LATE WHIPLASH SYNDROME: A CLINICAL SCIENCE APPROACH TO EVIDENCEBASED DIAGNOSIS AND MANAGEMENT.

Keith Poorbaugh, PT, ScD, OCS, CSCS, FAAOMPT Clinical Director, Advanced Physical Therapy, Anchorage, AK Faculty, International Academy of Orthopedic Medicine, Tucson, AZ, USA

Jean-Michel Brisme, PT, ScD, OCS, FAAOMPT Assistant Professor, Texas Tech University Health Science Center, Lubbock, TX, USA Senior Faculty, International Academy of Orthopedic Medicine, Tucson, AZ, USA

Valerie Phelps, PT, OCS, FAAOMPT Owner/Director Advanced Physical Therapy, Anchorage, AK Senior Faculty, International Academy of Orthopedic Medicine, Tucson, AZ, USA

Phillip S. Sizer Jr, PT, PhD, OCS, FAAOMPT Professor & Program Director, Texas Tech University Health Science Center, Lubbock, TX, USA Senior Faculty, International Academy of Orthopedic Medicine, Tucson, AZ, USA

Corresponding Author Phillip S. Sizer Jr, PT, PhD, OCS, FAAOMPT Professor & Program Director, ScD Program in PT Dept of Rehabilitation Sciences, School of Allied Health Sciences Texas Tech University Health Science Center 3601 4th St. Lubbock, TX, USA 79430

Abstract The purpose of this article is to narrow the gap that exists in the clinical application of scientific research and empirical evidence for the evaluation and management of late whiplash. Considering that 14% to 42% of patients are left with chronic symptoms following whiplash injury, it is unlikely that only minor self-limiting injuries result from the typical rear-end impact. As psychosocial issues play a role in the development of persistent whiplash symptoms, discerning the organic conditions from the biopsychosocial factors remains a challenge to clinicians. The term whiplash represents the multiple factors associated with the event, injury, and clinical syndrome that are the end-result of a sudden accelerationdeceleration trauma to the head and neck. However, contentions surround the nature of soft-tissue injuries that occur with most motor vehicle accidents and whether these injuries are significant enough to result in chronic pain and limitations. The stark contrast in litigation for whiplash that exists amongst industrialized nations and less developed countries suggests another factor that could influence ones interpretation of persistent symptoms associated with Late Whiplash Syndrome. There are no gold standard tests or imaging techniques that can objectify whiplash associated disorders. A lack of supporting evidence and disparity in medico-legal issues has created distinct camps in the scientific interpretations and clinical management of late whiplash. It is likely that efforts in research and or clinical practice will begin to explain the disparity between acute and chronic whiplash syndrome. Recent evidence suggests that Late Whiplash Syndrome should be considered from a different context. The goal of this

article is to expound on several of the significant findings in the literature and offer clinical applications for evaluation and management of Late Whiplash Syndrome.

INTRODUCTION Late Whiplash Syndrome has been described as a disorder that is characterized by a constellation of clinical profiles including neck pain and stiffness, persistent headache, dizziness, upper limb paresthesia, and psychological emotional sequelae that persist more than six months after a whiplash injury.(Kasch et al. 1246-51;Karlberg et al. 874-82) Whiplash is the most common cause of neck pain associated with chronic musculoligamentous conditions.(Karlberg et al. 874-82;Narayan and Haid 21729) It is estimated that 6.2% of all Americans (approximately 15.5 million) currently suffer from Late Whiplash Syndrome.(Freeman MD 35-39;Freeman, Croft, and Rossignol 1043-49;Karlberg et al. 874-82) Annual medical costs associated with whiplash injuries are estimated to range from $3.6 billion in the United Kingdom to $10 billion in the United States.(Karlberg et al. 874-82;Yoganandan et al. 2443-48) The high incidence and exorbitant costs have elevated whiplash to international epidemic status. Late Whiplash Syndrome involves a broad spectrum of symptoms ascribed to few other conditions or injuries that may persist for months or years after the incident. (Evans 2117-18;Bunketorp, Nordholm, and Carlsson 227-34;Bosma and Kessels 56-65) It is estimated that only 10% of vehicle occupants exposed to a rear-end collision will develop whiplash syndrome.(Chester, Jr. 716-20) Of these, the incidence of chronic neck pain ranges from 18% to 40%.(Chester, Jr. 716-20) However, whiplash symptoms may not be evident for some time after the accident. Selected studies have demonstrated that the delay in the onset of whiplash symptoms can range from one hour to several days after the accident.(Balla 610-14;Hildingsson and Toolanen 35759;Kischka et al. 136-40) Moreover, patients that seek medical treatment for acute

whiplash injuries face a 33% chance of developing Late Whiplash Syndrome at more than 30 months after injury.(Freeman, Croft, and Rossignol 1043-49;Freeman MD 3539) However, when presented with chronic symptoms that are delayed in onset and present with few causal factors, there is a tendency right or wrong - to suspect underlying non-organic basis for the patients symptoms. Structural damage that persists beyond the average healing time for soft-tissue injuries is not common among patients with whiplash.(Cassidy et al. 1179-86) Thus, prolonged disability and limited treatment effectiveness have invoked conflicting views on the role of psychological factors and litigation in a patients recovery. Various investigators have reported the medico-legal aspects of chronic whiplash and have challenged organic causes for this disorder,(Ferrari and Russell 1-5;Ferrari and Russell 97-98;Schrader et al. 1207-11;Obelieniene et al. 279-83;Deans, McGalliard, and Rutherford 94-95;Evans 975-97) exemplified by the strong association found between retention of a lawyer and delayed recovery from whiplash injury.(Cassidy et al. 1179-86) Even worse, unresolved matters with an insurance provider are strongly associated with a poor outcome from whiplash associated disorders as far out as three years after the injury.(Miettinen et al. E47-E51) Thus, it has been contended that Late Whiplash Syndrome should be considered as much a behavioral disorder as a chronic injury. (Awerbuch 193-96)

Selected Pathoanatomy and Pathomechanics of Late Whiplash Syndrome Late Whiplash Syndrome involves a myriad of symptoms with considerable overlap between organic and psychosocial origins.(Kasch et al. 743-49) A single

anatomical site of whiplash injury has yet to be identified.(Sjostrom et al. 1725-34) The symbiotic relationship between the intervertebral disc, uncovertebral joints and zygapophyseal joints in the cervical spine lends these structures to complex mechanical loading in response to injury. Because structures such as the intervertebral discs and zygapophyseal joints are extensively innervated,(Mendel, Wink, and Zimny 13235;Johnson 71-76) they could serve as primary pain generators in Late Whiplash Syndrome.(Aprill and Bogduk 744-47;Barnsley et al. 20-25;Yoganandan et al. 2317-23) For example, cervical facet joints have been implicated as the cause of neck pain in 60% of a study group with chronic pain after whiplash exposure.(Lord et al. 1737-44) A primary function of the cervical spine is to facilitate and control motion of the head and neck, while disruption of the cervical kinematics may contribute to late whiplash symptoms.(Reitman et al. 2832-43) Although overall cervical movement remains within physiological limits during a low velocity impact, injury appears to emerge in response to pure posterior rotation, anterior shear, and upward thrust of the segment about an abnormally high instantaneous axis of rotation (IAR).(Tencer, Mirza, and Bensel 34-42) The role of the IAR in whiplash-related pathology is apparent, as abnormal instantaneous axes have been detected in at least one segmental level within almost half of patients examined with a similar history.(Amevo, Aprill, and Bogduk 74856) Inertial loading of the trunk and head appears to contribute to the consequences of whiplash injury mechanisms.(Yoganandan et al. 2443-48;Bogduk and Yoganandan 267-75;Tropiano et al. 1709-16) Inertial loads experienced during a whiplash event create an elongated S-shaped curve in the cervical spine that is considerably different

from the typical lordotic C-curve that is witnessed in the cervical spine at rest.(Stemper, Yoganandan, and Pintar 1764-71;Kumar, Ferrari, and Narayan 760-68;Kumar, Ferrari, and Narayan 760-68) \ This aphysiological behavior produces pathomechanical tissue responses and potential clinical consequences that have been previously described. (Sizer P, Poorbaugh K, and Phelps V 249-66) For example, trauma may injure cervical facet capsular ligaments that have been shown to tear under combined shear, bending, and compression loads witnessed in a whiplash event.(Siegmund et al. 2095-101) The end result of the early phase of whiplash involves anterior separation of the vertebral bodies, shear of the posterior annulus and compression of the zygapophyseal joints, lending to tears of anterior annulus fibrosis and bony contusions or fractures of the zygapophyseal joint articular processes.(Kaneoka et al. 763-69) Accompanying this response are strain levels in the upper cervical spine ranging from 15% to 26% in the posterior longitudinal ligament and intervertebral discs. Moreover, the order of segmental recruitment during the whiplash event might lend selected segments to more stress than others, especially witnessed at the C5-6 segmental level.(Kaneoka et al. 763-69) These conditions could persist for an extended period of time, lending to the development of the symptoms associated with Late Whiplash Syndrome. Integrity of the cervical musculoskeletal complex depends on three subsystems: bony architectural structures, capsuloligamentous systems and neuromuscular control mechanisms.(Panjabi 383-89;Panjabi 390-96) Each of these systems could be implicated in Late Whiplash Syndrome. For example, disc pathology can serve as a contributing factor in the development of chronic symptoms after whiplash injury, (Pettersson et al. 283-87) where trauma to the cervical spine may accelerate normal

age-related disc deterioration.(Buckwalter 1307-14;Watkinson, Gargan, and Bannister 307-09) Peak disc strains appear to occur early in the second phase of whiplash, where disc shear strain is highest in the posterior annulus and axial elongation is greatest at the anterior annulus, especially at the C5-6 segment.(Panjabi et al. 1217-25) The stability of the functional spinal units for the cervical spine is achieved through a symbiotic relationship of all supporting structures. Therefore, disc changes not only produce disc related symptoms, but additionally contribute to the eventual development of pain in other tissues. Loss of integrity or segmental stiffness from a disc injury can cause undue stress to other supporting structures, such as the zygapophyseal joint. This phenomenon supports the contribution of the zygapophyseal joint to the symptoms associated with Late Whiplash Syndrome.(Lord et al. 1737-44) Of equal importance is the impact that whiplash has on the cervical neural structures in response to changes in their surrounding architectural container. A rear impact causes a graduated decrease in the diameter of the spinal canal at C2-3 and C3-4 but remains nearly constant from C4-5 to C6-7.(Debois et al. 1996-2002) Other researchers have found that hyperextension of the lower cervical spine occurs in the early phase of whiplash and results in a narrowed spinal canal, due to decreased spinal canal diameter and increased cord diameter.(Ito et al. 1330-39) This decrease in the sagittal diameter of the canal may contribute to symptomology in Late Whiplash Syndrome. A study of 48 consecutive whiplash patients demonstrated that spinal canal was significantly narrower in patients with persistent symptoms versus a recovered group, especially in those patients with pre-existing cervical spondylosis.(Borchgrevink et al. 425-28)

