Take a look at the Recent articles

Abstract

Background: The Neck Pain Task Force (NPTF) invites a constructive dialogue on how to best decrease the personal and societal burden of neck pain and its associated disorders. A critical review of the NPTF own literature synthesis on the onset and epidemiology of whiplash associated disorders (WAD) is well suited to ascertain whether the NPTP has achieved its stated goal concerning linking onset, course and care of a condition which contrasting views are no less conflicting now than almost seventy years ago.

Discussion: The NPTP review of possible mechanisms of injury to the neck is not trustworthy. Firstly, the NPTF choose to skip all research, expect 2 experimental studies. Secondly, the NPTF then states that the current evidence does not allow us to draw any conclusions about a specific injury mechanism if one exists. A literature review was conducted by the author on this issue, within the frame of NPTF literature review period, 1980-2006, which showed remarkable consistency both across different methodologies and different research teams which possess high degrees of external validity to the aforementioned biomechanical research on low velocity whiplash biomechanics.

Scrutinizing the NPTF work on incidence, prevalence, course, and prognosis of WAD, it was striking how often the members of the NPTF scientific jury emphasize that neck pain and its associated disorders is also prevalent in the general population. A closer look at the NPTF own literature synthesis revealed that prior neck injuries are a confounding factor that must be controlled for in future studies about the prevalence of neck pain in the general population.

Summary: The onset and epidemiology of WAD are controversial as demonstrated by NPTF and the critical considerations presented herein. It is of major concern to rule in the late whiplash syndrome and identifying predictors and potentially mitigating chronic neck pain, and especially so in more severe cases.

Key words

whiplash, injury mechanisms, onset, epidemiology

Background

The results of the work by The Bone and Joint Decade 2000–2010 Task Force on Neck Pain and its Associated Disorders was published as a supplement in the February 15, 2008 issue of the Spine [1]. This work was generated through ongoing discussions by a multidisciplinary Scientific Secretariat, spanning 6 years, reviewing the international literature on this topic [2]. The NPTF has delivered a major undertaking towards bringing neck pain of musculoskeletal origin, which maintains a low status within the hierarchy of contemporary medicine [3], into the limelight. The NPTF recommendations about research priorities and methodological implications are invaluable guidelines for researchers [4]. Broadly, it can be asserted that the NPTF research priorities as well as recommendations suggest what should be done (emphasis added) and the NPTF review articles highlight what has been done (emphasis added). It is therefore of concern how the mismatch between the two highlighted matters is interpreted. Whiplash associated disorders (WAD) is well suited to ascertain whether the NPTP has achieved its stated goal concerning linking onset, course and care of a condition which contrasting views are no less conflicting now than nearly seventy years ago [5].

The NPTF states “The Neck Pain Task Force hopes that our new conceptual model for the onset, course, and care of neck pain will signal a shift in our thinking about this widespread problem, and that it will open a constructive dialogue on how to best decrease the personal and societal burden of neck pain and its associated disorders” [2].

The objective of the present debate is to open such a dialogue about the onset and epidemiology of WAD.

Discussion

The onset of WAD

The NPTP review of possible mechanisms of injury to the neck is not trustworthy. Firstly, the NPTF choose to skip all research, expect 2 experimental studies involving volunteers’ exposure to low-speed collision (speed changes 4-8 km/h) and a sham collision, exploring possible mechanisms of injury to the neck [6]. Secondly, the NPTF then states “However, the current evidence does not allow us to draw any conclusions about a specific injury mechanism, if one exists” [6]. Therefore, the NPTF prior citation in the same article to Farmer et al. [7] at Insurance Institute for Highway Safety seems to be out of context, but it reads as follows “…found that active devices such as active head rests and seat backs were associated with an overall 43% reduction in WAD claims in favour of the devices” [6].

What is the function of the aforementioned devices? The device, which is activated in rear – end collisions, is to have seat and head restraint which reduces the opposite movements of the head and trunk, i.e., keep the body and the head moving together to reduce the strain on the neck and to reduce the risk of neck injury [8]. Therefore, it is difficult to understand why NPTF scientific jury omitted the literature about low speed whiplash biomechanisms. In fact, biomechanical research into low velocity whiplash biomechanics, conducted within the frame of NPTF literature review period, 1980-2006, has shown remarkable consistency both across different methodologies and different research teams which possess high degrees of external validity to the aforementioned biomechanical research. A research conducted in 2010 into low velocity whiplash biomechanics came to the following conclusion “The present results underscore the importance of neck injury prevention systems in minimizing spinal rotations during whiplash to reduce the resulting residual instability, pain, and chronic symptoms” [9].

