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Whiplash Injury Diagnosis, Symptoms & Treatment | 2024

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Whiplash Injury Diagnosis, Symptoms & Treatment

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Whiplash injury is an acceleration–deceleration mechanism of energy transfer to the neck. It may result from rear-end or side-impact motor vehicle collisions, but it can also occur through diving and other mishaps. The impact may result in bony or soft tissue injuries (whiplash injury), which in turn may lead to a variety of clinical manifestations.


The Whiplash medical term was introduced in 1928 by the American orthopedist H. E. Crowe, and it was defined as the effects of sudden acceleration–deceleration forces on the neck and upper trunk as a result of external forces exerting a whiplash Crowe emphasized that the term “lash-like effect” describes only the manner in which a head was moved, suddenly to produce a sprain in the neck.

There is little agreement as to the definition of Whiplash-Associated Disorders (WAD injury). Some authors of whiplash articles, such as Gay and Abbot, do not define whiplash clearly. Neither Gotten, nor Macnab offered definitions, although Macnab noted that, a significant soft tissue injury can result from the application of an extension strain to the neck by sudden acceleration.

And Farbman classified the whiplash injury as a musculoligamentous neck sprain, which did not involve nerve root damage, fractures, and other complications. Nordhoff describes the whiplash injury in equally simplistic terms, as an injury that occurs because of occupant motions within a vehicle that is rapidly decelerating or accelerating, without reference to the body parts involved.

See Also: Atlas Fracture

Mechanism of Injury

A number of mechanisms have been proposed that result in a WAD injury. These include:

  1. Motor vehicle accidents (MVAs);
  2. Sporting injuries involving a blow to the head or neck, or a heavy landing;
  3. Pulls and thrusts on the arms;
  4. Falls, landing on the trunk or shoulder.

Perhaps the most common mechanism of WAD injury is the MVA. According to reports, more than 1 million whiplash injuries occur each year in the United States. Eighteen percent of MVAs involving passenger cars in the United States in 1994 were rear-end impacts.

The extent of injury from a WAD following an MVA depends, in part, on three factors:

  1. The position of the head at the point of impact,
  2. The amount of force involved,
  3. The direction of those forces.
Whiplash car accedent
Whiplash injury in Car Accident

Head Position

Pure extension injuries seem to be uncommon in a WAD, because most injuries involve forced combinations of motion. These include a flexion or extension force applied to a rotated head and neck, resulting from a turned position on impact.

As many as 57% of persons sustaining whiplash injury, with symptoms persisting 2 years after collisions, reported having their heads rotated out of the anatomic position at the time of impact. In fact, head position has been reported as the only accident feature of a collision event that has a statistically significant correlation with symptom duration.

Amount of Force

The amount of force applied to the neck is approximately equal to the weight of the head and the speed with which the head moves. Consequently, the heavier the head or the faster it moves, the greater the stress that is put through the neck.

However, it is well recognized by clinicians with any experience with post-MVA patients that some patients who have survived high-velocity accidents do better than many who appear to have been involved in trivial impacts.

Force Direction

Force direction plays a significant role in the degree of damage sustained by the patient. The direction of the applied forces depends on:

  1. where the car is hit, that is, front end, rear end, or side;
  2. symmetry of the impact, that is, directly head on or rear end, or the forward or backward side;
  3. whether the car is pushed ahead into another vehicle, the curb, or other stationary object;
  4. the position of the victim in relation to the impact.

During the early phase of a rear-end collision, the occupant’s trunk is forced upward toward the head, and the cervical spine undergoes a sigmoid deformation, resulting in the head being moved upward and backward. During this motion, at about 100 milliseconds after impact, the lower cervical vertebrae undergo extension, but without translation. This motion causes the vertebral bodies to separate anteriorly and the zygapophyseal joints to impact posteriorly. These forces may lead to posterior dislocations.

The reason for the greater severity of hyperextension injuries over the other force directions is believed to be related to several factors, including:

  1. whether the seat back breaks;
  2. whether the occupant hits the front of the occupant space;
  3. the differential motion between the seat back and occupant;
  4. hyperextension of the neck over the head restraint;
  5. rebound neck flexion as the head rebounds off the head rest.