Any of the structures innervated by the upper cervical segmental nerves can be influenced by a whiplash event, lending to prolonged symptomology.(Bogduk 67-70) For instance, the trigeminal nerve located in the upper cervical segments of the spinal cord has been implicated in the cephalic symptoms associated with whiplash. The trigeminal nucleus is located in the upper cervical segments of the spinal cord.(Bogduk 67-70) Thus, any increased afferent signaling from selected structures innervated by these segmental nerves could trigger cervicogenic headache in this population. (Bogduk 6770) These segments receive afferent information from the distribution inherent to the trigeminal nerve and upper cervical nerves. Because chronic pain triggers the release of nerve growth factor (NGF) and increased interneuron growth, there is reasonable basis for afferent convergence within the cervical trigeminal nucleus. The potential neural adaptations and the increased incidence of convergence serve as physiological bases for cervicogenic headaches associated with Late Whiplash Syndrome. Women may be at greater risk for developing Late Whiplash Syndrome and this predisposition may be, in part, related to differences in anatomical and pathomechanical tissue responses. There is more than 2:1 preponderance for women to suffer whiplash injuries when compared to their male counterparts.(Dolinis J 173-79) The Quebec Task Force on Whiplash-Associated Disorders reported that females sustained 60% of all injuries in a cohort of 3,014 whiplash patients.(Spitzer et al. 1S-73S) Not only are women more likely to sustain a whiplash injury, but they may be additionally less likely to recover.(Radanov, Sturzenegger, and Di 281-97) However, the explanation for these differences is controversial. (Radanov, Sturzenegger, and Di 281-97;Sapir and Gorup E268-E273;Spitzer et al. 1S-73S;Borchgrevink et al. 425-28) Pettersson observed that

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the spinal canal of female patients was significantly narrower than that of males, (Pettersson et al. 1664-67) suggesting one of the causal factors that may explain this disparity. Other explanations for the higher incidence of whiplash injuries among women point to gender-specific segmental spinal stability and tissue response to injury. Whiplash injury appears to cause a greater instance of segmental hypermobility in women with whiplash-associated disorder (WAD) in comparison to women with idiopathic onset of neck pain, especially in combined rotational and translational hypermobility in the middle cervical spine segments.(Kristjansson et al. 2215-21) Similarly, female cadaveric specimens demonstrated significantly greater dorsal shear motion at C4-5 during simulated whiplash when compared with males.(Stemper, Yoganandan, and Pintar 1764-71) Females may be predisposed to greater incidence in facet injury during whiplash. This may be related to less extensive cartilage available to cushion the subchondral bone, accompanied by an increased cartilage gap in the dorsal facet observed in females.(Yoganandan et al. 2317-23) Simulated rear impact using human volunteer subjects showed greater degrees of cervical retraction in females that were unaware at time of rear impact.(Siegmund et al. 671-79) This additional translation could result in increased strains experienced by restraining structures, such as the facet capsule. Soft-tissue injuries that are common with a rear impact could lead to spinal column instability, due to a loss of integrity in the spinal stabilizing system.(Panjabi 38389;Panjabi 390-96) Simulated frontal impacts demonstrated strains in excess of the physiologic limits for supraspinous and interspinous ligaments, as well as ligamentum

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flavum.(Panjabi et al. 1217-25) Disruption of these soft-tissue structures could lead to segmental instability, which could result in pain associated with aberrant or excessive motion. The stability of the craniocervical region is afforded by the alar and transverse ligaments and trauma to these structures can contribute to Late Whiplash Syndrome. (Dvorak et al. 452-61;Dvorak and Panjabi 183-89) The occipital portion of the alar ligament courses from each of the occipital condyles to the posterior aspect of the dens, whereas the atlantal portion of the alar ligament connects the atlas with the ventral aspect of the dens.(Sizer P, Phelps V, and Brisme JM 136-52) The alar ligaments not only provide the primary restraint to lateral flexion and rotation but additionally act as secondary restraints to sagittal flexion in this region. Together, these ligaments serve as a primary restraint to extension, axial rotation and sidebending in the upper cervical spine.(Willauschus et al. 2493-98) When the head is rotated and flexed, the alar ligaments are maximally stretched and susceptible to injury from sudden acceleration during a vehicle accident.(Dvorak et al. 452-61;Dvorak and Panjabi 183-89) Complete ruptures of the alar ligament are rare in survivors of whiplash injury. However, suspected ligamentous lesions of the craniocervical region should be evaluated with clinical manual testing(Sizer P, Poorbaugh K, and Phelps V 249-66) and functional stress radiographic imaging.(Derrick LJ and Chesworth BM 6-11), Moreover, the transverse ligament of atlas (TLA) stabilizes the atlantoaxial joint by securing the dens against the inner aspect of the atlas, where it functions to hold the dens in place and prevent posterior translation of the process into the spinal canal during cervical flexion.

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(Uitvlugt and Indenbaum 918-22) Lesions of the TLA are life threatening and require immediate referral to physician for further evaluation and management. The locomotor system works along with ligaments to stabilize segments of the cervical spine and whiplash can possibly produce dysfunction in this system, lending to subsequent instability and latent symptoms. Neck muscle dysfunction is an early correlate of subclinical neck pain.(Lee et al. E60-E67) Muscle spasms have the capacity to reduce range of motion (ROM) and to alter IARs.(Amevo, Aprill, and Bogduk 748-56) In addition, a pattern of muscle fiber transformation from slow oxidative to fast glycotic has been observed in patients who underwent spondylodesis for cervical dysfunction. (Uhlig et al. 240-49) Biopsies of ventral neck muscles (sternocleidomastoid, omohyoid, longus colli) and dorsal neck muscles (rectus capitus posterior major, obliqus capitus inferior, splenius capitus, and trapezius) were taken from 64 patients who underwent spondylodesis for cervical dysfunction (whiplash and rheumatoid arthritis). The same pattern of muscular transition was found in patients with soft-tissue injuries of the neck (whiplash). In the ventral muscles, transformation was more prevalent among women and in patients with shorter duration of symptoms (less than two years). Muscles in which transformations had ceased displayed a significantly higher percentage of type IIB fibers than were found in muscles with ongoing transformations. A higher ratio of type IIB fibers indicated that the muscles transformed from slow oxidative to fast glycolytic in nature, suggesting a decrease in the muscles resistance to fatigue. A loss of endurance among local muscles responsible for segmental control may impair segmental spinal stability due to reduced neuromuscular control. This may be one of the factors that cause muscle spasms in the presentation of Late Whiplash Syndrome.

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Resultant Pathology Investigators have examined the soft tissue injuries that are sustained during whiplash. Deng et al suggested five possible whiplash injury mechanisms: (1) excessive cervical hyperextension; (2) muscle tensile forces; (3) facet capsular impingement due to local tilting and compression; (4) dorsal root ganglion deformation during transient pressure increases in spinal canal; and (5) facet joint shearing and loading.(Deng B, Begeman PC, and Yang KH 171-88) Cryomicrotome examination of cadaveric specimens exposed to whiplash trauma revealed extensive tissue abnormalities, such as anterior annulus tears, disruption of anterior longitudinal ligament, separation of ligamentum flavum with hematoma, and capsular tears of zygapophyseal joint. These injuries, which were mainly confined to the lower cervical spine, reflect anatomical changes that could partially explain the persistence of clinical symptoms.(Yoganandan et al. 2443-48) The zygapophyseal joint appears to be the single most common pain generator associated with chronic neck pain after whiplash.(Barnsley et al. 20-25;Lord et al. 173744) Lord found that the cervical zygapophyseal joint was the primary cause of chronic neck pain after whiplash in 60% of their subjects in a double blind, placebo-controlled study.(Lord et al. 1737-44) However, In a study of 318 patients suffering chronic neck pain (symptoms longer than six months), April observed a different pattern of zygapophyseal joint involvement determined through provocative discography and cervical zygapophyseal joint blocks.(Aprill and Bogduk 744-47) They found that 53% of

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the patients suffered a symptomatic disc, while 26% demonstrated a symptomatic zygapophyseal joint either in isolation or in conjunction with a symptomatic disc. A comprehensive evaluation of zygapophyseal joint kinematics and capsular ligament strains in whole cervical spine specimens with muscle force replication models during simulated whiplash support that the zygapophyseal joint is at risk for injury. (Pearson et al. 390-97) The mechanism of zygapophyseal joint injuries during whiplash may involve excessive articular compression and or capsular strain associated with aphysiological translation and loading.(Pearson et al. 390-97) This strain triggers cervical pain, as the joint capsule is well innervated by the medial branches of the dorsal rami, where each medial branch segmentally innervates multiple zygapophyseal joints.(Bogduk 319-30) Mechanoreceptors are present within the joint capsule that may respond to noxious stimuli from excessive capsular loading.(McLain 495-501) The S-curvature of the cervical spine during the early phase of the whiplash event causes compression in the dorsal region of the zygapophyseal joint accompanied by ventral joint distraction.(Stemper, Yoganandan, and Pintar 1764-71) As a consequence, zygapophyseal capsular strain occurs in the second phase of whiplash due to the separation of the joint surfaces. If a whiplash event is severe enough to injure the joint capsule, zygapophyseal capsule overstretch is a possible cause of persistent neck pain.(Cavanaugh et al. 63-67;Winkelstein et al. 1238-46) Segmental instability can develop in a whiplash event and complicate zygapophyseal involvement. When present, excessive segmental translation can compromise the stability of the functional spinal unit. Besides creating pain from abnormal loading, this excessive motion at a facet that exhibits degenerative articular

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processes could cause irritation of the medial branch of the dorsal ramus as it courses dorsolaterally around that process.(Zhang et al. 1379-84) Painful zygapophyseal joints associated with Late Whiplash Syndrome can be challenging to manage. Clinicians can implement joint-specific mobilization and stability skills training to reduce pain and normalize motion. If clinicians fail to consider the prevalence of zygapophyseal joint pain in Late Whiplash Syndrome, it is possible that many patients may go undiagnosed.(Aprill and Bogduk 744-47) The inability of imaging to adequately detect injuries of the zygapophyseal joints after whiplash increases the diagnostic controversy amongst clinicians. Yet, further evidence for joint pain has been demonstrated using short versus long lasting diagnostic blocks of the cervical zygapophyseal joints .(Barnsley et al. 20-25) Using this approach, Barnsley et al demonstrated a 40% to 68% prevalence of zygapophyseal joint pain, where the most common levels for symptomatic joints were C2-3 and C5-6. The role of disc pathology in whiplash injuries is relatively clear. The intervertebral discs of the cervical spine receive innervation from the ventral primary ramus via the sinuvertebral nerves.(Bogduk, Windsor, and Inglis 2-8) These nerve fibers enter the disc in the posterolateral direction and are present throughout the annulus but are most numerous in the middle third of the discs annular material.(Mendel, Wink, and Zimny 132-35) The posterolateral region of the disc contains receptors resembling Pacinian corpuscles and Golgi tendon organs demonstrating a mechanoreceptive function. (Mendel, Wink, and Zimny 132-35) Disc pathology could potentially produce persistent symptoms after whiplash injury by virtue of irritation of these nerves.(Bogduk, Windsor, and Inglis 2-8;Davis et al. 245-51;Hamer et al. 549-50)

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The primary mechanisms for discogenic neck pain associated with Late Whiplash Syndrome are strain or tears at the anterior annulus and strain of the posterior longitudinal ligament when stretched by a bulging disc.(Debois et al. 1996-2002) The integrity of the disc may be compromised during the whiplash injury and lead to acute injury or accelerated disc degeneration. Without surprise, a significantly higher rate of disc degeneration was found in whiplash patients 10 years after the accident when compared to age-matched controls.(Watkinson, Gargan, and Bannister 307-09) Using whole cervical spine specimens, Panjabi et al found that the greatest strains occurred at the posterior region of the C56 disc during simulated whiplash. (Panjabi et al. 1217-25) These data suggest that the C5-6 disc is the most common location for disc lesions in late whiplash syndrome. Clinically confirming this finding, Pettersson combined clinical examination and MRI findings to evaluate 39 whiplash patients within 11 days of injury and at a 2-year follow-up.(Pettersson et al. 283-87) This prospective study demonstrated that 25% of the whiplash patients had positive MRI findings for disc pathology, mainly witnessed at C4-5 and C5-6.