The epidemiology of WAD

One of the most important conclusions made by the NPTF is that the annual incidence of WAD in North America and Western Europe is estimated to be at least 300 per 100,000 inhabitants [6]. As the incidence of WAD is among the most controversial epidemiological issues in medicine today [10,11] a more thorough analysis of the underlying causes for the diverging incidence rates between countries and even within the same country as reported by the NPTF [12] would have been much appreciated.

However, the most likely explanation for the diverging incidence rates across the Nordic countries [13] and other countries [10], which share a common cultural background and life-style standard, is the different registration strategies and/or different injury registration sources. Moreover, the editorial – “Stopping late whiplash: Which way to Utopia?” [14] may give interested readers some insight into other reasons for the diverging incidence rates. Unpublished observations made by the author indicate that the diagnosis of WAD (ICD-9 diagnostic code 847.0 -cervical sprains and strains, including whiplash injuries) may be hidden by other diagnostic codes in some countries like Norway.

Scrutinizing the NPTF work on incidence, prevalence, course and prognosis of WAD, it was striking how often the members of the NPTF scientific jury emphasize that neck pain and its associated disorders is also prevalent in the general population [1]. The NPTF states “The best evidence suggests that between 20% and 40% of the general population reports having experienced neck pain during the previous month” [12]. The NPTF estimates the 12-month prevalence of neck pain in the general population to be 30-50% [15]. Accordingly, referring to WAD, the NPTF states “The clinical diagnosis is also confused by the high prevalence of neck pain and other WAD-like symptoms in the general population and in the working population” [13]. When reporting about the course and prognosis of WAD, the NPTF states: “The preponderance of evidence indicates that, in adults, recovery of WAD is prolonged, with approximately half of those affected reporting neck pain symptoms 1 year after the injury. However, this should be interpreted in light of the background prevalence of neck pain” [12]. These disclaimers, made by the NPTF, gave the author the impression that symptoms in WAD have similar characteristics to symptoms vocalized by people in the general population.

The NPTF also implies that patients with WAD may simply be attributing some prior symptoms, prone in the general population, to an accident or a mishap [12]. It seems appropriate, therefore, to take a closer look at the evidences put forward by the NPTF, which underpinned their incidence and prevalence rates of neck pain in the general population versus patients with WAD.

The age distribution in adults exposed to a whiplash mechanism to the neck has shown a remarkable consistency across countries with preponderance of the younger age groups between 16-24 years of age [16-19]. This is in contrast to the incidence rates of neck pain in the general population, reported by the NPTF, which peak incidence coincided with middle-age groups peaking at ages 40-49 and ages 35-44, respectively [13]. This is in accordance with the fact, emphasised by the NPTF, that younger (WAD) age groups are at greater risk (emphasis added) to seek compensation for their pain and suffering as well as filing disability claims than older (WAD) age groups [6].

Quoting the references in the NPTF own literature synthesis reveals that their review has some essential shortcomings. Regarding incidence, the study by Croft et al., [20] who carried out a one-year prospective study on 7.669 individuals with no neck pain at baseline, came to the following conclusion “We have carried out a prospective study in a general population sample and demonstrated that established risk factors for chronic pain predict future episodes of neck pain, and shown that in addition a history of neck injury is an independent and distinct risk factor”. Croft et al., further stated “This finding may have major public health and medicolegal implications” [20]. Unfortunately, the NPTF dismiss the word injury (emphasis added) when referring to this work, only stating “a history of neck pain, poor self-assessed health…” as independent risk factors for neck pain [13].

According to the NPTF, most estimates of 12-month prevalence of neck pain in the general population were between 30-50% [13]. However, when ascertaining the literature cited by the NPTF reporting the highest prevalence rates, over lifetime, at twelve-month and at one-month, it became apparent that few studies claim that prior neck pain is a significant risk factor for subsequent neck pain [21,22], while most studies in the NPTP literature synthesis did not mention at all whether people with prior neck injury (emphasis added) were included [23-31]. Prior neck injuries in the general population seems therefore to be a confounding factor that must be controlled for in future studies about incidence and prevalence rates of neck pain in the general populations. The aforementioned disclaimers, made by the NPTF, regarding the incidence and prevalence rates in WAD, are therefore based on weak evidences. Few studies have been conducted comparing the prevalence of neck pain and disability in WAD with those in the general population [32-34]. In conclusion, a past history of neck injury appears to have a substantial impact on future persistent neck pain and disability [34].