Hyperflexion injuries are typically less severe because the amount of head excursion is limited by the chin striking the chest. The damage incurred by cervical side-bending traumas depends on whether the head hits an object or the shoulder.

A number of other variables also determine the type and extent of the WAD injury:

  • seat position.
  • occupant size, height, and posture.
  • vehicle interior design.
  • size of vehicle.
  • Sex of driver: Women generally position their seats more forward than men, which places their bodies closer to the front car structures and, therefore, at higher risk of impacting the front interior.
  • Seat belt: The subject of seat belts is controversial, because the seatbelt appears to be responsible for more injuries than any other contact source in the car, albeit minor ones.340 This is, in part, because of their design, which restrains only one shoulder, and because the belt acts as a fulcrum for energy concentration on the occupant.
  • Headrest height: Headrest height appears to play a role, with the driver often setting the head rest too low, or sitting too far forward to obtain adequate support from the head rest. However, the fatal accidents involving hyperextension appear to occur in the absence of a head restraint, where there is no structural limitation to the head movement except anatomic structures.
Whiplash Associated Disorder

Clinical Findings

It should be obvious that a meticulous examination of the traumatized patient is of paramount importance. Signs and symptoms to alert the clinician include:

  • Upper motor neuron signs and symptoms;
  • periodic loss of consciousness
  • that the patient does not move the neck, even slightly (fractured dens);
  • painful weakness of the neck muscles (fracture);
  • gentle traction and compression of the neck that are painful (fracture);
  • severe muscle spasm (fracture);
  • complaints of dizziness.

Interscapular area and neck pain after car accident usually seen within a few hours of the WAD injury.

See Also: Occipital Condyle Fractures

Sources of Symptoms

The causes for symptoms following a whiplash injury are numerous. The resulting damage from a WAD injury can include an injury to one or more of the following types of structures:

Soft tissue structures

A cervical strain may be produced by an overload injury to the cervical muscle– tendon unit because of excessive forces. These forces can result in the elongation and tearing of muscles or ligaments, edema, hemorrhage, and inflammation. Many cervical muscles do not terminate in tendons but, instead, attach directly to bone by myofascial tissue that blends into the periosteum. Muscles respond to injury in a variety of ways, including reflex contraction, which further increases the resistance to stretch and serves as a protection to the injured muscle.

Joint capsule and ligaments

Both mechanoreceptors and nociceptors have been identified in the human cervical joint capsule and ligaments, indicating a neural input in pain sensation and proprioception. Postmortem studies have found that after whiplash injury, ligamentous injuries are extremely common in the cervical spine, but that herniation of the NP is a rare event.

The motion segment lesions found in the cervical spine included bruising and hemorrhage of the uncinate region, the so-called rim lesions or transections of the anterior annulus fibrosus, rupture of the alar ligaments, and avulsions of the vertebral end plate. As in the lumbar spine, the outer layers of the cervical annulus are innervated, and are, therefore, a reasonable source of pain.

Zygapophyseal joint

Fractures or contusions of the zygapophyseal joints can occur, although postmortem studies reveal that many of these injuries are undetectable by plain radiographs. Zygapophyseal joint pain is the only basis for chronic neck pain after whiplash that has been subjected to scientific scrutiny. However, it cannot be diagnosed clinically or by medical imaging. The diagnosis relies on fluoroscopically guided, controlled diagnostic blocks of the painful joint.

Although there is uncertainty about the exact pathway that elicits neck pain, the cervical zygapophyseal joint has been identified as a source of pain in between 25 and 65% of people with neck pain. Specifically, the prevalence of lower cervical facet joint pain has been reported to be 49%. It is worth remembering that although the so-called neck sprains from MVAs usually involve the cervical spine, one of the upper eight thoracic spinal joints is sometimes found to be affected, so these structures should be assessed in the examination of a whiplash injury.

Central or peripheral neurologic systems

These systems may be injured secondary to traction, impingement, hemorrhage, avulsion, or concussion. Although neck pain and headache are the two most common symptoms of a whiplash injury, other symptoms such as visual disturbances, balance disorders, and altered cerebral function are reported.