Whiplash-Related Sensorimotor Control Deficits Late Whiplash Syndrome is associated with disturbances in the sensorimotor control system.(Treleaven, Jull, and Lowchoy 224-29) Soft tissue injuries during the whiplash event appear to create pathomechanical changes in segmental control. Thus, a whiplash injury can cause microtrauma to the high density of muscle spindles that act as receptors for proprioception and provide afferent information about extent and rate of change in muscle length, thus impairing the integrity of the functional spinal unit.

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(Richmond and Bakker 49-61) Similarly, whiplash-associated local pain and muscle inflammation may inhibit gamma-motorneuron discharge that could degrade the accuracy of proprioceptive information relayed to the central nervous system by the muscle spindles.(Loudon, Ruhl, and Field 865-68) The ability to reproduce head motions requires integration of proprioceptive information with neuromuscular control. These impairments can lead to control deficits. For example, Loudon et al found not only that the ability to replicate a target position through neck rotation was compromised in chronic whiplash patients, but also that most of these patients were inaccurate in their assessment of neutral, with a tendency to hold their head in a slightly rotated or sidebent position.(Loudon, Ruhl, and Field 865-68) The total range of each rotatory and translatory movement observed in the cervical spine can be divided into neutral and elastic zones.(Klein et al. 141-48) The neutral zone involves the range of movement that occurs with minimal resistance from physiological constraints, while the elastic zone is encountered at the end of the range where tissues tighten and constrain motion. The evaluation of the elastic and neutral zones within the rotatory and translatory motions of a moving segment is a more sensitive parameter detecting changes caused by traumatic injury than a simple measure of ROM.(Panjabi et al. 1111-15)Simulated injury of the spine has been shown to cause an increase of the neutral zone before any significant changes in the ROM were observed.(Oxland and Panjabi 1165-72;Zhu et al. 440-44) A loss of segmental constraint in the elastic zone with an increase in the neutral zone can produce cervical segmental motion control loss, constituting the segmental instability that can persist

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after whiplash trauma and a potential etiology of the pain associated with Late Whiplash Syndrome. Zhu et al found that cadaveric cervical spine specimens responded to high-speed axial trauma in a manner that demonstrated multi-directional movement control loss and resultant instability.(Zhu et al. 440-44) Although late whiplash patients often suffer a reduction in total ROM, the neutral zone increases even in the absence of observable anatomic lesions through imaging.(Panjabi 383-89;Panjabi 390-96) The neutral zone harbors greater possibilities for spinal injury, leaving the spinal segment poorly guided by supporting structures through the movement sequence and setting the stage for aberrant motion control. The segmental instability that can accompany Late Whiplash Syndrome could produce a painful clinical profile with latent, subtle soft-tissue trauma. (Bogduk and Yoganandan 267-75) The longus coli has been shown to play a key role in the stability and control of the head and neck. A study of 36 healthy subjects utilized computerized tomography to compare muscle force and cross-sectional area of neck muscles in relation to cervical spine lordosis and length.(Mayoux-Benhamou et al. 367-71) The longus coli was found to provide support of the cervical lordosis and withstand physiologic loads presented by the head and extension moment generated by contraction of the dorsal neck muscles. This postural function of the longus coli is complimented by the multifidus muscles. (Kristjansson 83-88) Together, these muscles form a sleeve that encloses and stabilizes the cervical spine in all positions of the head.(Mayoux-Benhamou et al. 367-71) Patients with Late Whiplash Syndrome demonstrate performance deficits during the

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craniocervical flexion test, indicating dysfunction or impaired ability to activate the deep cervical flexor muscles that include the longus coli.(Jull GA 143-54) Chronic Whiplash Syndrome can disturb an individuals complex postural control system. Chronic WAD leads to a characteristic pattern of trunk sway that is different from other patient groups with balance disorders, where chronic whiplash patients exhibit trunk sway for stance tasks and complex gait tasks that required task-specific gaze control. These results suggest a pathological vestibular-cervical interaction, making it difficult for chronic whiplash patients to integrate the visual, vestibular, and neck proprioceptive signals needed for generating appropriate balance control mechanisms.(Sjostrom et al. 1725-34)

Neurophysiological Adaptation Chronic whiplash patients may experience widespread sensory hypersensitivity associated with neurophysiological sensitization. Scott et al. conducted a case control study of 29 subjects with chronic WAD, 20 subjects with chronic idiopathic neck pain and 20 pain-free volunteers.(Scott, Jull, and Sterling 175-81) Patients with whiplash were the only group to demonstrate a generalized hypersensitivity to pressure, heat, and cold stimuli independent of anxiety levels. A prolonged and continued barrage of afferent nociceptive stimuli is capable of leading to peripheral and central sensitization. (Cote et al. E445-E458) Peripheral sensitization: The initial tissue injury associated with whiplash may trigger an inflammatory response that can induce sensitization of peripheral nerves. The release of potassium ions, substance P, bradykinin, prostaglandins, and other

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cytokines produces a local sensitization.(Rang, Bevan, and Dray 534-48) This chemical sensitization increases the activity of silent nociceptors, producing clinical hyperpathia that has been observed in patients suffering from chronic WAD. Moreover, gene expression is induced in the dorsal root ganglion due to the peripheral histochemical response. This leads to increased synthesis of peripheral receptors that equates to increased sensitivity of the nociceptive afferent system.(Michael and Priestley 1844-54) Peripheral sensitization results in an increased nociceptive input to the spinal cord. (Curatolo, Arendt-Nielsen, and Petersen-Felix 469-76) Even if the original injury involves an isolated site or tissue, sensitization can lead to diffuse symptoms that imitate a more severe and broad sweeping condition. Central sensitization: Central sensitization involves adaptation within various central nervous system locations, (including the dorsal horn of the spinal cord), to the previously described prolonged peripheral sensitization event and resultant persistent afferent signaling. Chronic whiplash patients display pain hypersensitivity due to an alteration of the central processing of sensory input. This condition appears to be more than a simple psychogenic event.(Curatolo, Petersen-Felix, and Arendt-Nielsen 151730) Relying solely on psychological factors as an explanation for central sensitization ignores the prevailing evidence that injury and tissue damage induces neural hypersensitivity within the central nervous system. It is suggested that central hypersensitivity can be prevented or resolved with the following management approaches: interventional block to reduce nociceptive input from the injured areas, pharmacological intervention to impact central nervous system mechanisms that underlie central hypersensitivity, and pharmacologic or psychological intervention to

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affect the descending modulatory system.(Curatolo, Arendt-Nielsen, and Petersen-Felix 469-76) Reduced cortical inhibition and amplified sensory response involve adaptations in multiple neurophysiological processes. Prolonged afferent nociceptive input may lead to increased excitability of central afferent pathways.(Woolf and Salter 1765-69) Activation of voltage-gated channel receptors involves the entire spinal cord and supraspinal centers in addition to the neural structures connected to the original site of the initiating lesion.(Samad et al. 471-75) Increased peripheral nociception leads to the increased release of substance P,(Rang, Bevan, and Dray 534-48;Alpar et al. 807-11) calcitonin gene-related polypeptide (CGRP),(Alpar et al. 807-11;Cavanaugh et al. 6367) and other substances that sensitize the post-synaptic membranes in both the peripheral and central nervous system. Thus, peripheral sensitization is responsible for primary hyperalgesia, as well as triggering secondary hyperalgesia associated with central sensitization.(Mannion and Woolf S144-S156) These changes have been observed in patients with chronic neck pain following whiplash, suggesting an appreciable hypersensitivity of the nociceptive system to peripheral stimulation. (Curatolo, Petersen-Felix, and Arendt-Nielsen 1517-30)

Role of Psychological Distress An account of psychological distress among whiplash patients with different levels of pain and disability demonstrated that all patients exhibited both impaired motor function and varying degrees of psychological distress. Patients with moderate and severe levels of pain showed greater psychological distress and generalized

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hypersensitivity to a variety of stimuli than those patients with mild symptoms.(Sterling et al. 182-88) This likely has a neurogenic origin, as the force generated with whiplash is capable of causing brainstem lesions, cerebral concussion and stretching of cranial nerves.(Ommaya and Hirsch 13-21) These changes may account, in part, for the psychological changes demonstrated in selected cases of Late Whiplash Syndrome. Gargan et al. studied 50 consecutive patients after rear impact motor vehicle collisions, recording their symptoms and psychological status. For psychological status, the investigators used the General Health Questionnaire to assess factors related to somatic response, social relations, presence of insomnia and depression.(Gargan et al. 523-26) They discovered that the severity of symptoms after a whiplash injury appears to be related both to the physical restriction of neck movement and the accompanying psychological disorder. Whiplash sufferers involvement in litigation regarding their cases gives cause for suspicion that malingering or secondary gain is a contributing factor to the recognizant nature of the symptoms.(Miettinen et al. E47-E51) Noncompliance or non-adherence should not be surprising to the clinician, especially when a patient is frustrated with being sent to treatments that are less probable to succeed.(Bogduk 409-14) In this light, malingering is likely not a medical diagnosis, but rather should be considered a clinical opinion.(Bogduk 409-14) Wallis and Bogduk(Wallis and Bogduk 223-27) compared the psychological profiles, as well as patient responses on pain rating scales, of chronic WAD patients versus students instructed to simulate chronic pain. They concluded that it was quite difficult for an individual to fake a psychological profile typical of a chronic WAD patient.

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The impact of litigation on whiplash patient recovery is controversial. In a large, population-based sample, the accident impact direction was not a determinant of the reported symptoms following the incident, whereas litigation status was a determinant. (Cassidy et al. 1179-86) Alternately, the response to radiofrequency medial branch neurotomy was prospectively compared in two groups of whiplash patients (litigant or non-litigant) with persistent whiplash symptoms that were refractory to prior conservative treatments.(Sapir and Gorup E268-E273) There was no significant difference between the two groups in the degree of symptoms or response to treatment, where both groups experienced significant and equivalent pain reduction with the selected treatment. Thus, the authors refuted the contention that litigation exacerbates whiplash symptoms suggesting that a consideration for whiplash injury only as a secondary gain syndrome and a denial of treatment based on a presumption of malingering could create a grave injustice to patients. Ferrari and Russel asserted that there are different rates of chronic whiplash in countries other than the United States and that chronic injury-related damage cannot account for the wide differences.(Ferrari and Russell 97-98;Ferrari and Schrader 72226) Conversely, the role of litigation may account for these differences, as the use of litigation is relatively low for all purposes in undeveloped countries. Moreover, an ongoing dispute for persistence of whiplash symptoms being mired in the legal system is associated with increased duration of symptoms.(Gun et al. 386-91;Osti OL, Gun RT, and Abraham G 90-94) For example, in Finland a poor outcome at three years after whiplash injury was significantly related to whether the injured persons had unfinished matters with the insurance company.(Miettinen et al. E47-E51)