Ruling in the late whiplash syndrome

The NPTF states “In North-America, about 5% of the general population is disabled because of neck pain” [1]. Freeman et al., cautiously estimated that 6.2% of the US population, or circa 15.5 million individuals, have late whiplash syndrome [35]. Based on prior methodological objections made by the author in this paper, one may wonder: is this the same population? Whilst the NPTF looks upon WAD and other neck pain patients as the same population, explicitly stated by the NPTF “WAD and other neck pain do not differ once serious neck conditions have been ruled out” [36], there is no reason to assume that the NPTF overriding goal “to improve the health-related quality of life for people with musculoskeletal disorders throughout the world” [1], will be achieved.

Although about 50% of patients with WAD have favourable prognosis (benign WAD) [12], and only need advice, assurance and informed instructions it is the other half that needs therapeutic attention. Much more efforts must be put in mitigating the transition from the acute phase to the chronic phase. It is therefore important to consider modifiable prognostic factors that may be identified in the early acute stage of the condition such that interventions may be more specifically directed towards those circa 10-20% who are at the greatest risk of becoming most disabled and costly for societies [37,38]. The bottom line is that it will be more favourable for patients and societies to try to understand the aetiology and burden of chronic WAD, rather than belittling WAD.

Low velocity whiplash biomechanics

Crowe first used the term "whiplash" at a research meeting in 1928 to explain the effects of sudden external acceleration-deceleration forces on the neck [39]. Concomitant with the rise in popularity of the automobile after the Second World War, the term appeared first in the medical literature in 1945 [40]. Hyperflexion, associated with "extensor recoil" of the neck, was then proposed to be the injury mechanism [40]. In 1955, Severy et al. recorded whiplash loading to a human volunteer on film and recognised that hyperextension, followed by hyperflexion, was the correct sequence of events in rear-end collisions [41]. At that time, hyperextension of the head and neck was thought to be responsible for the possible injury mechanism [42,43]. In 1969, head restraints were made mandatory in cars in USA to prevent excessive movement of the head and neck [44]. Despite the introduction of head restraints, the frequency of injuries in low speed whiplash loading continued to rise [45]. It was not until 1993 that McConnell discovered that no whole cervical spine hyperextension took place in low speed MVCs [46].

The sequence of events in whiplash mechanism is over in the blink of an eye or less than half a second [46-49]. Modern technology, including high-speed photography, high-speed cineradiography and accelerometers, has been used to record the overall, local, segmental and component kinematic responses [48]. The overall picture given by McConnell et al. was scrutinised in 1994 by Matsushita et al. who for the first time used high-speed cineradiography to measure cervical inter-segmental motions in volunteers [50]. Since then, several separate research teams have added important pieces of information to the picture. The results across various animal, dummy, human neck cadaver [50-56] and volunteer studies [46,57,58] have been remarkably consistent. This knowledge serves as a basis for our present understanding of why and how injuries may occur in low speed MVCs and gives us insight into what soft tissues may be targeted [59].

The summary below is not all-inclusive but priorities what a clinician must know when examining and treating patients with WAD.

The neck experiences compression, tension, shear, flexion and extension at different cervical levels during the different phases of low speed MVCs [56,60]. The initial phase is crucial for understanding possible injury mechanisms in rear-end low speed MVCs [48]. The occupant's hips and low back are first thrust forwards and then upwards until this movement reaches the trunk (torso), which is accelerated forward by the seatback [45]. The trunk also moves upward due to straightening of the thoracic kyphosis and inclination of the seatback [47,56] (Figure 1). This upward movement (ramping) of the trunk causes axial compression of the cervical spine because the head is relatively stationary [47,48,56]. At the same time the forward acceleration impulse on the trunk is first transmitted to the lower cervical spine in the form of shear forces which cause straightening of the cervical lordosis followed by an S shaped dynamic form of the cervical lordosis [53,61,62]. The S shaped motion occurs about 100 milliseconds after the impact (depending on the acceleration impulse) and is produced by segmental extension at the lower cervical spine (induced from below) and local flexion at the upper cervical spine (induced from above) as a result of the inertia of the head [53,62-64]. Eventually the head catches up with the translating lower cervical spine and the whole cervical spine undergoes normal C shaped extension and finally rebounds into flexion [52,53]. This final phase may cause injuries in collisions at higher speed [65].

