patients may also be followed up by orthopedists, neurologists, neurosurgeons, rheumatologists, or family practitioners.


Most cervical strains are a by-product of our industrial society and the primary means of transportation, the motor vehicle.

Motor vehicle safety appears to be a primary focus for deterrence.


Chronic pain syndrome may develop in certain individuals. This syndrome may be characterized by excessive disability, dependence, prescription drug use, depression, and dramatization of pain behavior. Referral to a chronic pain specialist may be indicated.

A study by Watanabe et al found that individuals who suffered whiplash-associated disorders were more likely to have shoulder stiffness, headache, and arm pain at 20-year follow-up, with the odds ratios being 3.36, 2.39, and 3.82, respectively. Comparing persons who had experienced whiplash-associated disorders with controls, the investigators reported the prevalence of shoulder stiffness to be 72.0% versus 45.9%, respectively; of headache to be 24.0% versus 12.2%, respectively; and of arm pain to be 13.3% versus 3.9%, respectively.[92]


Short-term recovery

Many patients improve within 8 weeks, although complete resolution in this period may not be common. If pain persists for longer than 3 months, severe ligamentous, disc, or associated facet injury is suggested. Recovery after whiplash occurs mostly in the first 2-3 months after the accident. After that, recovery slows dramatically, with no further change in symptoms after 2 years.[93]

At 6 months after the injury, 20-70% of patients with neck injury due to an automobile accident still experience pain.

Long-term recovery

Dreyer and Boden examined patients 10 years after the onset of neck pain and found that 79% had improved, 43% were pain-free, and 32% had persistent, moderate to severe pain.[47] In a group of patients with significant symptoms at 10 years after whiplash injury, Barnsley and colleagues found that everyone had degenerative changes on radiographs, at a significantly higher rate than that of a control group.[45]

Whiplash patients with ongoing moderate or severe symptoms at 2-3 years continued to show decreased ROM, increased electromyographic activity during craniocervical flexion, and sensory hypersensitivity. They also showed elevated levels of psychological distress compared with those of patients with milder symptoms or with individuals who had recovered.[94]

The greatest risk for long-term symptoms occurs in patients with point tenderness and limited ROM.[95]

In a study by Gun and colleagues, bodily pain scores and role emotional scores of the 36-Item Short Form Survey (SF-36) health questionnaire were consistently and significantly positively associated with improved outcomes. Consulting a lawyer was associated with a decreased likelihood of claim settlement and an increased likelihood that the patient would still be receiving treatment after 1 year. However, such consultation was not significantly associated with a return to work. The degree of damage to the vehicle was not a predictor of outcome.[96]

A Japanese study, by Oka et al, found that, among persons involved in a traffic collision, patients with whiplash-associated disorder suffering from intractable neck pain tended to have worse psychological test scores than did controls suffering from minor neck pain successfully treated within 3 months. The two groups differed significantly with regard to their scores on the Tampa Scale of Kinesiophobia, the Pain Catastrophizing Scale, the SF-36 mental health component summary, and the EuroQol-5 dimension questionnaire (with this last used to assess general quality of life).[97]

Similarly, a study by Elphinston et al found that reductions in fear of movement and reinjury, as well as a decrease in pain catastrophizing, were linked to a rising expectation of recovery in patients.[98]

According to a study by Hendriks et al, factors related to poor recovery from whiplash-associated disorder include female sex, a low level of education, high initial neck pain, severe disability, and high levels of somatization and sleep difficulties. Neck pain intensity and work disability were the most consistent predictors for poor recovery.[99]

Similar results were found by Walton et al in a study investigating factors affecting prognosis in patients who have sustained whiplash injury in a motor vehicle accident.[100] Their meta-analysis of 3,193 patients found 9 significant predictors: absence of postsecondary education, female sex, history of neck pain, neck pain intensity of more than 55/100, presence of neck pain at baseline, presence of headache at baseline, catastrophizing, whiplash-associated disorder grade 2 or 3, and failure to use a seat belt at the time of collision. Of those factors, 4 were robust to publication bias: neck pain intensity, whiplash-associated disorder grade, headache, and absence of postsecondary education.

Sterling et al evaluated a prognostic model for chronic whiplash injury-related disability that used the Neck Disability Index as an outcome measure, and age, decreased cold pain thresholds and peripheral vasoconstriction (indices of central sensitization), decreased cervical range of motion, post-traumatic stress symptoms, and initial disability as predictors. They found that their model demonstrated good accuracy for predicting which patients would have moderate to severe disability one year after injury.[101]

Use of a "fear-avoidance model" may prove effective for understanding the development of persistent complaints following an acute whiplash injury. It is postulated that the injured patient is caught in a downward spiral of increasing avoidance, disability, and pain.[102]

Associated comorbidities

Petterson and colleagues proposed a possible association between whiplash injury and cervical disc disease, suggesting that trauma to the cervical spine may accelerate normal age-related deterioration of the discs.[43]

One study showed that increasing age, injury-related cognitive impairment, and severity of the initial neck pain were predictive of persistent symptoms at 6 months.[103]

In another study, Radanov and co-investigators examined patients with injury-related symptoms at 2 years.[103] Compared with other patients, symptomatic patients were older and had an increased incidence of rotated or inclined head position at the time of impact, an increased prevalence of pretraumatic headache, and an increased intensity of initial neck pain and headache. Symptomatic patients also had more symptoms (including those of radicular deficit), higher average scores on a multiple-symptom analysis, and more degenerative signs (osteoarthritis) on radiographs.

Disabling neck pain is associated with other comorbidities (headache, cardiovascular problems, digestive problems, low back pain) that negatively affect the patient's health. The prevalence of neck pain and disability is increased in individuals with a lifetime history of neck injury who are involved in a motor vehicle collision.[104]  Low back pain is a common injury with prolonged recovery. Biopsychosocial factors, such as the type of compensation system that exists, affect the incidence and prognosis.[105]

Chronic psychiatric disease is more common in patients with chronic symptoms (chronic whiplash-associated disorder) than in others. The dominant psychiatric diagnosis before and after the injury is depression. Psychiatric morbidity may be a patient-related risk factor for chronic symptoms after a whiplash injury and seems to be associated with psychiatric vulnerability.[106]

Depressive symptomatology after whiplash is common, occurs early, and often persists or becomes recurrent.[107]

The incidence of widespread pain disorders increases after cervical spinal injury. In a study of 161 cases of traumatic injury, fibromyalgia syndrome was 13 times more frequent after neck injury than after lower-extremity injury.[108]

Chronic whiplash-associated disorders are characterized by mechanical hyperalgesia over the cervical spine and by widespread hypersensitivity to mechanical pressure and thermal stimuli; this finding was independent of state of anxiety and may represent changes in central pain-processing mechanisms.[109]

A study of a large cohort of individuals involved in traffic accidents showed that patients with whiplash-associated disorders may demonstrate symptoms well beyond the neck, including fatigue, dizziness, paresthesias, headaches, spinal pain, nausea, and jaw pain.[110, 111]

Medicolegal considerations

The prognosis of acute whiplash varies according to the population sampled and the insurance/compensation system under which individuals are allowed to claim benefits.[112] See also Medical/Legal Pitfalls.

Patient Education

Patient education in self-care is important in preventing dependence on health-care providers, as well as in preventing excessive disability.

A physical therapist can teach patients with chronic cervical strains how to use proper postural and body mechanics.

For excellent patient education resources, visit eMedicineHealth's First Aid and Injuries Center and Osteoporosis Center. Also, see eMedicineHealth's patient education articles Neck Strain, Shoulder and Neck Pain, Sprains and Strains, and Whiplash.