eMedicine Specialties > Physical Medicine and Rehabilitation > Cervical Spine Disorders

Cervical Sprain and Strain

Author: Oregon K Hunter Jr, MD, Physiatrist, Southeastern Rehabilitation Medicine, SIMED
Coauthor(s): Michael D Freeman, PhD, MPH, DC, Clinical Associate Professor of Epidemiology, Department of Public Health and Preventive Medicine, Oregon Health Sciences University; Adjunct Associate Professor of Forensic Medicine and Epidemiology, Institute of Forensic Medicine, Faculty of Health Sciences at Aarhus University, Denmark
Contributor Information and Disclosures

Updated: Jul 15, 2009

Introduction

Background

Cervical strain is one of the most common musculoskeletal problems encountered by generalists and neuromusculoskeletal specialists in the clinic.

One cause of cervical strain is termed cervical acceleration-deceleration injury; this is frequently called whiplash injury.

Whiplash, one of the most common sequela of nonfatal car injuries, is one of the most poorly understood disorders of the spine, and the severity of the trauma is often not correlated with the seriousness of the clinical problems.1 A history of neck injury is a significant risk factor for chronic neck pain.2 Pretorque of the head and neck increases facet capsular strains, supporting its role in the whiplash mechanism.3

The Quebec Taskforce on Whiplash-Associated Disorders has suggested the following system for classifying the severity of cervical sprains4 :

  • 0 - No neck pain complaints, no physical signs
  • 1 - Neck pain complaints, only stiffness or tenderness, no other physical signs
  • 2 - Neck complaints and musculoskeletal signs (decreased range of motion [ROM] and point tenderness)
  • 3 - Neck complaints and neurologic signs (weakness, sensory and reflex changes)
  • 4 - Neck complaints with fracture and/or dislocation

Related eMedicine topics:
Cervical Facet Syndrome
Cervical Spine Sprain/Strain Injuries
Cervical Strain
Neck Trauma

Related Medscape topic:
Resource Center Spinal Disorders

Pathophysiology

Relevant anatomy and physiology

Consistent with known biologic models, injuries to bony, articular (disks 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.

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 disk 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.5

Chronic pain associated with cervical strains is most likely to affect the zygapophysial (facet) joints, intervertebral disks, and upper cervical ligaments. The C2-3 facet joint is the most common source of referred pain in patients with a dominant complaint of 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 diskogenic 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.

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.6

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.7

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.8   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.9

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.10

In a clinical review, Barnsley and colleagues described the classic whiplash scenario in which the patient's car has been struck from behind (ie, rear ended).11 This type of accident 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.12 Direct facial impact has shown a flexion motion of the upper or middle cervical spine, with extension of the lower cervical spine.13

The forces involved in an impact speed of 20 mph (32 km/h) cause the human head to reach a peak acceleration of 12 G during extension. 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 disks, 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.14,15,16,17,18

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.19

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.20 Head-turned rear impacts up to 8 G do not typically injure the alar, transverse, and apical ligaments.21

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 C6-7.22

A rear-end collision is most likely to injure the lower cervical spine, with intervertebral hyperextension at a peak acceleration of 5 G and above.23,24 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.25

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 C6.6 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.26

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.27   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.28

The risk of whiplash injury in motor vehicle collisions increases when subjects are surprised and unprepared for the impact.29

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 disk 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.30

Complications

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

Cord compression after whiplash due to physiologic extension loading is not likely. However, individuals with a narrow spinal canal have an increased risk of quadriparesis-causing injury to the spinal cord.24

Postmortem studies have shown that ligamentous injuries are common after whiplash injuries, but disk herniation is a rare event.31

In one study, 33% of patients with whiplash injury had disk herniations with medullary or dura impingement over 2-year follow-up after injury.32

In another study, whiplash-type distortions were associated with a 16% incidence of diskoligamentous injuries. On magnetic resonance imaging (MRI), most patients with severe, persisting, radiating pain had large disk protrusions that were confirmed as herniations at surgery. Neck and radiating pain were alleviated with early disk excision and fusion.33

Strain or tears of the anterior annulus and the alar portions of the posterior longitudinal ligament (when stretched by a bulging disk) are possible causes for diskogenic 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.34

Upper cervical disk 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. Radiculopathy is more likely than are cord signs.