Figure 1. Transient unphysiological S-shaped motion of the cervical spine during a rear-end collision

Compression of the cervical spine segments loosens the lower cervical spine ligaments and renders them less capable to withstanding shear forces [66]. The coupled compression/sliding of the facet joints results in abnormal posterior rotation around an instantaneous axis of rotation (IAR) located in the moving vertebra. The rostral location of the IAR causes gapping anteriorly and further compression posteriorly in the lower cervical spine segments [62]. In some cases, this injury mechanism may exceed the normal physiological limits [53,60,67]. The initial small upper cervical flexion generated by the compressive forces and the inertia of the head is immediately reinforced by local tension in the upper cervical spine due to the relatively faster upward motion of the head compared with that of the much heavier trunk [59,60]. It is therefore hypothesized that the lower cervical spine segments may be injured as a result of abnormal coupled compression, shear and rotational forces, while abnormal tension-flexion seems to be the main force induced in the upper cervical spine [56,59,60]. Research has identified soft tissue injuries in unembalmed cadavers subjected to rear impacts at low speed [68,69]. Although research into low speed whiplash biomechanics has enormously enriched our understanding of possible injury mechanisms in WAD, the clinical side of the problem is still unsolved.

Summary

The onset and epidemiology of WAD are controversial as demonstrated by the NPTF literature review on these topics and the critical considerations presented herein. A comprehensive literature review on low velocity whiplash biomechanics, omitted by the NPTF, shows that whiplash consists of complicated injury mechanisms. It can be substantiated that the incidence and prevalence rates of WAD cannot be compared with the incidence and prevalence rates of neck pain in the general population as presented by the NPTF. Prior neck injuries in the general population are a confounding factor that must be controlled for in future epidemiologic studies about neck pain in the general and working populations. It is of major concern to rule in the late whiplash syndrome and identifying predictors of and potentially mitigating chronic neck pain, and especially so in more severe cases.

Conflict of Interest

There are no competing interests.

Acknowledgements

This work was conducted as deputyship researcher at Communication and Research Unit for Musculoskeletal Disorders, Division for Neuroscience and Musculoskeletal Medicine (FORMI), Oslo University Hospital, Ullevål, 0407, Oslo, Norway.

