Biomechanics of Minor Automobile Accidents (printer-friendly)

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www.medscape.com Abstract and Introduction

Abstract

Biomedical experimental data indicate that automobile accidents with no vehicle damage are unlikely to cause injury to the occupants. Soft tissue injuries heal in a few weeks. Chronic pain has never been produced by experimental injury and is much less common in countries without financial payments for accident victims. Chronic pain after no-damage collisions is probably caused by psychologic factors. Psychologic treatment should be added to conventional nonoperative treatment when no objective explanation for chronic symptoms is found.
Introduction

Whiplash is a term commonly used to describe the motion of and injuries to the neck of an occupant in an automobile that sustains an impact from the rear. This neck motion is complex and includes shear, tension, head rotation, and extension followed by flexion.[1] True whiplash describes a wave motion traveling down a tapered whip and creating a sonic boom, and does not describe neck motion at all.[1] Neck injuries from rear-end impacts are a significant problem in the United States and, including litigation, cost more than $29 billion per year.[2] Rear-end impact is most likely to injure the neck, since the thoracic and lumbar spine is protected by the seat and restraints. Unless a headrest is present, hyperextension is prevented only by facet joints, ligaments, and to a lesser extent, muscles and other soft tissues. In front-end impact, the seat/shoulder belt protects the neck less than the lumbar area, while the thoracic area is most protected by the combination of the ribs and a seat/shoulder belt. The neck is less vulnerable in flexion than extension because of a larger range of motion, limitation by chin hitting chest, and muscles and ligaments being farther from the pivot point at the back of the head.[1] Degeneration of a disk (due to the aging process) precedes herniation of a disk.[3,4] About one third of lumbar magnetic resonance imaging (MRI) scans on subjects who had never had low back or leg pain showed disk herniations or spinal stenosis.[5] Therefore, an abnormality found on MRI must be strictly correlated with age and clinical signs and symptoms before conclusions are made.[5] Disk bulges, protrusions, and herniations are found on lumbar MRI[6] in 80% of asymptomatic patients, which is consistent with the degenerative etiology of disk abnormality. Disk herniations are uncommon in front and side impact automobile accidents severe enough to cause other serious spinal injuries.[7-10] In laboratory spinal testing, pure compression, torsion, and flexion do not result in disk herniation.[4,11] Only a combination of lateral bending, hyperflexion, and severe compression can sometimes cause disk herniation.[11] This combination can occur in the lumbar disks during heavy lifting, but rarely occurs anywhere in the spine during automobile accidents. Herniation of a degenerated disk frequently occurs without injury. Although an automobile accident is an unlikely cause of disk herniation, an automobile accident could cause herniation of a previously degenerated disk. Comparison of preinjury and postinjury MRI can objectively determine what abnormality is due to the injury. Otherwise, disk abnormality should be attributed to an automobile accident only if it is of a type not normally seen in the aging process, or if there is neural compression on MRI and appropriate localized new symptoms or objective findings. For a given occupant and vehicles, likelihood of injury increases as the speed of the impacting vehicle increases. Likelihood of injury to the occupant is also affected by various internal and external factors. Internal factors include the occupant's sex, weight, height, age, and musculature, as well as preexisting arthritis. External factors include the relative mass and velocity of vehicles, as well as the type of bumper, restraint system, headrest, and seat.
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Biomechanics of Minor Automobile Accidents (printer-friendly)