MRI or computed tomography (CT) myelography are necessary for the diagnosis.35

Frequency

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 rate for neck and shoulder pain is 16-18%.36

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.34 Freeman and co-investigators cautiously estimated that 6.2% of the US population, or 15.5 million individuals, have late whiplash syndrome.37

International

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.

Mortality/Morbidity

  • 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.

Sex

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

Age

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

Clinical

History

The most common symptoms of cervical disorders are suboccipital headache and/or ongoing or motion-induced neck pain. Other 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 disk in the upper cervical spine.35
  • Headache
    • Headache is a frequent symptom of cervical strain.38
    • 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 disk damage have been implicated in the pathology of headaches due to neck injury.6
    • 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.6
  • 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.39
    • Bladder or bowel dysfunction - These may be symptoms of complication of myelopathy (spinal cord involvement).

Physical

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 - This 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. Palpation of the zygapophysial joints may be helpful in determining the painful joints, because of osteoarthritis or posttraumatic irritation of the joint capsule.
    • ROM - 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.40 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.41
    • 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.42
    • Special maneuvers - Cervical neurocompression 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
    • 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 upper extremities may be decreased. 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, 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. By contrast, 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 pattern in the upper extremities.
    • 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.

Causes

  • 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.43

More on Cervical Sprain and Strain

Overview: Cervical Sprain and Strain
Differential Diagnoses & Workup: Cervical Sprain and Strain
Treatment & Medication: Cervical Sprain and Strain
Follow-up: Cervical Sprain and Strain
Multimedia: Cervical Sprain and Strain
References
[ CLOSE WINDOW ]

References

  1. Riley LH 3rd, Long D, Riley LH Jr. The science of whiplash. Medicine (Baltimore). Sep 1995;74(5):298-9. [Medline].

  2. Croft PR, Lewis M, Papageorgiou AC, et al. Risk factors for neck pain: a longitudinal study in the general population. Pain. Sep 2001;93(3):317-25. [Medline].

  3. Winkelstein BA, Nightingale RW, Richardson WJ, et al. The cervical facet capsule and its role in whiplash injury: a biomechanical investigation. Spine. May 15 2000;25(10):1238-46. [Medline].

  4. Spitzer WO, Skovron ML, Salmi LR, et al. Scientific monograph of the Quebec Task Force on Whiplash-Associated Disorders: redefining "whiplash" and its management. Spine. Apr 15 1995;20(8 Suppl):1S-73S. [Medline].

  5. Siegmund GP, Myers BS, Davis MB, et al. Mechanical evidence of cervical facet capsule injury during whiplash: a cadaveric study using combined shear, compression, and extension loading. Spine. Oct 1 2001;26(19):2095-101. [Medline].

  6. Anderson AV. Cervicogenic processes: results of injury to the cervical spine. Pain Practitioner. 2001;11:9-11.

  7. Igarashi A, Kikuchi S, Konno S, et al. Inflammatory cytokines released from the facet joint tissue in degenerative lumbar spinal disorders. Spine. Oct 1 2004;29(19):2091-5. [Medline].

  8. Bogduk N. Point of view. Spine. 2002;27:40-1.

  9. Siegmund GP, Myers BS, Davis MB, et al. Human cervical motion segment flexibility and facet capsular ligament strain under combined posterior shear, extension and axial compression. Stapp Car Crash J. Nov 2000;44:159-70. [Medline].

  10. Ferrari R. The many facets of whiplash. Spine. Oct 1 2001;26(19):2063-4. [Medline].

  11. Barnsley L, Lord S, Bogduk N. Comparative local anaesthetic blocks in the diagnosis of cervical zygapophysial joint pain. Pain. Oct 1993;55(1):99-106. [Medline].

  12. Pearson AM, Panjabi MM, Ivancic PC, et al. Frontal impact causes ligamentous cervical spine injury. Spine. Aug 15 2005;30(16):1852-8. [Medline].

  13. Fukushima M, Kaneoka K, Ono K, et al. Neck injury mechanisms during direct face impact. Spine. Apr 15 2006;31(8):903-8. [Medline].