References

1. Guzman J, Hurwitz E, Carroll L, Haldeman S, Côté P, et al. (2008) Results of the Bone and Joint Decade 2000-2010 Task Force on Neck Pain and its Associated Disorders. Spine 33: S1-220.
2. Guzman J, Hurwitz EL, Carroll LJ, Haldeman S, Côté P, et al (2008) A conceptual model for the course and care of neck pain. Results of the Bone and Joint Decade 2000-2010 Task Force on Neck Pain and its Associated Disorders. Spine 33: S14-23. [Crossref]
3. Freedman K, Bernstein J (1998) The adequacy of medical school education in musculoskeletal medicine. J Bone Joint Surg 80: 1421-1427. [Crossref]
4. Carroll LJ, Hurwitz EL, Côté P, Hogg-Johnson S, Carragee E, et al. (2008) Research priorities and methodological implications. Results of the Bone and Joint decade 2000–2010 Task Force on Neck Pain and Its Associated Disorders. Spine 33: S214-220. [Crossref]
5. Gay JR, Abbott KH (1953) Common whiplash injuries of the neck. J Am Med Assoc 152: 1698-1704. [Crossref]
6. Holm L, Carroll L, Cassidy D, Hogg-Johnson S, Côté P, et al. (2008) The Burden and determinants of neck pain in whiplash-associated disorders after traffic collisions. Results of the Bone and Joint decade 2000–2010 Task Force on Neck Pain and Its Associated Disorders. Spine 33: S52-59. [Crossref]
7. Farmer CM, Wells JK, Lund AK (2002) Effects of Head Restraint and Seat Redesign on Neck Injury Risk in Rear-End Crashes. Arlington, VA: Insurance Institute for Highway Safety.
8. http://www.youtube.com/watch?v=rXH3auUmOkM
9. Ivancic PC, Sha D, Lawrence BD, Mo F (2010) Effect of active head restraint on residual neck instability due to rear impact. Spine 35: 2071-2078. [Crossref]
10. Ferrari R, Russell A (1999) Epidemiology of whiplash: an international dilemma. Ann Rheum Dis 58: 1-5. [Crossref]
11. Bogduk N (2000) Epidemiology of whiplash. Ann Rheum Dis 59: 394-396. [Crossref]
12. Carroll L, Holm L, Hogg-Johnson S, Côté P, Cassidy D, et al. (2008) Course and prognostic factors for neck pain in whiplash – associated disorders (WAD). Results of the Bone and Joint Decade 2000-2010 Task Force on Neck Pain and Its Associated Disorders. Spine 33: S83-82. [Crossref]
13. Kristjansson E (2004) Clinical characteristics of whiplash associated disorders (WAD), grades I-II: Investigation into the stability system of the cervical spine. PhD thesis ISBN: 99979-9513-3-8. University of Iceland, Faculty of Medicine, Reykjavik, Iceland.
14. Harth M (2008) Stopping late whiplash: Which way to Utopia? J Rheumatol 35: 2303-2305.
15. Hogg-Johnson S, van der Velde G, Carroll L, Holm L, Cassidy D, et al. (2008) The Burden and determinants of neck pain in the general population. Results of the Bone and Joint Decade 200-2010 Task Force on Neck Pain and Its Associated Disorders. Spine 33: S39-51. [Crossref]
16. Bring G (1996) Whiplash-associated injuries and disorders – Biomedical aspects of a multifaceted problem. PhD thesis. ISBN: 91-7045-569-4 Umeå University, Sweden, Department of Family Medicine.
17. Spitzer WO, Skovron ML, Salmi LR, Cassidy JD, Duranceau J, et al. (1995) Scientific Monograph of the Quebec Task Force on Whiplash-Associated Disorders: Redefining "Whiplash" and its Management. Spine 20: 1S -73S. [Crossref]
18. Quinlan KP, Annest JL, Myers B, Ryan G, Hill H (2004) Neck strains and sprains among motor vehicle occupants—United States. Accid Anal Prev 36: 21-27. [Crossref]
19. Ferrando J, Plaséncia A, MacKenzie E, Orós M, Arribas P, et al. (1998) Disability Resulting from traffic injuries in Barcelona, Spain: 1-year incidence by age, gender and type of user. Accid Anal Prev 30: 723-730. [Crossref]
20. Croft PR, Lewis M, Papageorgiou AC, Thomas E, Jayson MI, et al. (2001) Risk factors for neck pain: a longitudinal study in the general population. Pain 93: 317-325. [Crossref]
21. Lau EM, Sham A, Wong KC (1996) The prevalence of and risk factors for neck pain in Hong Kong Chinese. J Publ Health Med 18: 396-399. [Crossref]
22. Makela M, Heliovaara M, Sievers K, Impivaara O; Knekt P, et al. (1991) Prevalence, determinants, and consequences of chronic neck pain in Finland. Am J Epidemiol 134: 1356-1367. [Crossref]
23. Chiu TT, Leung AS (2006) Neck pain in Hong Kong: a telephone survey on prevalence, consequences, and risk groups. Spine 31: E540-E544. [Crossref]