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A number of studies demonstrate convincing evidence of psychological distress as a contributing factor and possibly the determining factor for whiplash outcome. (McLean et al. 783-90;Ferrari and Russell 1-5;Ferrari and Russell 97-98;Ferrari and Schrader 722-26;Ferrari 2063-64;Ferrari et al. 1337-42;Radanov et al. 442-48) However, there is no conclusive evidence that an individuals psychological status is solely responsible for the development or outcome of Late Whiplash Syndrome. In addition, there is no special psychiatric profile that exists for this disorder. Finally, the psychiatric outcome of whiplash sufferers is no different than other types of injuries caused by road traffic injuries.(Mayou, Bryant, and Duthie 647-51) Post-traumatic stress disorder occurs in roughly 10% of car accident survivors during the first year after the accident.(Mayou, Bryant, and Duthie 647-51) Thus, it is important for the clinician to appreciate the interaction of physical and psychological factors in determining the latent outcome of whiplash.(Mayou, Bryant, and Duthie 64751) It is highly plausible that many conditions have a certain degree of psychological distress that impacts the persons physical response to the injury. Patients with chronic neck pain and headache after whiplash injury have been shown to exhibit psychological profiles that are similar to patients with chronic neck pain alone. In their comparison of chronic whiplash patients and chronic neck pain, Wallis et al reported that a reactive pattern of distress was exhibited among both groups.(Wallis et al. 101-05) This secondary response can involve fear avoidance behaviors and distress associated with somatization, which can be interpreted as the patients belief that something is causing pain in the head or neck, further complicated by the pain-impaired cognitive functioning and subsequent insecurity. Eventually, depression develops as the patient concludes

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that the pain is permanent. This realization triggers hostility, especially if the accident was not the patients fault, or when medical science offered no explanation or cure. (Wallis et al. 101-05)

CLINICAL EXAMINATION OF LATE WHIPLASH SYNDROME PATIENTS While a myriad of signs and symptoms can be observed in Late Whiplash Syndrome, neck pain and headache comprise the cardinal clinical features and are best predicted based on severity of the initial injury.(Barnsley 394-96;Radanov et al. 442-48) Accurate determination of the pain generators responsible for the symptoms associated with whiplash can be arduous and no single diagnostic feature can completely describe the atypical presentation of patients involved in motor vehicle accidents. However, the patients reported pain intensity soon after the accident has been deemed as one of the few prognostic factors linked to clinical management outcome, where a more severe pain intensity is linked with persistent symptoms and the development of Late Whiplash Syndrome.(Radanov, Sturzenegger, and Di 281-97;Cote et al. E445-E458) Minor cervical spine injuries are defined as injuries that do not involve a fracture. (Bogduk and Yoganandan 267-75) This broad description encompasses all of the potential injuries described to this point. Of course, the connotation of a minor injury is that it should heal relatively quickly with little or no intervention. A typical example of this prognostic expectation is the clinical symptoms of muscle spasm and point tenderness. The Quebec Task Force on Whiplash Associated Disorders (WAD) graded whiplash related disorders based on severity and clinical presentation, which has been

26

previously described (Table 1).(Sizer P, Poorbaugh K, and Phelps V 249-66) The risk for WAD at follow-up ranging from 6 to 24 months after injury increases with higher WAD grade classification.(Hartling et al. 36-41) While the Quebec Task Force grading scheme offers selected guidelines for classifying whiplash patients based upon their clinical presentation, it offers little guidance to differentiate the underlying cause of the chronic whiplash patients conditions. In spite of the shortcomings associated with the classification system, Grade II WAD becomes interesting in terms of Late Whiplash Syndrome, as the patients with this condition can suffer from persistent neck pain with muscle spasm and limited ROM that frequently characterize chronic whiplash.(Spitzer et al. 1S-73S) Muscle dysfunction is suspected in many Late Whiplash Syndrome patients but remains difficult to quantify, since the use of palpation to assess point tenderness or muscle spasm is questionable in context with poor interexaminer reliability.(Viikari-Juntura E 1526-32) Muscle dysfunction was used to distinguish patients with chronic Grade II WAD from healthy controls in a study using surface EMG to assess upper trapezius muscle function. (Nederhand et al. 1938-43) Patients with chronic Grade II WAD demonstrated a higher coactivation level of the upper trapezius in the resting arm during performance of unilateral dynamic tasks, along with an inability to relax this muscle to baseline levels after completion of the task. The authors interpreted this unnecessary muscle activation as a generalized decrease in the ability to relax the trapezius muscles. Nederhand et al continued this research into muscle activation patterns with a similarly designed study to determine whether upper trapezius EMG activity could be used to differentiate between patients with chronic Grade II WAD and those with

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nonspecific neck pain.(Nederhand et al. 1056-61) The lack of any statistically significant differences led the authors to conclude that cervical muscle dysfunction is not specific to whiplash trauma but appears to be a general sign in diverse chronic neck pain syndromes.(Nederhand et al. 1056-61) Hence, the presence of palpable point tenderness or hardness of muscles is of little specific diagnostic value. While the presence of muscle tenderness and spasm is a salient feature in whiplash patients, an accurate diagnosis relies on the use of examination tools and methods that are quantifiable and contribute to the differential diagnosis of the patient. The lack of significant findings with advanced imaging among chronic whiplash sufferers often leads to misdiagnosis and generalized treatment. Thus, the clinician is led to believe that if the injury cannot be demonstrated upon imaging, perhaps there is no injury.(Bogduk and Yoganandan 267-75) Even todays advanced imaging lacks credible correlation with clinical and experimental studies of whiplash injuries, which have revealed joint capsule tears, hemarthroses, and fractures of articular cartilage. (Jonsson, Jr. et al. 2733-43;Matsumoto et al. 19-24;Taylor and Twomey 1115-22;Abel 469-553;Bogduk and Mercer 633-48) While cervical spine imaging can give an

appreciation of age-related changes that have the same prevalence in asymptomatic individuals,(Borchgrevink et al. 425-28;Ellertsson AB, Sigurjonsson K, and Thorsteinsson T 269-70;Ronnen et al. 93-96) it is possible for lesions to exist in the cervical spine and escape detection on conventional radiography,(Clark et al. 74247;Davis et al. 245-51;Jonsson, Jr. et al. 251-63;Streitwieser et al. 538-42;el-Khoury, Kathol, and Daniel 43-50) magnetic resolution imaging (MRI),(Boden et al. 403-08;Davis et al. 245-51;Fletcher et al. 817-20;el-Khoury, Kathol, and Daniel 43-50) or computed

28

tomography (CT) scanning.(Antinnes et al. 98-101;Fletcher et al. 817-20;el-Khoury, Kathol, and Daniel 43-50) Minor radiographic findings, such as loss of cervical lordosis, can be interpreted as normal or simply a response to local muscle spasm. However, reduced cervical lordosis is a classical sign reflecting the early stages of disc degeneration with a potential kyphotic kink due to internal disc disruption that can occur in response to a whiplash.(Borchgrevink et al. 425-28) The goal of a thorough clinical examination should be to differentially diagnose the pain generators based upon a detailed history and functional examination. The clinician must develop a thorough understanding of the whiplash event and subsequent clinical sequelae. The history of a patient experiencing whiplash syndrome is paramount to understanding the diagnosis and promoting the patients recovery. The history-taking process will require an investigative approach into the mechanism of insult. Moreover, the answers should be forthcoming on the chronic whiplash patients position at time of impact, type of impact, and the level of the patients awareness at the time of the incident. If the history is to be relevant, it must examine details associated with the five clinical questions, or clinical Ws, that include Who?, What?, Where?, When? and Why?. The question of Who? refers to the patients gender, age, occupation and coping style. The question What? identifies the primary or chief complaints of the patient that includes pain, sensory changes, and motor deficits. The question Where? addresses the location of the symptoms, whereas When? examines the initiation and changes in symptoms since initial onset. The answers to these questions help identify patterns of symptom aggravation or alleviation. Lastly and most important in the history

29

of a whiplash patient, the question Why? addresses the etiology of symptom onset and aggravation. The symptom presentation of chronic whiplash patients can be vague in nature. Nonetheless, these symptoms warrant a clinical explanation to educate and reassure the patient. The most common symptoms reported for WAD are neck pain and stiffness, headache, and shoulder pain.(Miettinen et al. E47-E51) Headaches are often the unexplained side-effect of Late Whiplash Syndrome, while they can occasionally serve as the primary complaint.(Lord et al. 1187-90) The prevalence of a broad spectrum of chronic symptoms after whiplash can serve to complicate the interpretation of the clinical examination. The clinician must remain focused on performing a consistent battery of tests in relation to the patients symptoms while maintaining a respect for symptom irritability and severity. A thorough clinical examination should include the assessment of posture, ROM, cervical spine movement behavior, strength and sensorimotor function (Appendix A). Each patient

should be screened to determine the appropriateness for conservative management and indications for referral to the appropriate specialist to rule out or confirm instability or major trauma. A thorough historical account should be followed by observation of posture and presence of any aberrant movement patterns during active movements. Pain provocation tests appear to be the most effective method to evaluate back and neck pain, whereas soft-tissue paraspinal palpatory diagnostic tests are the least reliable. (Seffinger et al. E413-E425) Examination testing is initiated by instructing the patient to perform neck motions in all cardinal planes to assess quantity and quality of movement.

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Symptom behavior is noted throughout the movements to establish a motion limitation and or provocation pattern that indicates one or more particular lesions (see Case Profiles). Reduced ROM after whiplash injury is a prognostic factor that may suggest a recovery delay and can be helpful in categorizing patients when interpreted along with age and gender.(Dall'Alba et al. 2090-94) In the acute stage, whiplash patients will often present with global limits of neck ROM. Guarded movement and painful response in all planes of motion indicate the presence of muscle splinting and the potential for underlying articular and or ligamentous lesions. However, chronic WAD produces a pattern of limited motion suggesting one or more pain generators (see Case Profiles). Segmental instability, or the loss of segmental movement control, may emerge as a consequence of Late Whiplash Syndrome. While greater than 20 in single-level intervertebral rotation is a suggested criterion for identifying abnormal cervical spinal motion,(White AA III) radiographically appreciable cervical spine instability (RACSI) is not present in all patients suffering with cervical segmental instability.(Cook et al. 895906) While the presence of instability in motion studies acutely suggests potentially significant injury and should initiate further appropriate clinical assessment , there is limited evidence to support the use of flexion-extension radiographs to clear the spine of injury acutely following trauma because the sensitivity of the test for identifying substantial injury will likely be very low.(Brown et al. E503-E508) Thus, objectifying whiplash-associated segmental instability becomes a clinical challenge.(Panjabi et al. 1217-25;Derrick LJ and Chesworth BM 6-11)

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Clinical testing of the alar ligament and transverse ligament of atlas (TLA) ligaments has been previously described.(Sizer P, Phelps V, and Brisme JM 136-52) However, outcomes from clinical testing of these ligaments may be unclear. Additionally, the validity or reliability of segmental testing for lower cervical instability has not been established. Therefore, the clinician may be forced to rely on symptom presentation for identifying nonradiographically appreciable cervical instability. Cook et al conducted a comprehensive study to identify subjective and objective clinical identifiers associated with this form of clinical cervical spine instability(Cook et al. 895906) The authors identified subjective symptoms that were most suggestive of nonradiographically appreciable instability, where the top three were: (1) intolerance to prolonged static postures; (2) fatigue and inability to hold head up; and (3) improvement with external support, including use of the hands or a collar. Similarly, the top three objective physical examination findings suggestive of the same condition included (1) poor coordination/neuromuscular control, including poor recruitment and dissociation of cervical segments with movement; (2) abnormal joint play; and (3) motion that is not smooth throughout range (of motion), including segmental hinging, pivoting, or fulcruming.