  14. Kumar S, Ferrari R, Narayan Y. Cervical muscle response to head rotation in whiplash-type left lateral impacts. Spine. Mar 1 2005;30(5):536-41. [Medline].

  15. Kumar S, Ferrari R, Narayan Y. Effect of head rotation in whiplash-type rear impacts. Spine J. Mar-Apr 2005;5(2):130-9. [Medline].

  16. Kumar S, Ferrari R, Narayan Y. Electromyographic and kinematic exploration of whiplash-type rear impacts: effect of left offset impact. Spine J. Nov-Dec 2004;4(6):656-65; discussion 666-8. [Medline].

  17. Kumar S, Ferrari R, Narayan Y. Looking away from whiplash: effect of head rotation in rear impacts. Spine. Apr 1 2005;30(7):760-8. [Medline].

  18. Kumar S, Ferrari R, Narayan Y. The effect of trunk flexion in healthy volunteers in rear whiplash-type impacts. Spine. Aug 1 2005;30(15):1742-9. [Medline].

  19. Stemper BD, Yoganandan N, Pintar FA. Gender- and region-dependent local facet joint kinematics in rear impact: implications in whiplash injury. Spine. Aug 15 2004;29(16):1764-71. [Medline].

  20. Panjabi MM, Ivancic PC, Maak TG, et al. Multiplanar cervical spine injury due to head-turned rear impact. Spine. Feb 15 2006;31(4):420-9. [Medline].

  21. Maak TG, Tominaga Y, Panjabi MM, et al. Alar, transverse, and apical ligament strain due to head-turned rear impact. Spine. Mar 15 2006;31(6):632-8. [Medline].

  22. Tominaga Y, Maak TG, Ivancic PC, et al. Head-turned rear impact causing dynamic cervical intervertebral foramen narrowing: implications for ganglion and nerve root injury. J Neurosurg Spine. May 2006;4(5):380-7. [Medline].

  23. Ito S, Ivancic PC, Panjabi MM, et al. Soft tissue injury threshold during simulated whiplash: a biomechanical investigation. Spine. May 1 2004;29(9):979-87. [Medline].

  24. Ito S, Panjabi MM, Ivancic PC, et al. Spinal canal narrowing during simulated whiplash. Spine. Jun 15 2004;29(12):1330-9. [Medline].

  25. Tropiano P, Thollon L, Arnoux PJ, et al. Using a finite element model to evaluate human injuries application to the HUMOS model in whiplash situation. Spine. Aug 15 2004;29(16):1709-16. [Medline].

  26. Cusick JF, Pintar FA, Yoganandan N. Whiplash syndrome: kinematic factors influencing pain patterns. Spine. Jun 1 2001;26(11):1252-8. [Medline].

  27. Kumar S, Narayan Y, Amell T. An electromyographic study of low-velocity rear-end impacts. Spine. May 15 2002;27(10):1044-55. [Medline].

  28. Vasavada AN, Brault JR, Siegmund GP. Musculotendon and fascicle strains in anterior and posterior neck muscles during whiplash injury. Spine. Apr 1 2007;32(7):756-65. [Medline].

  29. Siegmund GP, Sanderson DJ, Myers BS, et al. Awareness affects the response of human subjects exposed to a single whiplash-like perturbation. Spine. Apr 1 2003;28(7):671-9. [Medline].

  30. Freeman MD, Croft AC, Nicodemus CN. Significant spinal injury resulting from low-level accelerations: a case series of roller coaster injuries. Arch Phys Med Rehabil. Nov 2005;86(11):2126-30.

  31. Mercer S, Bogduk N. The ligaments and annulus fibrosus of human adult cervical intervertebral discs. Spine. Apr 1 1999;24(7):619-26; discussion 627-8. [Medline].

  32. Pettersson K, Hildingsson C, Toolanen G, et al. Disc pathology after whiplash injury. A prospective magnetic resonance imaging and clinical investigation. Spine. Feb 1 1997;22(3):283-7; discussion 288. [Medline].

  33. Jonsson H, Cesarini K, Sahlstedt B, et al. Findings and outcome in whiplash-type neck distortions. Spine. Dec 15 1994;19(24):2733-43. [Medline].

