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April 2005, Vol. 15, Iss. 2

Table of Contents

Altered Cervical Lordosis and DJDChiropractor Invents Car Seat HeadpieceDACBRs Cause Professional Embarrassment at RACEight Major Aberrant Forms of the Lumbo-Pelvic SpineEuropean Spine Journal to Publish 6th CBP® Clinical Control TrialEvidence Based or NotGlutamate/Aspartame - Pain and Your BrainGreg Buchanan Donates $30,000 to CBP® NonprofitInappropriate Characterization of CBP® TechniqueMissed Appointments and Patient EducationMoney, Taxes, Life and PracticePalmer College Takes Alumni Group to CourtPosturePrint™ Research with ICAPresenting Defendable Care Options to PatientsPublished Papers Near 81Resign or be TerminatedThermography: Renewed InterestUsing Silence to CommunicateWhiplash Injuries: Pathophysiology, Diagnosis, Medical Management and Prognosis

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Whiplash Injuries: Pathophysiology, Diagnosis, Medical Management and Prognosis

By Rene Cailliet, MD

 

 

 

         

               The term “whiplash” was first introduced by an American orthopedist, Dr. H.E. Crowe (1928) when he described the syndrome as a tissue insult from a sudden acceleration-deceleration force,1  but thirty-six years later2 he stated, “This expression was intended to be a description of motion and not a disease which it has been so termed by physicians, patients and attorneys.” As ultimately there were so many injuries to the cervical spine sustained from vehicular accidents, a Canadian Task Force (1995) on Whiplash-Associated Disorders was created.3 They defined Whiplash injuries as “An acceleration-deceleration mechanism of energy transfer to the neck which may result from rear end or side impact, predominantly in motor vehicle collisions but also from diving accidents or other mishaps.

              In spite of the frequency of whiplash injuries, the medical literature remains sparse. A review of an article in Muscle Nerve Journal4 reviewed the medical literature from 1995 and claimed that only 20 papers had methodological significance. Most were papers without scientific data and/or single case reports. These articles claimed that the diagnosis of Whiplash was exclusively clinical with no confirmation based on specific imaging studies or with any physiological basis. Treatment results are not dependent on the modalities used. Acute care using a collar or any form of immobilization does not shorten the duration of neck pain.  The summary of the Stapp Car Conference held in October 1967 stated that the mechanics of whiplash were not clear and that animal simulations did not correlate.

              An editorial in the Spine Journal in year 20012 even questioned the existence and verification of the whiplash syndrome asking “what is a whiplash injury” and “how do we measure the clinical picture of whiplash associated disorders”? This editorial alluded to the influence of cultural, social and psychological factors being predominant in the syndrome and its sequelae         

              Malleson3 termed Whiplash a “Useful and Fashionable Illness”. He accepted the physiological factors of the injury but refuted the validity of chronic, persistent disabling pain considering the injury as a convenient diagnosis “masking depression”. Neck sprain poses a difficult diagnostic problem as there are no objective diagnostic findings.

               Denny-Brown and Russell4 demonstrated that acceleration-deceleration forces could cause brain damage even in the  absence of direct head trauma as an  affect of contra-coup of the brain within the skull. Ian Macnab, a prominent orthopedic surgeon from Toronto (1971), stated, “the client incapacitated by subjective symptoms, the existence of which could neither be proved or disproved was manna for the plaintiff’s attorney and represented a pain vacation for the unscrupulous patient...more disabled by the diagnosis than be the injury.”5 By statements like this from prominent physicians culpability was introduced as was litigation potential.

              The Quebec Task Force suggested the following classification as to the severity of a whiplash injury:

              Grade O: Whiplash exposure but no pain, no symptoms and no signs      

              Grade 1: Delayed neck pain, minor stiffness, non-focal tenderness only, and no physical signs.

              Grade 2: Early neck pain, focal neck tenderness, spasm, stiffness and radiating symptoms.

              Grade 3: Early onset of neck pain, focal  neck tenderness, spasm, stiffness, radiating symptoms and evidence of neurological deficit.

              Grade 4: Neck complaints (like Grade 2 or 3)  and  fracture dislocation.

              These grades except 3 and 4 are all subjective.  The ambiguity of the definition using terms such as “stiffness,” “spasm,” “focal tenderness” and “radiating symptoms” beg definition. The acute phase of a cervical injury is not confirmable by clinical examination, nor by radiological studies including magnetic resonance studies (MRI) or CT Scanning as these latter studies fail to identify soft tissue changes.