LATE WHIPLASH SYNDROME GENERAL MANAGEMENT PRINCIPLES Prevention of Whiplash Injury The preventive role of the seat headrest in motor vehicles to limit rearward angular displacement of the occupants head in relation to the torso during a rear-end collision has been investigated. A study conducted soon after the introduction of head

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restraints demonstrated that 29% of drivers without head restraints reported neck injuries during a rear impact, compared to 24% of drivers with head restraints.(O'Neill et al. 399-406) The lack of a clear indication for the preventive use of head restraints was blamed on the improper adjustment of the head restraints. Because there is a relative time lag between the peak accelerations of the torso upon its contact with the seat back and the head upon its contact with the head restraint,(Tencer, Mirza, and Bensel 243240) the distance between the head and headrest should not exceed 10cm.(Svensson et al. 221-27) This differential displacement can be altered by adjusting the head restraint to create a more uniform contact between the torso and the seat and between the head and head restraint.(Tencer, Mirza, and Bensel 2432-40) If adjustable headrests were placed in the up-position, there would be a 28.3% reduction in whiplash injury risk. (Viano and Gargan 665-74)

Prognostic indicators The prognostic factors for a poor recovery from whiplash involves pre-traumatic neck pain, female gender, low education level, a WAD grade of II or III,(Sterner et al. 195-99) work disability, high levels of somatization, sleep difficulties,(Hendriks et al. 408-16) and high initial neck pain intensity.(Hendriks et al. 408-16;Miettinen et al. E47E51) The Fear Avoidance Behavior Questionnaire (FABQ) has been used in a study evaluating the role of fear in the prognosis of recovery. Patients with neck pain were more likely to have a chronic condition but had lower disability scores than low back pain patients. Disability in patients with chronic neck pain was not as highly associated with pain intensity and fear-avoidance beliefs about work activities in comparison with

33

patients with chronic lumbar pain.(George, Fritz, and Erhard 2139-45) The patients individual coping style will significantly influence treatment outcomes.

Conservative Management The primary role of intervention must be centered on patient education, so to improve the patients understanding of the symptoms related to tissue strain and muscle spasm while stressing the high probability of recovery. Clinicians must stress the importance of returning to normal activity for the sake of preventing the development of more disabling and persistent symptoms. Proper patient education is critical to aid patients in overcoming their fears, since the fears are often based on unsubstantiated concerns. The clinician must describe the difference between activities that simply hurt and those that are harmful. Detailed explanation regarding the underlying factors that sustain the patients pain generator(s) and lead to symptoms could aid the patient in recovery, where greater acceptance of pain can be associated with a significant decrease in multiple measurable domains: pain intensity, pain-related anxiety, depression, and physical and psychosocial disability.(McCracken 21-27) Studies of multimodal management for Late Whiplash Syndrome offer promising outcomes for management of persistent whiplash symptoms. Vendrig conducted a study of 26 patients with chronic whiplash symptoms (WAD I or II).(Vendrig, van Akkerveeken, and McWhorter 238-44) All patients received intervention based upon a multimodal treatment program designed to restore normal daily activities and return to work with no real emphasis on pain reduction. The primary emphasis of the treatment regime involved operant conditioning with graded activity to eliminate inappropriate pain

34

behaviors. At a 6-month follow-up, significant gains were observed in terms of pain intensity, activity tolerance and return to work. However, more than 50% of patients did not demonstrate a clinically significant change and 35% did not return to work. The authors suggest that deep-rooted beliefs about pain (avoid activity until symptoms resolved) impaired healing prognosis. The patients individual coping style could significantly influence treatment outcomes. Obvious patterns of avoiding daily activities and non-harmful functions indicate a tendency to avoid, rather than confront, behaviors where the patient fears could result in pain. Proper patient education is critical to aid patients in overcoming these fears, since they are often based on unsubstantiated concerns. According to consensus-based recommendations from the Quebec Task Force on WAD, range of motion exercises should be immediately implemented.(Spitzer et al. 1S-73S) A number of studies point to the importance of early activation as a preferred treatment program for acute whiplash patients.(Mealy, Brennan, and Fenelon 65657;McKinney 1006-08;Borchgrevink et al. 25-31) When asked about the best advice for acute whiplash patients, 90% of clinicians agreed that a return to normal activity , even if it produces symptoms, should be recommended and that exercise therapy is an effective treatment approach in these cases.(Ferrari et al. 1337-42) A systematic review of randomized trials concluded that there is no beneficial evidence for use of manipulation and/or mobilization as the sole treatment for mechanical neck pain.(Gross et al. 1541-48) However, when these treatment procedures were combined with exercise the effects are beneficial for persistent mechanical neck disorders with or without headaches.(Bronfort et al. 788-97) A

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prospective randomized clinical trial evaluated an active intervention program involving manual therapy and gentle exercise that resulted in reduced pain intensity, less sick leave and improved neck range of motion. These results suggested that an active intervention was more effective in reducing pain intensity and sick leave, as well as in retaining/regaining total range of motion versus the standard intervention for chronic whiplash patients.(Rosenfeld et al. 2491-98) The careful application of manual techniques to encourage restoration of physiological articular motion is a valuable treatment tool for persistent neck pain associated with Late Whiplash Syndrome. The clinician must incorporate keen attention to the patients history to rule-out the presence of any red flags or contraindications to mobilization. This pretreatment screening should include a thorough assessment for ligamentous instability and vertebral artery insufficiency, which have been previously described.(Sizer P, Phelps V, and Brisme JM 136-52) After screening, manual therapy should be applied based upon the basic goals of reducing pain and or restoring motion. The decision regarding which of these two therapy goals should be emphasized is based upon the severity of the symptoms and the specificity of the clinical profile. If the patient presents with minor symptoms of pain and stiffness, the goal for manual therapy should focus on restoration of physiological spinal motion. However, a patient complaining of severe neck pain may best benefit from gentle manual techniques to reduce pain and sensitivity.

LATE WHIPLASH SYNDROME CASE PROFILES

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The published contentions that surround Late Whiplash Syndrome are noteworthy, but offer few clinical solutions for guiding the clinician in diagnosis or treatment. Additionally, there is not a single symptom profile for whiplash patients other than the common complaint of neck pain, making the treatment of Late Whiplash Syndrome troublesome. Proper treatment of Late Whiplash Syndrome requires identification of the primary pain generators and development of a comprehensive, individualized treatment program. The presentation associated with Late Whiplash Syndrome include neck pain and stiffness, persistent headache, dizziness, upper limb paresthesia, and psychological emotional symptoms. These symptom characteristics can be further delineated into case profiles that assist the clinician in proper diagnosis and management (Figure 1). For specifically treating the different types of pain generators associated with Late Whiplash Syndrome, the clinician can reflect on the categories that have been established for patients with neck pain that are based on symptom location, including Local Cervical Syndrome, Cervico-Cephalic Syndrome and Cervico-Brachial Syndrome.(Winkel D et al.) In addition, clinicians should give consideration to another clinical profile of Late Whiplash Syndrome, which includes Behavioral Manifestations.

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Late Whiplash Syndrome Clinical Profile 1: Local Cervical Syndrome Local Cervical Syndrome is a disorder that involves local neck symptoms, such as neck pain and stiffness. The primary pain generator may be associated with a disc-related or joint-related disorder. In the case of Late Whiplash Syndrome, the symptoms may arise due to a combination of these etiologies. Local Cervical Syndrome involves complaints of neck pain and stiffness that are local and referred in a non-radicular distribution. For example, cervical internal disc disruption has been shown to cause local and referred symptoms.( Schellhas KP, Smith MD, Gundry CR, Pollei SR. Cervical discogenic pain. Prospective correlation of magnetic resonance imaging and discography in asymptomatic subjects and pain sufferers. Spine. 1996 Feb 1;21(3):300-11; discussion 311-2. Grubb S, Kelly C. Cervical discography: Clinical implications from 12 years of experience. Spine. 2000; 25,11: 1832-1839.) The patient typically describes symptoms that include aching pain that extends from the mid-cervical region down to the mid-thoracic level. Local Cervical Syndrome caused by a disc-related disorder involves symptoms originating from disc. The most frequent spinal segments to present as Local Cervical Syndrome are C5-6 and C6-7,(Barnsley, Lord, and Bogduk 99-106;Lord et al. 1737-44) however a whiplash injury may cause disc lesions at more cranial disc levels (C2 to C4) in response to the trauma. Selected lesions, such as a disc protrusion or herniation, may be radiographically observable with advanced imaging. However, Local Cervical Syndrome may result from an internal disc disruption that fails to show any findings on standard MRI or CT. Painful limits in the sagittal plane are most indicative of a discogenic lesion, with extension being more painful and limited than flexion.
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Painful limits in the transverse plane are more predictive of a zygapophyseal lesion, particularly if the symptoms are aggravated with three-dimensional movements that stress the capsule or cartilage.(Onan, Heggeness, and Hipp 430-39;Goel and Clausen 684-91) Three-dimensional movement behaviors of the cervical spine can be assessed by separately testing the upper and lower cervical spine. To provoke symptoms coming from the upper cervical spine, the clinician would facilitate a threedimensional movement of retraction (producing upper cervical flexion) or protraction (producing upper cervical extension) with rotation or sidenodding. The capsuloligamentous structures of the C0C1 would be best stressed through protraction or retraction and sidenodding. Conversely, C1C2 is most stressed when rotation is added to the same sagittal movements.(Sizer P, Phelps V, and Brisme JM 136-52) Consistent three-dimensional behaviors in the cervical disc segments (C2C3 through C7T1) allow for predictable stress of the articular versus capsuloligamentous structures in those levels.(Cook et al. 895-906;Sizer P, Phelps V, and Brisme JM 2135) To stress the lower cervical zygapophyseal joint capsule, the clinician could facilitate a three-dimensional movement of rotation, followed by ipsilateral sidebending and flexion or extension. The sagittal components of the three-dimensional patterns would emphasize the side contralateral to the direction of rotation during flexion versus the side ipsilateral to rotation during extension. On the other hand, pain from the zygapophyseal articular surface is best provoked on the side contralateral to rotation when the rotation is accompanied by sidebending in the opposite direction. To stress the uncovertebral joint capsule in a similar fashion, testing would require that the first motion be sidebending accompanied by ipsilateral rotation. Conversely, the

39

uncovertebral joint surface is best stressed with sidebending accompanied by contralateral rotation (Appendix A).(Sizer P, Phelps V, and Brisme JM 21-35) Local Cervical Syndrome caused by a disc-related disorder should be managed by specific manual techniques to restore the cervical lordosis and improve mobility throughout the cervical spine and cervicothoracic junction. Joint specific treatment for the cervical spine could involve segmental traction and dorsoventral mobilization to reduce disc loading and improve segmental mobility(Winkel D et al.;Sizer P, Phelps V, and Brisme JM 136-52). General and local manual techniques can be applied to the cervicothoracic junction to improve extension and rotation for the purpose of reducing the movement related stress at cranial segments. An individualized exercise program should involve proprioceptive exercises for the neck and head using saccadic eye movements. Diaphragmatic breathing and other relaxation techniques can be prescribed to reduce elevated resting tone in superficial neck muscles. Gentle conditioning exercise could be utilized to address strength deficits in the scapulothoracic and local cervical muscles. A joint-related disorder can involve the zygapophyseal joints or uncovertebral joints, as these structures respond to adverse loading and stress from microtrauma over a prolonged course. These cocnditions should be managed by specific manual techniques to unload articular joints of the cervical spine. The articular pillar is quite easily palpated during mobility testing. Pain can be provoked from either the zygapophyseal or uncovertebral articular surfaces as these structures are compressed during two-dimensional movements that stress the joint structures (contralateral sidebending and rotation). The painful segments should be treated with gentle pain-

40

relieving techniques such as segmental traction. The stiff or restricted cervical segments can be mobilized to improve rotation or sidebending. The patients home exercise program could include gentle conditioning exercises and postural training for reducing load of the posterior column by emphasizing vertical spine orientation. Finally, a progressive exercise program should be prescribed to improve postural awareness, local cervical muscle strength, and proprioception re-education that incorporate saccadic eye motions. Based upon the work by Mossiman et al, an extra-ocular muscle training program could be used to influence the volitional control of eye movements through a series of alternating memory guided and antireflexive eye movements with and without movement of the head.(Mosimann et al. 828-35) Intervention offered by pain specialists may be indicated to address persistent symptoms related to Late Whiplash Syndrome. The prevalence of cervical zygapophyseal joint pain in chronic neck syndromes has been determined to be as high as 60%.(Lord et al. 1737-44), Randomized clinical trials offer limited evidence that radiofrequency (RF) denervation can afford relief of chronic neck pain of zygapophyseal joint origin.(Lord et al. 1737-44;Wallis, Lord, and Bogduk 15-22;Sapir and Gorup E268E273) In a prospective, double-blind, placebo-controlled study, the effectiveness of RF ablation of the cervical medial branch nerves provided patients a median of 263 days of adequate pain relief,(Lord et al. 1737-44) while acceptable pain relieve was reported one year following cervical radiofrequency neurotomy in patients with chronic whiplash. (Prushansky et al. 365-73).