24. Côté P, Cassidy JD, Carroll L (1998) The Saskatchewan health and back pain survey. The prevalence of neck pain and related disability in Saskatchewan adults. Spine 23: 1689-1698. [Crossref]
25. Fejer R, Hartvigsen J, Kyvik KO (2006) Heritability of neck pain: a population based study of 33,794 Danish twins. Rheumatology 45: 589-594. [Crossref]
26. MacGregor AJ, Andrew T, Sambrook PN, Spector TM (2004) Structural, psychological, and genetic influences on low back and neck pain: a study of adult female twins. Arthritis Rheum 51: 160-167. [Crossref]
27. Bovim G, Schrader H, Sand T (1994) Neck pain in the general population. Spine 19: 1307-1309. [Crossref]
28. Palmer KT, Syddall H, Cooper C, Coggon D (2003) Smoking and musculoskeletal disorders: findings from a British national survey. Ann Rheum Dis 62: 33-36. [Crossref]
29. Picavet HS, Schouten JS (2003) Musculoskeletal pain in the Netherlands: prevalences, consequences and risk groups, the DMC (3)-study. Pain 102: 167-178. [Crossref]
30. Ektor-Andersen J, Isacsson SO, Lindgren A, Ørbæk P (1999) The experience of pain from the shoulder-neck area related to the total body pain, self-experienced health and mental distress. The Malmø Shoulder-Neck Study group. Pain 82: 289-295. [Crossref]
31. Kim K, Uchiyama M, Liu X, Shibui K, Ohida T, et al. (2001) Somatic and psychological complaints and their correlates with insomnia in the Japanese general population. Psychosom Med 63: 441-446. [Crossref]
32. Berglund A, Alfredsson L, Cassidy JD, Jensen I, Nygren A (2000) The association between exposure to a rear-end collision and future neck or shoulder pain: a cohort study. J Clin Epidemiol 53: 1089-1094. [Crossref]
33. Côté P, Cassidy JD, Carroll L (2001) Is a lifetime history of neck injury in a traffic collision associated with prevalent neck pain, headache and depressive symptomatology? Accid Anal Prev 32: 151-159. [Crossref]
34. Bunketorp L, Stener-Victorin E, Carlsson J (2005) Neck pain and disability following motor vehicle accidents – a cohort study. Eur Spine J 14: 84-89. [Crossref]
35. Freeman MD, Croft AC, Rossignol AM, Weaver DS, Reiser M (1999) A review and methodologic critique of the literature refuting whiplash syndrome. Spine 24: 86-96. [Crossref]
36. Nordin M, Carragee E, Hogg-Johnson S, Weiner S, Hurwitz E, et al. (2008) Assessment of neck pain and its associated disorders. Results of the Bone and Joint Decade 2000–2010 Task Force on Neck Pain and Its Associated Disorders. Spine 33: S101-122. [Crossref]
37. Sterling M, Jull G, Kenardy J (2006) Physical and psychological factors maintain long-term predictive capacity post whiplash injury. Pain 122: 102-108. [Crossref]
38. Sterling M, Hendrikz J, Kenardy J (2010) Compensation claim lodgment and health outcome developmental trajectories following whiplash injury: a prospective study. Pain 150: 22-28. [Crossref]
39. Crowe H (1928) Injuries to the cervical spine. Presented at the annual meeting of the Western Orthopaedic Association, San Francisco.
40. Davis AG (1945) Injuries of the cervical spine. JAMA 127: 149-155
41. Severy DM, Mathewson JH, Bechtol CO (1955) Controlled automobile rear-end collisions, an investigation of related engineering and medical phenomena. Can Serv Med J 11: 727-759. [Crossref]
42. Macnab I (1964) Acceleration injuries of the cervical spine. J Bone Joint Surg Am 46: 1797-1799. [Crossref]
43. Mertz HJ, Patrick LM (1967) Investigation of the kinematics and kinetics of whiplash. In: Proceedings of the 11th Stapp Car Crash Conference. Society of Automotive Engineers, New York: 269-317.
44. McKenzie JA, Williams JF (1971) The dynamic behaviour of the head and cervical spine during "whiplash". J Biomech 4: 477-490. [Crossref]
45. Insurance institute for highway safety (2002). Status Report 37: 1-8.
46. McConnell WE, Howard RP, Guzman HM, Bomar JB, Raddin JH, et al. (1993) Analysis of human test subject kinematic responses to low velocity rear end impacts. In: Proceedings International Congress and Exposition. Detroit MI: Society of Automotive Engineers: 21-30.
47. Hell W, Schick S, Langwieder K (2000) Epidemiology of cervical spine injuries in rear-end collisions and influence of different anthropometric parameters in human volunteer tests. In: Yoganandan N, Pintar FA, eds. Frontires in Whiplash Trauma. Clinical & Biomechanical. Amsterdam: IOS Press pp.146-163.