  34. Barnsley L, Lord S, Bogduk N. Whiplash injury. Pain. Sep 1994;58(3):283-307. [Medline].

  35. Chen TY. The clinical presentation of uppermost cervical disc protrusion. Spine. Feb 15 2000;25(4):439-42. [Medline].

  36. Dreyer SJ, Boden SD. Nonoperative treatment of neck and arm pain. Spine. Dec 15 1998;23(24):2746-54. [Medline].

  37. Freeman MD, Croft AC, Rossignol AM, et al. A review and methodologic critique of the literature refuting whiplash syndrome. Spine. Jan 1 1999;24(1):86-96. [Medline].

  38. Haldeman S, Dagenais S. Cervicogenic headaches: a critical review. Spine J. Jan-Feb 2001;1(1):31-46. [Medline].

  39. Lorberboym M, Gilad R, Gorin V, et al. Late whiplash syndrome: correlation of brain SPECT with neuropsychological tests and P300 event-related potential. J Trauma. Mar 2002;52(3):521-6. [Medline].

  40. Dall'Alba PT, Sterling MM, Treleaven JM, et al. Cervical range of motion discriminates between asymptomatic persons and those with whiplash. Spine. Oct 1 2001;26(19):2090-4. [Medline].

  41. Prushansky T, Pevzner E, Gordon C. Performance of cervical motion in chronic whiplash patients and healthy subjects: the case of atypical patients. Spine. Jan 1 2006;31(1):37-43.

  42. Kasch H, Stengaard-Pedersen K, Arendt-Nielsen L, et al. Headache, neck pain, and neck mobility after acute whiplash injury: a prospective study. Spine. Jun 1 2001;26(11):1246-51. [Medline].

  43. Giannoudis PV, Mehta SS, Tsiridis E. Incidence and outcome of whiplash injury after multiple trauma. Spine. Apr 1 2007;32(7):776-81. [Medline].

  44. Uhrenholt L, Grunnet-Nilsson N, Hartvigsen J. Cervical spine lesions after road traffic accidents: a systematic review. Spine. Sep 1 2002;27(17):1934-41; discussion 1940. [Medline].

  45. Kristjansson E, Leivseth G, Brinckmann P, et al. Increased sagittal plane segmental motion in the lower cervical spine in women with chronic whiplash-associated disorders, grades I-II: a case-control study using a new measurement protocol. Spine. Oct 1 2003;28(19):2215-21. [Medline].

  46. Matsumoto M, Fujimura Y, Suzuki N, et al. MRI of cervical intervertebral discs in asymptomatic subjects. J Bone Joint Surg Br. Jan 1998;80(1):19-24. [Medline].

  47. Hino H, Abumi K, Kanayama M, et al. Dynamic motion analysis of normal and unstable cervical spines using cineradiography. An in vivo study. Spine. Jan 15 1999;24(2):163-8. [Medline].

  48. Buonocore E, Hartman JT, Nelson CL. Cineradiograms of cervical spine in diagnosis of soft-tissue injuries. JAMA. Oct 3 1966;198(1):143-7. [Medline].

  49. Zheng Y, Liew SM, Simmons ED. Value of magnetic resonance imaging and discography in determining the level of cervical discectomy and fusion. Spine. Oct 1 2004;29(19):2140-5; discussion 2146. [Medline].

  50. Leppanen R. Intraoperative monitoring of trapezius function. Spine J. 2003;3:248.

  51. Pezzin LE, Dillingham TR, Lauder TD, et al. Cervical radiculopathies: relationship between symptom duration and spontaneous EMG activity. Muscle Nerve. Oct 1999;22(10):1412-8. [Medline].

  52. Scholten-Peeters GG, Bekkering GE, Verhagen AP, et al. Clinical practice guideline for the physiotherapy of patients with whiplash-associated disorders. Spine. Feb 15 2002;27(4):412-22. [Medline].

  53. Rosenfeld M, Gunnarsson R, Borenstein P. Early intervention in whiplash-associated disorders: a comparison of two treatment protocols. Spine. Jul 15 2000;25(14):1782-7. [Medline].

  54. Rosenfeld M, Seferiadis A, Carlsson J, et al. Active intervention in patients with whiplash-associated disorders improves long-term prognosis: a randomized controlled clinical trial. Spine. Nov 15 2003;28(22):2491-8. [Medline].