Abnormal peripheral vestibular function was found using platform posturography in about 90% of the 48 patients examined by Chester. Fractures and dislocations, many causing cord damage, have been demonstrated on human victims of hyperextension injuries, who had no radiographic evidence of the severity of these lesions.

Intervertebral disk

Experimental and clinical studies have consistently demonstrated how poorly and slowly disk lesions heal after a hyperextension trauma, with very small lesions taking as long as 18 months to heal. A follow up study, averaging a review time of nearly 11 years, found that 40% of patients were still having intrusive or severe symptoms (12% severe and 28% intrusive). The same study also found that in general, there is no alter in neck pain 2 years after car accident.

Posterior (dorsal) root ganglia

Vascular structures (vertebrobasilar arteries)

Postmortem studies have shown that vertebral artery lesions are found in about one-third of fatally injured MVA victims with vertebral atlas injury.

Visceral structures (secondary to ruptures, or contusions)

The physical examination usually reveals tenderness over the transverse and spinous processes, or over the anterior vertebral body, depending on the structures involved. Depending on the severity of the strain, motion can be markedly restricted as a result of muscle guarding. Other than perhaps to screen for possible fractures, there is no valid indication for medical imaging after whiplash, unless the patient has neurologic signs.

Findings on plain films are typically normal, although there may be a loss of the cervical lordosis. MRI reveals nothing but age-related changes with the same prevalence as in asymptomatic individuals. An enticing, but small, recent study suggests that, in patients with persisting acute neck pain, single photon emission computed tomography, at 4 weeks after injury revealed occult, small fractures of the vertebral rims or the synovial joints of the neck.

Whiplash Treatment

Once the physician has ruled out the possibility of fracture, dislocation, IVD injury, or neurovascular compromise, a conservative Whiplash injury treatment is recommended.

Whiplash Injury Treatment include the following:

  1. Initially, brief use of a cervical collar may be prescribed to reduce muscle guarding.
  2. Bed rest, along with analgesics and muscle relaxants, for no more than 2–3 days is prescribed for patients with a severe injury. However, in less severe cases, bed rest has not been shown to improve recovery and, when compared with mobilization or patient education, rest tends to prolong symptoms.
  3. Ice and electrical stimulation are applied to the neck during the first 48–72 hours to help control pain and inflammation.
  4. Range-of-motion exercises in the pain-free ranges of flexion and rotation are initiated as early as possible to reduce the likelihood of hypomobility. Gentle cervical isometrics also are introduced. Aggressive strengthening of the cervical musculature should not begin until full range of motion is restored. Strengthening of the trapezius muscle and other scapular stabilizers can be performed using upper extremity exercises, taking care to avoid an increase in symptoms.

Many patients improve within 8 weeks, although complete resolution is less common. If pain persists for more than months, more severe ligamentous, disk, associated zygapophyseal joint injuries, or other factors should be suspected. If significant neck pain persists past 6–8 weeks, flexion and extension radiographs may be useful to exclude, or confirm, instability.

The majority of studies reveal that, although most patients with WAD injury have a spontaneous resolution of symptoms, a small subgroup of patients are symptomatic beyond 1 year.