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Late Whiplash Syndrome Clinical Profile 2: Cervico-Cephalic Syndrome as Related to Cervicogenic Headache Post-whiplash cervicogenic headache has the typical characteristics of a benign headache with moderate intensity and a chronic course.(Drottning 384-86) The criteria that differentiate cervicogenic headache from a migraine are the absence of associated symptoms involving nausea, photo-phobia or aura. A migraine attack typically lasts 4 to 72 hours and requires the sufferer to avoid head movements and bright light or loud noises. Cervicogenic headaches are characterized by a symptom triad: neck pain, stiffness in the neck, and unilateral headache. (Drottning 384-86) Chronic cervicogenic headaches may be associated with reduced cervical range of motion (especially extension), dizziness, and ipsilateral shoulder pain. Internal Disc Disruption (IDD) may be an underlying cause of persistent neck pain and headaches. (Schellhas et al. 300-11) The pathological features of IDD are radial fissures extending from the nucleus pulposus to the innervated outer third of the anulus fibrosis that allow the nerve endings to be exposed to the noxious nucleus pulposus (NP). The IDD is a painful condition in which the internal architecture of the disc is disrupted even though its external appearance remains essentially unchanged.(Schwarzer et al. 1878-83) A normal MR imaging study of the entire cervical spine does not exclude the existence of clinically significant disc disease in patients suffering chronic neck, head, or radicular pain.(Schellhas et al. 300-11) The cervical zygapophyseal joint is another likely culprit for the symptoms associated with cervicogenic headache. Innervation of the joint by the medial branches of the segmental nerves dorsal ramus lends to producing cervicogenic headache

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symptoms when the joint is irritated. Comparative local anesthetic blocks revealed that C2-3 zygapophyseal joint pain was most likely to occur in patients with headache who rated their headache as worse than their neck pain.(Lord et al. 1187-90) Since the cervical zygapophyseal joint is a common pain generator for cervicogenic headache it is important to assess rotation mobility throughout the cervical segments. Joint specific treatment should be specifically applied in a segmental fashion towards either reducing pain at a provocative segment or restoring mobility at restricted levels. Previously described interventional techniques are indicated for these patients as well. Patients can suffer headache associated with craniovertebral instability. Typical symptoms of craniovertebral instability include occipital numbness or paresthesia, headaches, nausea, disorientation, malaise, vertigo, tinnitus, or visual disturbances (as previously described). When the lesion is radiographically appreciable, surgical intervention may be indicated. However, when it is not radiographically appreciable and the upper cervical ligaments are intact, the patient may be suffering from a sensorimotor control disturbance that can be best managed with a comprehensive exercise program. Craniocervical flexion exercise has been seen as an effective tool for the reduction of symptoms related to WAD and cervicogenic headache.(Jull et al. 1835-43) The specific exercise program involves upper cervical flexion and slight flattening of the cervical spine. The goal is to progressively flex or flatten the cervical lordosis with minimal use of the superficial flexors. The beneficial effects of this exercise are improved when combined with manual therapy.(Jull et al. 1835-43)

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Late Whiplash Syndrome Clinical Profile 3: Cervico-Cephalic Syndrome as Related to Cervicogenic Vertigo Cervicogenic vertigo has only recently been recognized in the clinical and scientific domain as a pathological condition that may result due to whiplash. Symptoms of dizziness and impaired balance may occur soon after the neck injury. The etiology of cervicogenic vertigo is based upon the strong interaction between the upper cervical spine and vestibular system. The upper cervical spine plays a significant role in position awareness and orienting the senses to the environment. This region acts as a third sensory organ due to the high neck muscle afference in concert with eye movements coordination. Any conflict or incongruity of input could result in dizziness, imbalance, or nausea.(Treleaven, Jull, and Sterling 36-43) There is no consensus on the methods used to diagnose cervicogenic vertigo. Neck afferents not only assist the coordination of eye, head, and body, but they additionally affect spatial orientation and control of posture.(Brandt 187-96) The complaint of dizziness in the whiplash patients history warrants careful evaluation of the potential triggers for this symptom. Upon physical examination, the presence of any complaints of dizziness or observation of nystagmus must be evaluated for its relation to position. Spontaneous nystagmus indicates a cortical control limitation that requires evaluation by a specialist. Positional nystagmus indicates that some component of balance or position awareness is impaired. A simple maneuver for testing positional nystagmus is to turn the patients head to one side while upright and simply wait for 30 seconds. Any nystagmus that changes direction according to the direction of the head on neck, rather than with gravity, makes cervical vertigo likely. The nystagmus and

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dizziness will normally subside as the position of cervical rotation is held, while in the presence of vascular compromise, the dizziness will increase as the position of cervical rotation is held. However, there is currently no clinical prediction rule that can accurately identify patients at risk for vertebrobasilar insufficiency and there is little evidence substantiating the accuracy of historical information, physical examination screening procedures, or diagnostic imaging to accurately identify patients at risk for vertebrobasilar insufficiency prior to manual therapy interventions.(Childs et al. 300-06) When stemming from proprioceptive disturbances, the clinical management approach includes gentle mobilization, exercise, and instruction in proper posture and use of the neck.(Karlberg et al. 874-82) In some patients the dizziness is due to pathology or dysfunction of upper cervical vertebral segments that can be treated with manual therapy.(Reid and Rivett 4-13) The difficulty in determining the underlying cause of symptoms of dizziness related to neck injury warrants a cautious application of manual therapy and ongoing reassessment. Exercises that incorporate postural awareness and proprioceptive re-education should be applied in a progressive fashion. An extra-ocular muscle retraining program (as previously described) can be utilized to reduce imbalance between cervical afferents and vestibular function.

Late Whiplash Syndrome Clinical Profile 4: Cervico-Brachial Syndrome Cervico-Brachial syndrome involves complaints in the local cervical area and one or both upper extremities. A simple description of this disorder is one that involves a lower cervical segment combined with nerve root irritation from either root tension around a primary disc lesion or root compression associated with stenosis. As

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observed with lower cervical segment, the neck complaints associated with cervicobrachial segment typically involve aching pain that extends from the mid-cervical region to the mid-thoracic level. The radicular symptoms may be described as sharp and shooting in nature indicating irritation of the dorsal root ganglion (DRG).(Winkel D et al.) The DRG is mechanosensitive and it lies in close proximity to its bony borders. (Ebraheim et al. 1619-23) Conversely, radicular arm pain that is slow in onset and aching in nature indicates an actual nerve root irritation. A nerve root compression syndrome is caused by compression that leads to a vascular compromise and an inflammatory response that sensitizes the nerve root to mechanical stimulus. This condition is often associated with bony changes in the uncovertebral joint and zygapophyseal joint articular processes that produce foraminal narrowing and nerve root compression.(Humphreys et al. 2180-84) The clinical examination can yield positive findings that indicate the presence of an irritation of a nerve. Symptoms can be elicited during a cervical sidebending movement away from the painful side, while a reduction of the arm pain follows when the patients painful shoulder is passively abducted. The Spurling test can be used to assess the paucity of the spinal foramen, where the head and neck are rotated and sidebent towards the painful side, followed by axial compression. Onset of the arm pain during this maneuver indicates a nerve root compression syndrome. A multimodal approach has been shown to improve functional outcomes for patients with cervical radiculopathy. A treatment regimen of intermittent mechanical cervical traction, thoracic joint manipulation, and conditioning exercises caused centralizing radicular symptoms and improving functional outcomes in 5 out of 6

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cervico-brachial syndrome patients.(Waldrop 152-59) General or local cervical traction can be utilized to reduce mechanical irritation of the nerve root or dorsal root ganglion. Over the door traction has been shown to be an effective treatment for chronic radiculopathy due to disc herniation.(Constantoyannis et al. 188-92) Finally, previously described cervical stabilization can augment symptom management by reinforcing segmental stability in the system. Interventions have been suggested for the management of cervical radicular pain associated with whiplash. (Slipman et al. 167-74) Investigators examined patients who had failed previous physical therapy management and demonstrated a positive response to fluoroscopically-guided diagnostic cervical selective nerve root blocks. However, they only observed good to excellent treatment results (indicated by VAS and Oswestry disability scores) in 14% of the subjects when treated with therapeutic blocks. A more recent study evaluating the effect of similar therapeutic blocks reported good to excellent results in 20% of their subjects(Slipman et al. 446-54). However, these findings are preliminary and further investigation that evaluates the role of interventions in these patients is merited.

Late Whiplash Syndrome Clinical Profile 5: Behavioral Manifestations Selected investigators suggest the biopsychosocial model should be used as a rationale to describe how pain can become a persistent problem independent of the precise physiologic etiology and extent of impairment in Late Whiplash Syndrome.(Nederhand et al. 1056-61) A prospective cohort study of car accident victims who filed compensation claims demonstrated that the patients coping style played a role in

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recovery during the first few weeks after the accident.(Buitenhuis, Spanjer, and Fidler 896-901) Those claimants who sought palliative relief of symptoms, and who experienced fear, annoyance, anger, or feelings of indadequacy but did not share their fears or concerns with others, were more likely to develop Late Whiplash Syndrome. Inadequate coping that is accompanied by somatization may play a role in the development of chronic symptoms.(Bosma and Kessels 56-65) The biopsychosocial model involves three systems (behavioral, cognitive, and psychophysiologic) that can be triggered in response to the trauma associated with the acceleration-deceleration injury.(Nederhand et al. 1056-61) Under this model, the actual injuries suspected from the trauma could have little influence on the symptom presentation. The biopsychosocial model views the patient as a system integrating biological, psychological, and social dimensions; here, the role of psychological and social factors has the most bearing on the patients recovery. A cornerstone of any treatment regime prescribed to patients with fear avoidance behaviors is active interventions and cognitive-behavioral training to reduce fear of reinjury. Patient education and encouragement are vital components of a treatment program aimed at restoring function and reducing chronicity.(Scholten-Peeters et al. 412-22) In addition, a three-year follow-up of a prospective randomized trial in 97 patients with acute whiplash associated disorders found that active intervention was more effective than a standard intervention for restoring ROM and reducing pain intensity and sick leave.(Rosenfeld et al. 2491-98) Therefore, while written information on injury mechanisms and advice on suitable activities and posture correction can be useful in managing the psychosocial attributes of Late Whiplash Syndrome, active

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exercises and general aerobic activation appear to improve the benefits of these measures.