  55. Ylinen J, Takala EP, Nykanen M, et al. Active neck muscle training in the treatment of chronic neck pain in women: a randomized controlled trial. JAMA. May 21 2003;289(19):2509-16. [Medline]. [Full Text].

  56. Chiu TT, Lam TH, Hedley AJ. A randomized controlled trial on the efficacy of exercise for patients with chronic neck pain. Spine. Jan 1 2005;30(1):E1-7. [Medline].

  57. Conlin A, Bhogal S, Sequeira K, et al. Treatment of whiplash-associated disorders--part II: medical and surgical interventions. Pain Res Manag. 2005;10(1):33-40. [Medline].

  58. Conlin A, Bhogal S, Sequeira K, et al. Treatment of whiplash-associated disorders--part I: non-invasive interventions. Pain Res Manag. 2005;10(1):21-32. [Medline].

  59. [Best Evidence] Rosenfeld M, Seferiadis A, Gunnarsson R. Active involvement and intervention in patients exposed to whiplash trauma in automobile crashes reduces costs: a randomized, controlled clinical trial and health economic evaluation. Spine. Jul 15 2006;31(16):1799-804. [Medline].

  60. [Best Evidence] Kongsted A, Qerama E, Kasch H, et al. Neck collar, "act-as-usual" or active mobilization for whiplash injury? A randomized parallel-group trial. Spine. Mar 15 2007;32(6):618-26. [Medline].

  61. Pietrobon R, Coeytaux RR, Carey TS, et al. Standard scales for measurement of functional outcome for cervical pain or dysfunction: a systematic review. Spine. Mar 1 2002;27(5):515-22. [Medline].

  62. Côté P, Hogg-Johnson S, Cassidy JD, et al. Early aggressive care and delayed recovery from whiplash: isolated finding or reproducible result?. Arthritis Rheum. Jun 15 2007;57(5):861-8. [Medline].

  63. Sampath P, Bendebba M, Davis JD, et al. Outcome in patients with cervical radiculopathy. Prospective, multicenter study with independent clinical review. Spine. Mar 15 1999;24(6):591-7. [Medline].

  64. Fouyas IP, Statham PF, Sandercock PA. Cochrane review on the role of surgery in cervical spondylotic radiculomyelopathy. Spine. Apr 1 2002;27(7):736-47. [Medline].

  65. Laporte C, Laville C, Lazennec JY, et al. Severe hyperflexion sprains of the lower cervical spine in adults. Clin Orthop Relat Res. Jun 1999;(363):126-34. [Medline].

  66. Soderlund A, Lindberg P. Long-term functional and psychological problems in whiplash associated disorders. Int J Rehabil Res. Jun 1999;22(2):77-84. [Medline].

  67. Peloso P, Gross A, Haines T, et al. Medicinal and injection therapies for mechanical neck disorders. Cochrane Database Syst Rev. Apr 18 2005;CD000319. [Medline].

  68. [Best Evidence] Peloso P, Gross A, Haines T, et al. Medicinal and injection therapies for mechanical neck disorders. Cochrane Database Syst Rev. Jul 18 2007;CD000319. [Medline].

  69. Sapir DA, Gorup JM. Radiofrequency medial branch neurotomy in litigant and nonlitigant patients with cervical whiplash: a prospective study. Spine. Jun 15 2001;26(12):E268-73. [Medline].

  70. Wallis BJ, Lord SM, Bogduk N. Resolution of psychological distress of whiplash patients following treatment by radiofrequency neurotomy: a randomised, double-blind, placebo-controlled trial. Pain. Oct 1997;73(1):15-22. [Medline].

  71. Schofferman J, Bogduk N, Slosar P. Chronic whiplash and whiplash-associated disorders: an evidence-based approach. J Am Acad Orthop Surg. Oct 2007;15(10):596-606. [Medline].

  72. Freund BJ, Schwartz M. Treatment of chronic cervical-associated headache with botulinum toxin A: a pilot study. Headache. Mar 2000;40(3):231-6. [Medline].

  73. Hurwitz EL, Aker PD, Adams AH, et al. Manipulation and mobilization of the cervical spine. A systematic review of the literature. Spine. Aug 1 1996;21(15):1746-59; discussion 1759-60. [Medline].