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The principle of conservation of momentum indicates that when two automobiles collide, the mass (m) of one vehicle times its change in velocity (DV) equals the product of m and DV for the other vehicle (m1 DV1 = m2 DV2). Knowing the masses of each car, accident reconstructionists use computer programs to calculate DV from car damage data; DV is used to evaluate the potential for occupant injury.[12] Potential for injury is proportional to energy absorbed by the body. Kinetic energy (E= 1/2 MV2) goes up at the rate of occupant velocity squared. The vehicle and occupant experience the same DV, but occupant and body segments experience different accelerations and displacements related to various internal and external factors.[12] In automobile accidents, the most vulnerable situation is a car hit from the rear, and the most vulnerable area of the spine is the occupant's neck. This situation has been studied using volunteers in automobiles hit from the rear by other automobiles. In a study by West et al,[13] cars traveling less than 5 mph impacting the rear of a stationary vehicle did not cause damage to vehicles, and the occupants had no symptoms. Slightly higher impact speeds caused damage to the stationary vehicle, yet the occupants still had no symptoms.[13] In a study by Szabo et al,[14] vehicles traveling at approximately 10 mph struck the rear of stationary vehicles of 5 volunteers; this caused DV of 5 mph of the rear-ended vehicle but no spinal pain in the volunteers during the subsequent year. Also, there were no changes on comparison preimpact and postimpact cervical and lumbar MRI scans in male and female volunteers up to 58 years old, some of whom had degenerative changes on MRI.[14] Castro et al[15] studied rearend impacts on 19 volunteers with DV between 5.4 and 8.8 mph; they found no signs of injury on physical examination or preimpact and postimpact MRI. In another study, seven volunteers up to age 59, some of whom had degenerative changes on cervical x-ray films, were subjected to rear-end collisions.[16] At DV less than 5 mph, car occupants experienced no neck pain; DV of 5.1 to 6.8 mph caused some neck pain lasting less than 3 days but with no long-term symptoms.[16] Neck flexion and extension after impact were less than the normal range.[16] Seven volunteers in vans and pickup trucks in 25 front and rear collisions with DV up to 6.8 mph and 5.6 mph respectively had no spinal pain.[17] The studies of Szabo et al[14] and Castro et al[15] indicate that thresholds of injury hold in the presence of arthritis. Patients with soft tissue injury and arthritis had rapid healing of soft tissue injury, as did those without evidence of arthritis.[16] Short-term symptoms did not result in chronic pain in any of the studies. Watts et al[1] reviewed the literature and concluded that a driver with headrest support can survive impacts of 40 mph and acceleration of 40 g's. Studies of normal volunteers with lax muscles in rear-end impacts indicate a DV of 6.8 mph can be tolerated without a headrest, and with a headrest a DV of 10 mph sometimes causes minor temporary (hours or days) pain.[1] Automobiles are designed to collapse on impact to decrease the likelihood of serious injury in high-speed impacts. This collapse, however, can result in large repair bills in low-speed collisions. Initiation of permanent frame damage can occur at very low impact speeds (about 1 mph into a rigid barrier). The soft side and upper panels can initiate damage even more easily.[1] Manufacturers are required by the government to provide bumpers with no damage at DV of 2.5 mph.[1] Bumper impacts at 5 mph DV on many 1997-1998 cars revealed all sustained some damage and most sustained substantial damage.[18] Nielson et al[17] found the threshold of bumper damage DV was between 3.4 and 5.4 mph. The threshold for spinal injury of an occupant is usually higher than the threshold for vehicle damage. Two thousand volunteer collisions have never produced chronic neck symptoms.[19] Collisions with no vehicle damage would usually not cause neck damage and would be even less likely to cause chronic symptoms. Psychologic factors are important in any discussion of the subjective phenomenon known as pain. In one study, Vietnamese patients were given only a 30th of the amount of morphine postoperatively as American patients for the same
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Biomechanics of Minor Automobile Accidents (printer-friendly)