SUMMARY There is no consensus on the optimal approach for evaluation and management of Late Whiplash Syndrome. The constellation of symptom presentation must be evaluated using an in-depth history and thorough clinical exam. The order of treatment must be guided by a specific diagnosis that determines potential pain generators and contributing factors. Successful treatment regimes involve a multidisciplinary approach. As expected in any instance of chronic pain, there are factors related to psychosocial and behavior, which have some impact not only on symptom presentation but also on treatment outcome. Not withstanding the need to screen patients for any precautions or contraindications to manual therapy it is crucial that a conservative approach includes opportunities for the patient to accept an active role in their recovery.

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REVIEW QUESTIONS:

Instructions: Select the correct answer from the list of alternatives offered with each question. (Alternatives are listed in alphabetical order)

1. The incidence of chronic neck pain associated with whiplash-related disorders is best described by which percentage range? a. b. c. d. 18% to 40% 40% to 55% 5% to 18% 55% to 70%

2. All of the following appear to contribute to a womans greater predisposition for late whiplash syndrome EXCEPT FOR: a. b. c. d. Increased cervical retraction during unanticipated rear impact Increased incidence of cervical segmental spinal instability Increased thickness of cartilage on zygapophyseal joint surfaces Increased transition of ventral neck muscles to a fast-glycolytic type

3. Which structure appears to be the most common pain generator associated with the chronic neck pain produced by whiplash? a. Cervical nerve root b. Dorsal root ganglion

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c. Intervetrebral disc d. Zygapophyseal joint

4. Which of the following best describes the change in passive control exhibited by a motion segment after a whiplash injury? a. Decreased range of motion in the elastic zone b. Decreased range of motion in the neutral zone c. Increased range of motion in the elastic zone d. Increased range of motion in the neutral zone

5. Which muscles appear to be most important in stabilizing the cervical spine? a. b. c. d. Longus Coli and Multifidus Scalenes and levator scapulae Sternocleidomastoid and semispinalis Upper trapezius and semispinalis cervicis

6. All of the following clearly relate to the psychological distress accompanying late whiplash syndrome, EXCEPT FOR: a. Fear-avoidance stemming from post-traumatic stress b. Participation in treatment approached that are destined to fail. c. Presence of a litigation in the patient experience d. The severity of symptoms experienced by the patient

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7. Which of the following WAD grades appears to be frequently related with the persistent neck pain and muscle spasms associated with late whiplash syndrome? a. Grade I WAD b. Grade II WAD c. Grade III WAD d. Grade IV WAD

8. Which element of the clinical examination process is the most critical to proper differential diagnosis of late whiplash syndrome? a. b. c. d. Neural examination Range of motion testing Relevant historical findings Results of advanced imaging

9. All of the following subjective historical findings are most suggestive of nonradiological clinical instability, EXCEPT FOR: a. Fatigue and inability to hold head up b. Intolerance to prolonged static postures c. Pain with coughing or sneezing d. Symptom improvement with external support

10. The first step for intervention in the treatment of patients with acute or Late Whiplash Syndrome involves.

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a. Education and reassure b. Home exercise c. Manual therapy d. Thermal modalities

11. When your late whiplash syndrome patient experiences the greatest pain provocation in the sagittal plane, which of the following lesions should be most suspected? a. b. c. d. Intervertebral disc lesion Muscle strain Uncovertebral joint irritation Zygapophyseal joint capsule sprain

12. Cervicogenic headaches have a symptom presentation that involves a triad of symptoms. All of the following are components of this triad, EXCEPT FOR: a. b. c. d. Neck pain Neck stiffness Tinnitus Unilateral headaches

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13. Nystagmus that initially increases with neck position change and then gradually subsides as that new position is held, is most likely which of the following? a. Abnormal Cortical control from a central nervous system disorder b. Cervicogenic vertigo from a proprioceptive disturbance c. Processing disturbances from a visual disturbance d. Vascular compromise, such as Vertebrobasilar insufficiency

14. Sharp-shooting upper extremity pain associated with late whiplash syndrome is most likely related to irritation of the: a. Dorsal root ganglion b. Nerve root c. Uncovertebral joint d. Zygapophyseal joint

15. All of the following systems are involved in a biopsychosocial model of treatment to chronic symptoms stemming from late Whiplash Syndrome, EXCEPT FOR: a. Behavioral system b. Cognitive system c. Psychophysiological system d. Sociocultural system

Answers:

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1. a 2. c 3. d 4. d 5. a 6. c 7. b 8. c 9. c 10. a 11. a 12. c 13. b 14. a 15. d

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See External File

Figure 1: Diagnosis and treatment algorithm of Whiplash Syndrome

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Table 1: Grades of Whiplash Related Disorders According to the Quebec Task Force on Whiplash Associated Disorders (WAD)

Grade 0 1 2 3 4

Description No Neck Symptoms or Physical Signs Neck Pain, Stiffness, or Tenderness only; No Physical Signs Neck Symptoms and Musculoskeletal Signs Neck Symptoms and Neurological Signs Neck Symptoms and Fracture or Dislocation

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Appendix A. Examination of the Cervical Spine Examination of the Cervical Spine Patients Name: Examiner: CHIEF COMPLAINTS Date:

INSPECTION

ACTIVE MOTIONS

Limited: Minimal (<20%), Moderate (20-50%), Severe (>50%) Pain (VAS): Minimal (1-3), Moderate (4-6), Severe (7-10)

Flexion Axial rotation, left Axial rotation, right Sidebend, left Sidebend, right Extension Extension with chin-tuck THREE DIMENSIONAL MOTION TESTS
Pain (VAS): Minimal (1-3), Moderate (4-6), Severe (7-10)

Sidebend with ipsilateral rotation with contralateral rotation Axial Rotation with ipsilateral sidebend with flexion with extension Axial Rotation with contralateral sidebend RESISTED TESTS
indicates ZAJ chondral indicates UVJ capsule indicates UVJ chondral indicates ZAJ capsule

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Strength Grade: Normal (5), Good (4), Fair (3), Poor (2), Trace (1), Absent (0)

Resisted shoulder girdle elevation: C2,3,4 Active Bilateral Arm Elevation Rule out shoulder dysfunction Resisted shoulder abduction: C5 Resisted shoulder adduction: C7 Resisted shoulder internal rotation: C5,6 Resisted shoulder external rotation: C5,6 Resisted elbow flexion: C5,6 Resisted elbow extension: C7 Resisted wrist extension: C6 Resisted wrist flexion: C7 Resisted thumb extension: C8 Resisted little finger adduction: T1 SENSORY TESTING REFLEX TESTING C4 (Supraclavicular) C5 (Shoulder) C6 (Thumb) C7 (Middle finger) C8 (Little finger) T1 (Medial forearm) T2 (Medial arm) Scapulohumeral: C0-4 Biceps: C5,6 Brachioradialis: C5 Triceps: C7 Achilles Tendon: Patellar Tendon: Babinski:

EXTRA TESTS: Positive test indicated by specific symptom provocation/alleviation . Foraminal compression test (Radicular UE symptoms) Rotation in retracted/protracted position (Suboccipital or head pain) Sidebend in retracted/protracted position (Suboccipital or head pain) Alar Ligament Test Transverse Ligament of Atlas Test Palpation:

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Assessment:

16.

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Reference List

Abel, M. S. "Occult traumatic lesions of the cervical vertebrae." CRC Crit Rev.Clin Radiol.Nucl.Med 6.4 (1975): 469-553. Alpar, E. K., et al. "Management of chronic pain in whiplash injury." J Bone Joint Surg Br. 84.6 (2002): 807-11. Amevo, B., C. Aprill, and N. Bogduk. "Abnormal instantaneous axes of rotation in patients with neck pain." Spine 17.7 (1992): 748-56. Antinnes, J. A., et al. "The value of functional computed tomography in the evaluation of soft-tissue injury in the upper cervical spine." Eur.Spine J 3.2 (1994): 98-101. Aprill, C. and N. Bogduk. "The prevalence of cervical zygapophyseal joint pain. A first approximation." Spine 17.7 (1992): 744-47. Awerbuch, M. S. "Whiplash in Australia: illness or injury?" Med J Aust. 157.3 (1992): 193-96. Balla, J. I. "The late whiplash syndrome." Aust.N.Z.J Surg 50.6 (1980): 610-14. Barnsley, L. "Epidemiology of whiplash." Ann.Rheum.Dis. 59.5 (2000): 394-96. Barnsley, L., S. Lord, and N. Bogduk. "Comparative local anaesthetic blocks in the diagnosis of cervical zygapophyseal joint pain." Pain 55.1 (1993): 99-106.

61

Barnsley, L., et al. "The prevalence of chronic cervical zygapophyseal joint pain after whiplash." Spine 20.1 (1995): 20-25. Boden, S. D., et al. "Abnormal magnetic-resonance scans of the lumbar spine in asymptomatic subjects. A prospective investigation." J Bone Joint Surg Am. 72.3 (1990): 403-08. Bogduk, N. "The clinical anatomy of the cervical dorsal rami." Spine 7.4 (1982): 319-30. ---. "The anatomical basis for cervicogenic headache." J Manipulative Physiol Ther. 15.1 (1992): 67-70. ---. "Diagnostic blocks: a truth serum for malingering." Clin J Pain 20.6 (2004): 409-14. Bogduk, N. and S. Mercer. "Biomechanics of the cervical spine. I: Normal kinematics." Clin Biomech (Bristol., Avon.) 15.9 (2000): 633-48. Bogduk, N., M. Windsor, and A. Inglis. "The innervation of the cervical intervertebral discs." Spine 13.1 (1988): 2-8. Bogduk, N. and N. Yoganandan. "Biomechanics of the cervical spine Part 3: minor injuries." Clin Biomech (Bristol., Avon.) 16.4 (2001): 267-75. Borchgrevink, G. E., et al. "Acute treatment of whiplash neck sprain injuries. A randomized trial of treatment during the first 14 days after a car accident." Spine 23.1 (1998): 25-31.

62

Borchgrevink, G. E., et al. "MR imaging and radiography of patients with cervical hyperextension-flexion injuries after car accidents." Acta Radiol. 36.4 (1995): 425-28. Bosma, F. K. and R. P. Kessels. "Cognitive impairments, psychological dysfunction, and coping styles in patients with chronic whiplash syndrome." Neuropsychiatry Neuropsychol.Behav.Neurol 15.1 (2002): 56-65. Brandt, T. "Cervical vertigo--reality or fiction?" Audiol.Neurootol. 1.4 (1996): 187-96. Bronfort, G., et al. "A randomized clinical trial of exercise and spinal manipulation for patients with chronic neck pain." Spine 26.7 (2001): 788-97. Brown, T., et al. "Intervertebral motion after incremental damage to the posterior structures of the cervical spine." Spine 30.17 (2005): E503-E508. Buckwalter, J. A. "Aging and degeneration of the human intervertebral disc." Spine 20.11 (1995): 1307-14. Buitenhuis, J., J. Spanjer, and V. Fidler. "Recovery from acute whiplash: the role of coping styles." Spine 28.9 (2003): 896-901. Bunketorp, L., L. Nordholm, and J. Carlsson. "A descriptive analysis of disorders in patients 17 years following motor vehicle accidents." Eur.Spine J 11.3 (2002): 227-34.