  74. Coulter ID, Hurwitz E, Adams AH, et al. The Appropriateness of Manipulation and Mobilization of the Cervical Spine. Santa Monica, Calif: RAND; 1996:36.

  75. Verhagen AP, Scholten-Peeters GG, van Wijngaarden S, et al. Conservative treatments for whiplash. Cochrane Database Syst Rev. 2007;(2):CD003338. [Medline].

  76. Sterling M, Jull G, Kenardy J. Physical and psychological factors maintain long-term predictive capacity post-whiplash injury. Pain. May 2006;122(1-2):102-8. [Medline].

  77. Hartling L, Brison RJ, Ardern C, et al. Prognostic value of the Quebec Classification of Whiplash-Associated Disorders. Spine. Jan 1 2001;26(1):36-41. [Medline].

  78. Gun RT, Osti OL, O'Riordan A, et al. Risk factors for prolonged disability after whiplash injury: a prospective study. Spine. Feb 15 2005;30(4):386-91. [Medline].

  79. Hendriks EJ, Scholten-Peeters GG, van der Windt DA, et al. Prognostic factors for poor recovery in acute whiplash patients. Pain. Apr 2005;114(3):408-16. [Medline].

  80. [Best Evidence] Walton DM, Pretty J, Macdermid JC, et al. Risk factors for persistent problems following whiplash injury: results of a systematic review and meta-analysis. J Orthop Sports Phys Ther. May 2009;39(5):334-50. [Medline].

  81. Vangronsveld K, Peters M, Goossens M, et al. Applying the fear-avoidance model to the chronic whiplash syndrome. Pain. Oct 2007;131(3):258-61. [Medline].

  82. Radanov BP, Sturzenegger M, Di Stefano G. Long-term outcome after whiplash injury. A 2-year follow-up considering features of injury mechanism and somatic, radiologic, and psychosocial findings. Medicine (Baltimore). Sep 1995;74(5):281-97. [Medline].

  83. Côté P, Cassidy JD, Carroll L. The factors associated with neck pain and its related disability in the Saskatchewan population. Spine. May 1 2000;25(9):1109-17. [Medline].

  84. Cassidy JD, Carroll L, Côté P, et al. Low back pain after traffic collisions: a population-based cohort study. Spine. May 15 2003;28(10):1002-9. [Medline].

  85. Kivioja J, Själin M, Lindgren U. Psychiatric morbidity in patients with chronic whiplash-associated disorder. Spine. Jun 1 2004;29(11):1235-9. [Medline].

  86. Carroll LJ, Cassidy JD, Côté P. Frequency, timing, and course of depressive symptomatology after whiplash. Spine. Jul 15 2006;31(16):E551-6. [Medline].

  87. Buskila D, Neumann L, Vaisberg G, et al. Increased rates of fibromyalgia following cervical spine injury. A controlled study of 161 cases of traumatic injury. Arthritis Rheum. Mar 1997;40(3):446-52. [Medline].

  88. Scott D, Jull G, Sterling M. Widespread sensory hypersensitivity is a feature of chronic whiplash-associated disorder but not chronic idiopathic neck pain. Clin J Pain. Mar/Apr 2005;21(2):175-81.

  89. Ferrari R, Russell AS, Carroll LJ. A re-examination of the whiplash associated disorders (WAD) as a systemic illness. Ann Rheum Dis. Sep 2005;64(9):1337-42.

  90. Côté P, Cassidy JD, Carroll L, et al. A systematic review of the prognosis of acute whiplash and a new conceptual framework to synthesize the literature. Spine. Oct 1 2001;26(19):E445-58. [Medline].

  91. Hoffberg HJ. Whiplash injuries in motor vehicle accidents. Pract Pain Manag. Sep/Oct 2002;24-37.

  92. Schrader H, Obelieniene D, Bovim G, et al. Natural evolution of late whiplash syndrome outside the medicolegal context. Lancet. May 4 1996;347(9010):1207-11. [Medline].

  93. Aprill C, Dwyer A, Bogduk N. Cervical zygapophyseal joint pain patterns. II: A clinical evaluation. Spine. Jun 1990;15(6):458-61. [Medline].