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orthopaedic procedure, and yet 10 times fewer of the Vietnamese patients considered their pain control inadequate. The authors of this study believe that pain depends less on tissue injury than on cultural norms and patient expectations.[20] In Lithuania, where car insurance and lawsuits are rare, 202 people involved in rear-end collisions were studied; none were disabled, and at an average of 22 months after injury, the prevalence of neck pain was the same as that in an age- and sex-matched control group of 202 individuals without history of injury.[21] Lawsuits and associated potential financial gain prolong and increase the severity of symptoms.[22-26] In several other countries, neck symptoms from automobile accidents resolve in 3 to 6 weeks, and the risk of chronic pain is no greater than in the otherwise healthy general population.[27] Chronic neck pain rarely occurs in the offending driver in the United States or after athletic activities in which acute neck sprains are common.[27] Cassidy et al[28] found that elimination of compensation for pain and suffering is associated with a decreased incidence and improved prognosis of whiplash injury. They concluded that insurance has a profound effect on frequency and duration of whiplash claims and that claimants recover faster if compensation for pain and suffering is not available.[28] Ferrari and Russel[27] gave an overview in their discussion of the whiplash literature review by Freeman et al.[2] Ferrari and Russel[27] stated that chronic damage does not explain chronic symptoms; psychologic and social factors create the setting of expectation of chronic pain and hypervigilance for symptoms and promote symptom amplification. Psychologic stress can cause pain by increasing muscle tension, sympathetic nerve activity, and muscle ischemia, which together cause a painful vicious cycle.[29,30] The longer the pain lasts after an injury, the more the psychologic factors predominate and the more psychologic modalities should be used in treatment.[29,31,32] Failure to appreciate and treat the psychologic component of chronic pain can lead to multiple unsuccessful operations.[33,34] Inconsistencies, unphysiologic history, and physical examination can alert the physician soon after injury to the presence of psychologic causes of pain.[31,35] The pathophysiology of cervical disk disease is the same as in other areas of the spine.[36] There are differences in the anatomy and biomechanics of the cervical and lumbar spine. The psychologic aspects of chronic pain are similar for various anatomic locations. For this reason, references regarding psychologic aspects of chronic low back pain are believed to be relevant to psychologic aspects of chronic neck pain. Cognitive-behavioral techniques have been found to be helpful in treating chronic spinal pain.[29,37,38] These techniques can be used successfully by the treating orthopaedic surgeon in a support group that meets in the office.[38] Psychologic counseling by psychologists or psychiatrists can help patients with major psychologic issues.[29] Cognitive-behavioral therapy is based on the idea that our feelings are not determined by what happens to us but how we react to what happens. If we want to change how we feel, we have to change how we react. This is done by changing the way we interpret events (cognition) and/or by changing how we act (behavior). Behavioral therapy for pain would include various relaxation techniques: meditation, self-hypnosis, affirmations, and guided imagery. The assumption is that by acting as if we are relaxed and peaceful, we will soon feel that way.[29,30] Conditioning exercise and activities that are of service to others (especially volunteer work) decrease depression and improve self-esteem. Patients with chronic pain are usually convinced that there is nothing they or anyone else can do to help the pain (helplessness and hopelessness). Cognitive therapy teaches that if we feel bad, we should look for the beliefs and attitudes that cause these feelings, and decide whether we are willing to give up these stress-producing beliefs for ones that are not. The following are examples of stress-relieving beliefs: 1. My beliefs determine how I react to events. 2. If I don't like how I feel, I can change my beliefs. 3. Everything is exactly as it should be, including my desire to change it.[39]

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Biomechanics of Minor Automobile Accidents (printer-friendly)

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Number 1 engenders responsibility and hope; No. 2 is empowering; No. 3 promotes humility and forgiveness of self and others, which increases peace of mind. Cognitive-behavioral therapy does not eliminate pain, but it improves quality of life and diminishes pain.[29,38] These psychologic techniques should be integrated with the usual conservative measures, including nonnarcotic pain medication, antidepressants, stretching and strengthening exercise, and education about pain. When no objective explanation for chronic symptoms is found, the combination of psychologic modalities and these conservative measures should be used to treat chronic spinal pain after automobile accidents that cause no damage to the occupant's car.
References