              With such vague terminology, a prognosis cannot be valued and the literature has been non-specific. The value of a treatment protocol is also questioned as the basis of any treatment remains unclear.6, 7  Further studies are necessary to verify more objective findings to clarify the symptomatology and the impairment  claimed.  More recent studies using electromyographic findings8 using mean peak normalized EMG amplitude of cervical muscles have implicated the specific  muscles involved in lateral and rotational forces upon the neck.

              Recently, there have been numerous articles in the medical literature upon a subject that was once ignored or denied. In 1990, April and Bogduk9 postulated that the facet joints were traumatized during a phase of whiplash and were the site of the resultant pain. While the mechanism of facet trauma appeared to be excessive flexion-extension,  L. Penning (1995) postulated that an “S” shape of the cervical spine occurred during the whiplash injury while the vertebral bodies were horizontal and underwent shear, thus damaging the facet surfaces.10 In 2001, Siegmond refuted that claim11 but offered no other mechanism and Panjabi et al again restated that shear mechanism was the culprit causing facet damage.12

              The mechanism of facet damage and cinematographic studies of the spine in simulated whiplash now have verified the shear forces. Pain is now considered to result from inflammatory cytokine liberated as they have been found to exist in degenerative disorders.13  As pain is the early and persistent complaint of patients suffering from a whiplash insult the facets and their inflammation are now known as the site and justifies anti-inflammatory medication and steroid injections into the joints.

              After a whiplash injury, neck pain is predominant and needs attention early in the treatment protocol. The earliest tissue reaction to the whiplash injury is muscular and thus the predominant site of pain. Muscle contraction termed  “spasm” is isometric contraction of skeletal  muscles that unleash several other tissue reactions such as facet compression and shear. All are factors in causing whiplash symptomatology and require attention. The pathophysiology of whiplash injury is gradually unfolding.

REFERENCES:

              1. Crowe HE. Injuries to the cervical spine. Paper presented at a meeting of the Western Orthopedic Association  San Francisco 1928.

              2. Crowe HE. 1984 . A new diagnostic sign in neck injuries.  California Med.,  100:12-3.

              3. Scientific Monograph of the Quebec Task Force on Whiplash-Associated Disorders: Redefining  “Whip[lash” and its Management.  Cassidy JD (Ed),  DSpine

1995:20:1S-735.

              4. Denny-Brown D, Russell R (1941) Experimental cerebral concussion. Brain, 647-164. 

              5. Macnab I. (1971) Acceleration injuries of the cervical spine.  J. Bone Joint Surg. 2:389-403.

              6. Rodriquez AA, Barr KP, Burns SP. Whiplash: pathophysiology, diagnosis, treatment and prognosis. Muscle Nerve. 2004 Jun; 29(6):768-81.

              7. Ferrari R.  The Many Facets of Whiplash (Editorial), Spine 26:19:2001, pp 2063-2064

              8. Kumar S, Ferrari R, Narayan Y. Cervical Muscle Response to Head Rotation in Whiplash Type Left Lateral Impacts,  Spine 10:5, 2005 pp 536-541.

              9. April , Dwer A, Bogduk N. Cervical zygapophyseal joint pain patterns II: A clinical evaluation.  Spine 1990;15:458-461.

              10. Penning L. Kinematics of cervical spine injuries. A functional radiological hypothesis.  Eur Spine J., 1995;4(2): 126-32.

              11. Siegmond GP, Myers BS, Davis MB, Bohnet HF, Winkelstein  BA.  Mechanical evidence of the cervical facet capsule injury during whiplash: a cadaveric study using combined shear, compression and extension.  Spine 2001;26(19):2063-64.

              12. Panjabi MM, Ito S, Pearson AM, Ivancic PC. Injury mjechanisms of the cervical intervertebral disc during simulated whiplash.  Spine 2004;29(11):1217-1225.

              13. Ha KY, Chang CV-H, Kim K-W, Kim Y-S, Na K-H, Lee J-S. Expression of Estrogen Receptor of the Facet Joints in Degenerative Spondylolisthesis.  Spine 30:(5) 2005, pp 562-566.

           14. Falla DL, Jull GA, Hodges PW.  Patients With Neck Pain Demonstrate Reduced Electromyographic Activity of the Deep Cervical Flexor Muscles  During Performance of the Craniocervical Flexion Test.  Spine 29;19: 2004,  2108-2114.

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