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  more...
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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.