Whiplash Disability Questionnaire

Download Whiplash Disability Questionnaire PDF File

References & More

  1. Dutton’s Orthopaedic Examination, Evaluation, And Intervention 3rd Edition.
  2. GAY JR, ABBOTT KH. Common whiplash injuries of the neck. J Am Med Assoc. 1953 Aug 29;152(18):1698-704. doi: 10.1001/jama.1953.03690180020006. PMID: 13069244.
  3. Spitzer WO, Skovron ML, Salmi LR, et al: Scientific monograph of the Quebec Task Force on Whiplash-Associated Disorders: Redefining 20:[Erratum, Spine 1995;20: Spine and its management. ,, whiplash ,, 2372], 1995.
  4. Evans RW: Some observations on whiplash injuries. Neurol Clin 10:975– 997, 1992.
  5. Ferrari R, Russell AS: Epidemiology of whiplash: An international dilemma. Ann Rheum Dis 58:1–5, 1999.
  6. Gotten N: Survey of 100 cases of whiplash injury after settlement of litigation. JAMA 162:854–857, 1956.
  7. Macnab I: The whiplash syndrome. Orthop Clin North Am 2:389–403, 1971.
  8. Nordhoff LS Jr: Cervical trauma following motor vehicle collisions. In: Murphy DR, ed. Cervical Spine Syndromes. New York, NY: McGrawHill, 2000:131–150.
  9. Scientific monograph of the quebec task force on whiplash-associated disorders. Spine 20:33S, 38S–39S, 1995.
  10. National Highway Traffic Safety Administration: Traffic Safety Facts 1994: A Compilation of Motor Vehicle Crash Data from the Fatal Accident Reporting System and the General Estimates System. Washington, DC: National Highway Traffic Safety Administration, 1995.
  11. Pennie B, Agambar L: Patterns of injury and recovery in whiplash. Injury 22:57–60, 1991.
  12. Sturzenegger M, Radanov BP, DiStefano G: The effect of accident mechanisms and initial findings on the long-term course of whiplash injury. J Neurol 242:443–449, 1995.
  13. Nikolai MD, Teasell R: Whiplash: The evidence for an organic etiology. Arch Neurol 57:590–591, 2000.
  14. Carrette S: Whiplash injury and chronic neck pain. N Engl J Med 330:1083–1084, 1994.
  15. Morris F: Do headrests protect the neck from whiplash injuries? Arch Emerg Med 6:17–21, 1989.
  16. Maimaris C, Barnes MR, Allen MJ: Whiplash injuries of the neck: A retrospective study. Injury 19:393–396, 1988.
  17. Grob D: Posterior surgery. In: Gunzburg R, Szpalski M, eds. Whiplash Injuries: Current Concepts in Prevention, Diagnosis and Treatment of the Cervical Whiplash Syndrome. Philadelphia: Lippincott-Raven Publishers, 1998:241–246.
  18. Jonsson H, Cesarini K, Sahlstedt B, et al: Findings and outcomes in whiplash-type neck distortions. Spine 19:2733–2743, 1994.
  19. Twomey LT, Taylor JR: The whiplash syndrome: Pathology and physical treatment. J Manual Manipulative Ther 1:26–29, 1993.
  20. Kaneoka K, Ono K, Inami S, et al: Motion analysis of cervical vertebrae during whiplash loading. Spine 24:763–769, 1999.
  21. Barnsley L, Lord S, Bogduk N: The pathophysiology of whiplash. In: Malanga GA, ed. Cervical Flexion-Extension/Whiplash Injuries. Spine: State of the Art Reviews. Philadelphia, PA: Hanley & Belfus, 1998:209– 242.
  22. Winkelstein B, Nightingale RW, Richardson WJ, et al: The cervical facet capsule and its role in whiplash injury: a biomechanical investigation. Spine 25:1238–1246, 2000.
  23. Lord SM, Barnsley L, Wallis BJ, et al: Chronic cervical zygapophyseal joint pain after whiplash: A placebo-controlled prevalence study. Spine 21:1737–1744, 1996.
  24. Livingston M: Common Whiplash Injury: A Modern Epidemic. Springfield, IL: Charles C Thomas, 1999.
  25. Viktrup L, Knudsen GM, Hansen SH: Delayed onset of fatal basilar thrombotic embolus after whiplash injury. Stroke 26:2194–2196, 1995.
  26. Ronnen HR, de Korte PJ, Brink PRG, et al: Acute whiplash injury: Is there a role for MR imaging? A prospective study of 100 patients. Radiology 201:93–96, 1996.
  27. Ellertsson AB, Sigurjonsson K, Thorsteinsson T: Clinical and radiographic study of 100 cases of whiplash injury. Acta Neurol Scand 57:269, 1978.
  28. Stovner LJ: The nosologic status of the whiplash syndrome: A critical review based on a methodological approach. Spine 21:2735–2746, 1996.
  29. Whiplash Disability Questionnaire. (From Pinfold M, Niere KR, O’Leary EF, et al: Validity and internal consistency of a whiplash-specific disability measure, Spine 29[3]:263–268, 2004.)
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