1. Watts AJ, Atkinson DR, Hennessy CJ: Low Speed Automobile Accidents. Tuscon, Ariz, Lawyer and Judges Publishing Co, 1996 2. Freeman MD, Croft AC, Rossignol AM, et al: A review and methodologic critique of the literature refuting whiplash syndrome. Spine 24:86-98, 1999 3. Osti OL, Vernon-Roberts B, Fraser DD: Annulus tears and intervertebral herniation. Spine 15:762-767, 1990 4. Roaf R: A study of the mechanics of spinal injuries. J Bone Joint Surg Br 42:822, 1960 5. Boden SD, Davis DO, Dina TS, et al: Abnormal magnetic-resonance scans of the lumbar spine in asymptomatic subjects. J Bone Joint Surg Am 72:403-408, 1990 6. Jensen MC, Brant-Zawadzki MN, Obuchowski N, et al: Magnetic resonance imaging of lumbar spine in people without back pain. N Engl J Med 331:69, 1994 7. Anderson PA, Rivara FP, Maier RV, et al: The epidemiology of seat belt associated injuries. J Trauma 31:60-67, 1991 8. Newman KD, Bowman LM, Eichelberger MR, et al: The lap belt complex. J Trauma 30:1133-1140, 1990 9. Hendey GW, Votey SR: Injuries in restrained motor vehicle accident victims. Ann Emerg Med 24:77-84, 1994 10. Mackey GM, Hill J, Parkin S, et al: Restrained occupants in non-struck side of lateral collisions. Accident Analysis Prevention 25:147-152, 1993 11. Adams MA, Hutton WC: Prolapsed intervertebral disc. a hyperflexion injury. Spine 7:184-191, 1982 12. Robinette RD, Fay RJ, Paulsen RE: Delta-V: basic concepts, computational methods and misunderstandings. Society of Automotive Engineers (SAE) Tech Paper Series 940915, 1994, pp 309-321 13. West DH, Gough JP, Harper TK: Low speed rear-end collision testing using human subjects. Accident Reconstruction J 5:22-26, 1993 14. Szabo TJ, Welcher JM, Anderson RA, et al: Human occupant kinematic response to low speed rear-end impacts. Society of Automotive Engineers Tech Paper Series 940532, 1994, pp 23-25 15. Castro WHM, Schilgon M, Meyer S, et al: Do whiplash injuries occur in low-speed rear-end impacts? Eur Spine J 6:366-375, 1997 16. McConnell WE, Howard RD, Poppel JV, et al: Human head and neck kinematics after low velocity rear-end impacts -- understanding "whiplash." SAE Tech Paper Series 952724, 1995, pp 215-238 17. Nielson GP, Gough JP, Little DM, et al: Human subject responses to repeated low speed impacts using utility vehicles. SAE Tech Paper Series 952724, 1997, pp 184-212 18. Stewart K (ed): Damage repair costs in low-speed crash tests at 5 mph. Status report. Insurance Institute for Highway Safety, Arlington, Va 33:5, 1998 19. Ferrari R, Russell AS: The whiplash syndrome; common sense revisited. J Rheumatol 24:618-622, 1997 20. Carragee EJ, Vittum D, Truong, TP, et al: Pain control and cultural norms and expectations after closed femoral shaft fractures. Am J Orthop 28:97-102, 1999 21. Shrader H, Obelieniene D, Bovim C, et al: Natural evolution of late whiplash syndrome outside the medicolegal context. Lancet 347:1207, 1996 22. Brand P, Yancey P: Pain. The Gift Nobody Wants. New York, Harper Collins Publisher, 1993, pp 243,244,270
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23. Fisbain DA, Rosomoff HL, Cutler RB: Secondary gain concept: a review of scientific evidence. Clin J Pain 11:6-21, 1995 24. Greenough CG: Recovery from low back injury. J Bone Joint Surg Br 76:859-860, 1994 25. Hayes B, Solyom CAE, Wing PC, et al: Use of psychometric measures and non-organic signs testing and detecting non-organic disorders in low back pain patients. Spine 18:1254-1262, 1993 26. Weisel W, Feffer HL, Borestein DG, et al: Low Back Pain. Charlottesville, Va, Michie Co, 1989, p 596 27. Feffari R, Russell AS: Whiplash; heading for a higher ground. Spine 24:97-98, 1999 28. Cassidy JD, Carroll LJ, Cote P, et al: Effect of eliminating compensation for pain and suffering on the outcome of insurance claims for whiplash injury. N Engl J Med 342:1179-1186, 2000 29. Sola AE: Textbook of Pain. Wall PW, Melzack R (eds). New York, Churchill-Livingstone, 1989 30. Sarno JE: The Mindbody Prescription, Healing the Body, Healing the Pain. New York, Warner Books, 1998, p 48 31. Waddell G, Main C, Morris E, et al: Chronic low back pain, psychological distress and illness behavior. Spine 9:209-215, 1984 32. Spengler D: Low Back Pain. New York, Grune & Stratton, 1982 33. Lee PN, Chow SP, Lieh-Mak F, et al: Psychosocial factors influencing outcome in patients with low back pain. Spine 14:838-843, 1989 34. American Medical Association Guide to Evaluation of Physical Impairment. Chicago, American Medical Association, 3rd Ed, 1988, pp 247-252 35. Waddell G, McCullock JA, Mamel E, et al: Non-organic physical signs in low back pain. Spine 5:117-125, 1980 36. Wood GW: Cervical disc disease. Campbell's Operative Orthopaedics. Canale ST (ed). St. Louis, CV Mosby Co, 1998, p 3038 37. Turner JA: Educational and behavioral interventions for back pain in primary care. Spine 21:2851-2959, 1996 38. Laborde JM: Cognitive-behavioral techniques in the treatment of chronic low back pain. JSOA 7:81-85, 1998 39. Davis M, Eshelman ER, McKay M: The Relaxation and Stress Reduction Workbook. Oakland, Calif, New Harbinger Publications, 14th Ed, 1997

Reprint Address Reprint requests to J. Monroe Laborde, MD, MS, 3525 Prytania St, Suite 402, New Orleans, LA 70115. J South Orthop Assoc. 2000;9(3) 2000 Southern Medical Association

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