48. McConnell WE, Howard RP, Krause R, Guzman HM, Bomar JB, et al. (1995) Human head and neck kinematics after low velocity rear-end impacts – understanding "whiplash". SAE Trans 104: 215-238.
49. Yoganandan N, Pintar FA, Kleinberger M (1999) Whiplash injury. Biomechanical experimentation. Spine 24: 83-85. [Crossref]
50. Matsushita T, Sato TB, Hirabayashi K, Fujimura S, Asazuma T, et al. (1994) X-ray study of the human neck motion due to head inertia loading. SAE Trans 105: 55-64.
51. Svensson MY, Lövsund P, Haland Y, Larsson S (1993) Rear-end collisions – A study of the influence of backrest properties on the head-neck motion using a new dummy neck. Proceedings International Congress and Exposition. Detroit MI: Society of Automotive Engineers 416-429.
52. Svensson MY, Aldman B, Hansson HA, Lövsund P, Seeman T, et al. (1993) Pressure effects in the spinal canal during whiplash extension motion: a possible cause of injury to the cervical spinal ganglia. In: Proceedings of the International Conference on the Biomechanics of Impacts. Eindhoven, The Netherland pp.189-200.
53. Winkelstein BA, Myers BS (2000) Cervical motion segment, combined loading, muscle forces and facet joint. In: Yoganandan N, Pintar FA, eds. Frontiers in Whiplash Trauma. Clinical & Biomechanical. Amsterdam: IOS Press pp.248-262.
54. Grauer JN, Panjabi MM, Cholewicki J, Nibu K, Dvorak J (1997) Whiplash produces an S-shaped curvature of the neck with hyperextension at lower levels. Spine 22: 2489-2494. [Crossref]
55. Panjabi MM, Cholewicki J, Nibu K, Babat LB, Dvorak J (1998) Stimulation of whiplash trauma using whole cervical spine specimens. Spine 23: 17-24. [Crossref]
56. Luan F, Yang KH, Deng B, Begeman PC, Tashman S, et al. (2000) Qualitative analysis of neck kinematics during low-speed rear-end impact. Clin Biomech 15: 649-657. [Crossref]
57. Geigel BC, Leinzinger P, Roll, Mühlbauer M, Bauer G (1995) The movement of head and cervical spine during rear-end impact. In: Proceedings of the International Conference on the Biomechanics of Impacts, Lyon, France 127-137.
58. Szabo TJ, Welcher JB (1996) Human subject kinematics and electromyographic activity during low speed rear impacts. Proceedings of the 40th Stapp Car Crash Conference. Warrendale, PA: Society of Automotive Engineers 295-315.
59. Cusick JF, Pintar FA, Yoganandan N (2001) Whiplash syndrome. Kinematic factors influencing pain patterns. Spine 26: 1252-1258. [Crossref]
60. Deng B, Begeman PC, Yang KH, Tashman S, King AI (2000) Kinematics of human cadaver cervical spine during low speed rear-end impacts. Stapp Car Crash J 44: 171-188. [Crossref]
61. Watanabe Y, Ichikawa, H, Kayama O, Ono K, Kaneoka K, et al. (2000) Influences of seat characteristics on occupant motion in low-speed rear impacts. Acc Anal Prev 32: 243-250. [Crossref]
62. Ono K, Kaneoka K, Wittek A, Kajzer J (1997) Cervical injury mechanism based on the analysis of human cervical vertebral motion and head-neck-torso kinematics during low speed rear impacts. In: Proceedings of the 41st Stapp Car Crash Conference, Society of Automotive Engineers, Inc 339-356.
63. Kaneoka K, Ono K, Inami S, Hayashi K (1999) Motion analysis of cervical vertebrae during whiplash loading. Spine 24: 763-769. [Crossref]
64. Yoganandan N, Pintar FA (2000) Mechanism of headache and neck pain in whiplash. In: Yoganandan N, Pintar FA, eds. Frontiers in Whiplash Trauma. Clinical & Biomechanical. Amsterdam: IOS Press pp.173–185.
65. Croft AC, Herring P, Freeman MD, Haneline MT (2002) The neck injury criterion: future considerations. Accid Anal Prev 34: 247-255. [Crossref]
66. Yang KH, Begeman PC, Muser M, Niederer P, Walz F (1997) On the role of the cervical facet joints in rear end impact neck injury mechanism. In: Proceedings of the 41st Stapp Car Crash Conference, Society of Automotive Engineers, Inc, 127-129.
67. Siegmund GP, Myers BS, Davis MB, Bohnet HF, Winkelstein BA (2001) Mechanical evidence of cervical facet capsule injury during whiplash. Spine 26: 2095-2101. [Crossref]
68. Yoganandan N, Pintar FA, Stemper BD, Schlick B, Philippens M, et al. (2000) Biomechanics of human occupants in simulated rear crashes: documentation of neck injuries and comparison of injury criteria. Stapp Car Crash J 44: 189-204. [Crossref]
69. Yoganandan N, Cusick JF, Pintar FA, Rao RD (2001) Whiplash injury determination with conventional spine imaging and cryomicrotomy. Spine 26: 2443-2448. [Crossref]