  94. Ashina M, Bendtsen L, Jensen R, et al. Muscle hardness in patients with chronic tension-type headache: relation to actual headache state. Pain. Feb 1999;79(2-3):201-5. [Medline].

  95. Banic B, Petersen-Felix S, Andersen OK, et al. Evidence for spinal cord hypersensitivity in chronic pain after whiplash injury and in fibromyalgia. Pain. Jan 2004;107(1-2):7-15. [Medline].

  96. Benthien H, Wohllebe W. [On the therapy of central venous thrombosis using streptokinase]. Z Arztl Fortbild (Jena). Apr 1 1968;62(7):388-90. [Medline].

  97. Castro WH, Schilgen M, Meyer S, et al. Do "whiplash injuries" occur in low-speed rear impacts?. Eur Spine J. 1997;6(6):366-75. [Medline].

  98. Cauthen JC, Kinard RE, Vogler JB, et al. Outcome analysis of noninstrumented anterior cervical discectomy and interbody fusion in 348 patients. Spine. Jan 15 1998;23(2):188-92. [Medline].

  99. Dvorak J. Epidemiology, physical examination, and neurodiagnostics. Spine. Dec 15 1998;23(24):2663-73. [Medline].

  100. Dwyer A, Aprill C, Bogduk N. Cervical zygapophyseal joint pain patterns, I: a study in normal volunteers. Spine. Jun 1990;15(6):453-7. [Medline].

  101. Kaiser JA, Holland BA. Imaging of the cervical spine. Spine. Dec 15 1998;23(24):2701-12. [Medline].

  102. Leclerc A, Niedhammer I, Landre MF, et al. One-year predictive factors for various aspects of neck disorders. Spine. Jul 15 1999;24(14):1455-62. [Medline].

  103. Leone M, D''Amico D, Grazzi L, et al. Cervicogenic headache: a critical review of the current diagnostic criteria. Pain. Oct 1998;78(1):1-5. [Medline].

  104. Lord SM, Barnsley L, Bogduk N. Percutaneous radiofrequency neurotomy in the treatment of cervical zygapophysial joint pain: a caution. Neurosurgery. Apr 1995;36(4):732-9. [Medline].

  105. Lord SM, Barnsley L, Wallis BJ, et al. Chronic cervical zygapophysial joint pain after whiplash. A placebo-controlled prevalence study. Spine. Aug 1 1996;21(15):1737-44; discussion 1744-5. [Medline].

  106. Lord SM, Barnsley L, Wallis BJ, et al. Percutaneous radio-frequency neurotomy for chronic cervical zygapophyseal-joint pain. N Engl J Med. Dec 5 1996;335(23):1721-6. [Medline].

  107. McCormack BM, Weinstein PR. Cervical spondylosis. An update. West J Med. Jul-Aug 1996;165(1-2):43-51. [Medline]. [Full Text].

  108. Nederhand MJ, Hermens HJ, IJzerman MJ, et al. Cervical muscle dysfunction in chronic whiplash-associated disorder grade 2: the relevance of the trauma. Spine. May 15 2002;27(10):1056-61. [Medline].

  109. Panjabi M. Whiplash trauma injury mechanism: a biomechanical viewpoint. In: Gunzburg R, Szpalski M, eds. Whiplash Injuries: Current Concepts in Prevention, Diagnosis, and Treatment of the Cervical Whiplash Syndrome. Philadelphia, Pa: Lippincott Williams & Wilkins; 1998.

  110. Panjabi MM, Ito S, Pearson AM, et al. Injury mechanisms of the cervical intervertebral disc during simulated whiplash. Spine. Jun 1 2004;29(11):1217-25. [Medline].

  111. Partheni M. Whiplash Injury Following Car Accident: Rate of Recovery. North American Spine Society, 12th Annual Meeting. 1997.

  112. Pope MH, DeVocht JW. The clinical relevance of biomechanics. Neurol Clin. Feb 1999;17(1):17-41. [Medline].

  113. Radanov BP, di Stefano G, Schnidrig A, et al. Role of psychosocial stress in recovery from common whiplash. Lancet. Sep 21 1991;338(8769):712-5. [Medline].

  114. Saper J. Whiplash: current concepts and treatment strategies. Top Pain Manag. 1996;11:25-7.

  115. Shafaie FF, Wippold FJ 2nd, Gado M, et al. Comparison of computed tomography myelography and magnetic resonance imaging in the evaluation of cervical spondylotic myelopathy and radiculopathy. Spine. Sep 1 1999;24(17):1781-5. [Medline].

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Further Reading

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Keywords

C-spine sprain, C-spine strain, acceleration/deceleration injury, acceleration-deceleration injury, cervical myofascial pain, cervical soft-tissue pain syndrome, cervical sprain, cervicobrachial strain, chronic cervical sprain, chronic cervical strain, chronic neck sprain, chronic neck strain, extension-flexion injury, extension/flexion injury, flexion-extension injury, flexion/extension injury, hyperflexion-hyperextension injury, hyperflexion/hyperextension injury, neck/shoulder girdle soft-tissue injury, neck sprain, neck strain, regional soft-tissue pain syndrome, WAD, whiplash-associated disorders, whiplash syndrome

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Contributor Information and Disclosures

Author

Oregon K Hunter Jr, MD, Physiatrist, Southeastern Rehabilitation Medicine, SIMED
Oregon K Hunter Jr, MD is a member of the following medical societies: American Academy of Pain Management, American Academy of Physical Medicine and Rehabilitation, American Association of Neuromuscular and Electrodiagnostic Medicine, American College of Forensic Examiners, American College of Legal Medicine, American College of Occupational and Environmental Medicine, American Congress of Rehabilitation Medicine, American Medical Association, Florida Medical Association, Florida Society of Physical Medicine and Rehabilitation, International Association for the Study of Pain, International Society of Physical and Rehabilitation Medicine, National Association of Disability Evaluating Professionals, and North American Spine Society
Disclosure: Nothing to disclose.

Coauthor(s)

Michael D Freeman, PhD, MPH, DC, Clinical Associate Professor of Epidemiology, Department of Public Health and Preventive Medicine, Oregon Health Sciences University; Adjunct Associate Professor of Forensic Medicine and Epidemiology, Institute of Forensic Medicine, Faculty of Health Sciences at Aarhus University, Denmark
Michael D Freeman, PhD, MPH, DC is a member of the following medical societies: American Academy of Forensic Sciences, American Academy of Pain Management, American College of Epidemiology, Association for the Advancement of Automotive Medicine, North American Spine Society, and Sigma Xi
Disclosure: Nothing to disclose.

Medical Editor

Martin K Childers, DO, PhD, Associate Professor, Department of Neurology, Wake Forest University Health Services
Martin K Childers, DO, PhD is a member of the following medical societies: American Academy of Physical Medicine and Rehabilitation, American Congress of Rehabilitation Medicine, American Osteopathic Association, Christian Medical & Dental Society, and Federation of American Societies for Experimental Biology
Disclosure: Allergan pharma Consulting fee Consulting

Pharmacy Editor

Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine
Disclosure: eMedicine Salary Employment

Managing Editor

Patrick M Foye, MD, FAAPMR, FAAEM, Associate Professor of Physical Medicine and Rehabilitation, Co-Director of Musculoskeletal Fellowship, Co-Director of Back Pain Clinic, Director of Coccyx Pain Service (Tailbone Pain Service: www.TailboneDoctor.com), University of Medicine and Dentistry of New Jersey, New Jersey Medical School
Patrick M Foye, MD, FAAPMR, FAAEM is a member of the following medical societies: American Academy of Physical Medicine and Rehabilitation, American Association of Neuromuscular and Electrodiagnostic Medicine, Association of Academic Physiatrists, and International Spine Intervention Society
Disclosure: Nothing to disclose.

CME Editor

Kelly L Allen, MD, Regional Medical Director, IMX-Medical Management Services
Disclosure: Nothing to disclose.

Chief Editor

Consuelo T Lorenzo, MD, Consulting Staff, Department of Physical Medicine and Rehabilitation, Alegent Health Care, Immanuel Rehabilitation Center
Consuelo T Lorenzo, MD is a member of the following medical societies: American Academy of Physical Medicine and Rehabilitation
Disclosure: Nothing to disclose.

 
 
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