63

Cassidy, J. D., et al. "Effect of eliminating compensation for pain and suffering on the outcome of insurance claims for whiplash injury." N.Engl.J Med 342.16 (2000): 1179-86. Cavanaugh, J. M., et al. "Pain generation in lumbar and cervical facet joints." J Bone Joint Surg Am. 88 Suppl 2 (2006): 63-67. Chester, J. B., Jr. "Whiplash, postural control, and the inner ear." Spine 16.7 (1991): 716-20. Childs, J. D., et al. "Screening for vertebrobasilar insufficiency in patients with neck pain: manual therapy decision-making in the presence of uncertainty." J Orthop.Sports Phys.Ther. 35.5 (2005): 300-06. Clark, C. R., et al. "Radiographic evaluation of cervical spine injuries." Spine 13.7 (1988): 742-47. Constantoyannis, C., et al. "Intermittent cervical traction for cervical radiculopathy caused by large-volume herniated disks." J Manipulative Physiol Ther. 25.3 (2002): 188-92. Cook, C., et al. "Identifiers suggestive of clinical cervical spine instability: a Delphi study of physical therapists." Phys.Ther. 85.9 (2005): 895-906. Cote, P., et al. "A systematic review of the prognosis of acute whiplash and a new conceptual framework to synthesize the literature." Spine 26.19 (2001): E445E458.

64

Curatolo, M., L. Arendt-Nielsen, and S. Petersen-Felix. "Evidence, mechanisms, and clinical implications of central hypersensitivity in chronic pain after whiplash injury." Clin J Pain 20.6 (2004): 469-76. Curatolo, M., S. Petersen-Felix, and L. Arendt-Nielsen. "Sensory assessment of regional analgesia in humans: a review of methods and applications." Anesthesiology 93.6 (2000): 1517-30. Dall'Alba, P. T., et al. "Cervical range of motion discriminates between asymptomatic persons and those with whiplash." Spine 26.19 (2001): 2090-94. Davis, S. J., et al. "Cervical spine hyperextension injuries: MR findings." Radiology 180.1 (1991): 245-51. Deans, G. T., J. N. McGalliard, and W. H. Rutherford. "Incidence and duration of neck pain among patients injured in car accidents." Br.Med J (Clin Res.Ed) 292.6513 (1986): 94-95. Debois, V., et al. "Soft cervical disc herniation. Influence of cervical spinal canal measurements on development of neurologic symptoms." Spine 24.19 (1999): 1996-2002. Deng B, Begeman PC, and Yang KH. "Kinematics of human cadaver cervical spine during low-speed rear-end impacts." STAPP Car Crash J 44 (2000): 171-88. Derrick LJ and Chesworth BM. "Post-motor vehicle accident alar ligament laxity." J Orthop Sports Phys Ther 16 (1992): 6-11.

65

Dolinis J. "Risk factors for "whiplash" in drivers: a cohort study of rear-end traffic crashes." Injury 28 (1997): 173-79. Drottning, M. "Cervicogenic headache after whiplash injury." Curr.Pain Headache Rep. 7.5 (2003): 384-86. Dvorak, J. and M. M. Panjabi. "Functional anatomy of the alar ligaments." Spine 12.2 (1987): 183-89. Dvorak, J., et al. "Biomechanics of the craniocervical region: the alar and transverse ligaments." J Orthop.Res. 6.3 (1988): 452-61. Ebraheim, N. A., et al. "The quantitative anatomy of the cervical nerve root groove and the intervertebral foramen." Spine 21.14 (1996): 1619-23. el-Khoury, G. Y., M. H. Kathol, and W. W. Daniel. "Imaging of acute injuries of the cervical spine: value of plain radiography, CT, and MR imaging." AJR Am.J.Roentgenol. 164.1 (1995): 43-50. Ellertsson AB, Sigurjonsson K, and Thorsteinsson T. "Clinical and radiographic study of 100 cases of whiplash injury." Acta Neurol Scand 57 (1978): 269-70. Evans, R. W. "Some observations on whiplash injuries." Neurol.Clin. 10.4 (1992): 97597. ---. "Chronic whiplash syndrome." Neurology 45.11 (1995): 2117-18. Ferrari, R. "The many facets of whiplash." Spine 26.19 (2001): 2063-64.

66

Ferrari, R. and A. S. Russell. "Epidemiology of whiplash: an international dilemma." Ann.Rheum.Dis. 58.1 (1999): 1-5. ---. "Whiplash: heading for a higher ground." Spine 24.1 (1999): 97-98. Ferrari, R., et al. "A re-examination of the whiplash associated disorders (WAD) as a systemic illness." Ann.Rheum.Dis. 64.9 (2005): 1337-42. Ferrari, R. and H. Schrader. "The late whiplash syndrome: a biopsychosocial approach." J.Neurol.Neurosurg.Psychiatry 70.6 (2001): 722-26. Fletcher, G., et al. "Age-related changes in the cervical facet joints: studies with cryomicrotomy, MR, and CT." AJR Am.J.Roentgenol. 154.4 (1990): 817-20. Freeman MD. A Study of Chronic Neck Pain Following Whiplash Injury. Ann Arbor: UMI Dissertation Services, 1998, 35-39. Freeman, M. D., A. C. Croft, and A. M. Rossignol. ""Whiplash associated disorders: redefining whiplash and its management" by the Quebec Task Force. A critical evaluation." Spine 23.9 (1998): 1043-49. Gargan, M., et al. "The behavioural response to whiplash injury." J.Bone Joint Surg.Br. 79.4 (1997): 523-26. George, S. Z., J. M. Fritz, and R. E. Erhard. "A comparison of fear-avoidance beliefs in patients with lumbar spine pain and cervical spine pain." Spine 26.19 (2001): 2139-45.

67

Goel, V. K. and J. D. Clausen. "Prediction of load sharing among spinal components of a C5-C6 motion segment using the finite element approach." Spine 23.6 (1998): 684-91. Gross, A. R., et al. "A Cochrane review of manipulation and mobilization for mechanical neck disorders." Spine 29.14 (2004): 1541-48. Gun, R. T., et al. "Risk factors for prolonged disability after whiplash injury: a prospective study." Spine 30.4 (2005): 386-91. Hamer, A. J., et al. "Whiplash injury and surgically treated cervical disc disease." Injury 24.8 (1993): 549-50. Hartling, L., et al. "Prognostic value of the Quebec Classification of WhiplashAssociated Disorders." Spine 26.1 (2001): 36-41. Hendriks, E. J., et al. "Prognostic factors for poor recovery in acute whiplash patients." Pain 114.3 (2005): 408-16. Hildingsson, C. and G. Toolanen. "Outcome after soft-tissue injury of the cervical spine. A prospective study of 93 car-accident victims." Acta Orthop.Scand. 61.4 (1990): 357-59. Humphreys, S. C., et al. "The natural history of the cervical foramen in symptomatic and asymptomatic individuals aged 20-60 years as measured by magnetic resonance imaging. A descriptive approach." Spine 23.20 (1998): 2180-84.

68

Ito, S., et al. "Spinal canal narrowing during simulated whiplash." Spine 29.12 (2004): 1330-39. Johnson, G. M. "The sensory and sympathetic nerve supply within the cervical spine: review of recent observations." Man.Ther. 9.2 (2004): 71-76. Jonsson, H., Jr., et al. "Hidden cervical spine injuries in traffic accident victims with skull fractures." J.Spinal Disord. 4.3 (1991): 251-63. Jonsson, H., Jr., et al. "Findings and outcome in whiplash-type neck distortions." Spine 19.24 (1994): 2733-43. Jull GA. " Deep cervical flexor muscle dysfunction in whiplash." J Musculoskeletal Pain 8 (2000): 143-54. Jull, G., et al. "A randomized controlled trial of exercise and manipulative therapy for cervicogenic headache." Spine 27.17 (2002): 1835-43. Kaneoka, K., et al. "Motion analysis of cervical vertebrae during whiplash loading." Spine 24.8 (1999): 763-69. Karlberg, M., et al. "Postural and symptomatic improvement after physiotherapy in patients with dizziness of suspected cervical origin." Arch.Phys.Med.Rehabil. 77.9 (1996): 874-82. Kasch, H., et al. "Development in pain and neurologic complaints after whiplash: a 1year prospective study." Neurology 60.5 (2003): 743-49.

69

Kasch, H., et al. "Headache, neck pain, and neck mobility after acute whiplash injury: a prospective study." Spine 26.11 (2001): 1246-51. Kischka, U., et al. "Cerebral symptoms following whiplash injury." Eur.Neurol. 31.3 (1991): 136-40. Klein, G. N., et al. "Trapped in the neutral zone: another symptom of whiplashassociated disorder?" Eur.Spine J. 10.2 (2001): 141-48. Kristjansson, E. "Reliability of ultrasonography for the cervical multifidus muscle in asymptomatic and symptomatic subjects." Man.Ther. 9.2 (2004): 83-88. Kristjansson, E., et al. "Increased sagittal plane segmental motion in the lower cervical spine in women with chronic whiplash-associated disorders, grades I-II: a casecontrol study using a new measurement protocol." Spine 28.19 (2003): 2215-21. Kumar, S., R. Ferrari, and Y. Narayan. "Looking away from whiplash: effect of head rotation in rear impacts." Spine 30.7 (2005): 760-68. Lee, H., et al. "Proprioception and rotation range sensitization associated with subclinical neck pain." Spine 30.3 (2005): E60-E67. Lord, S. M., et al. "Third occipital nerve headache: a prevalence study." J.Neurol.Neurosurg.Psychiatry 57.10 (1994): 1187-90. ---. "Chronic cervical zygapophyseal joint pain after whiplash. A placebo-controlled prevalence study." Spine 21.15 (1996): 1737-44.

70

Loudon, J. K., M. Ruhl, and E. Field. "Ability to reproduce head position after whiplash injury." Spine 22.8 (1997): 865-68. Mannion, R. J. and C. J. Woolf. "Pain mechanisms and management: a central perspective." Clin.J.Pain 16.3 Suppl (2000): S144-S156. Matsumoto, M., et al. "MRI of cervical intervertebral discs in asymptomatic subjects." J.Bone Joint Surg.Br. 80.1 (1998): 19-24. Mayou, R., B. Bryant, and R. Duthie. "Psychiatric consequences of road traffic accidents." BMJ 307.6905 (1993): 647-51. Mayoux-Benhamou, M. A., et al. "Longus colli has a postural function on cervical curvature." Surg.Radiol.Anat. 16.4 (1994): 367-71. McCracken, L. M. "Learning to live with the pain: acceptance of pain predicts adjustment in persons with chronic pain." Pain 74.1 (1998): 21-27. McKinney, L. A. "Early mobilisation and outcome in acute sprains of the neck." BMJ 299.6706 (1989): 1006-08. McLain, R. F. "Mechanoreceptor endings in human cervical facet joints." Spine 19.5 (1994): 495-501. McLean, S. A., et al. "The development of persistent pain and psychological morbidity after motor vehicle collision: integrating the potential role of stress response systems into a biopsychosocial model." Psychosom.Med. 67.5 (2005): 783-90.

71

Mealy, K., H. Brennan, and G. C. Fenelon. "Early mobilization of acute whiplash injuries." Br.Med.J.(Clin.Res.Ed) 292.6521 (1986): 656-57. Mendel, T., C. S. Wink, and M. L. Zimny. "Neural elements in human cervical intervertebral discs." Spine 17.2 (1992): 132-35. Michael, G. J. and J. V. Priestley. "Differential expression of the mRNA for the vanilloid receptor subtype 1 in cells of the adult rat dorsal root and nodose ganglia and its downregulation by axotomy." J.Neurosci. 19.5 (1999): 1844-54. Miettinen, T., et al. "The possibility to use simple validated questionnaires to predict long-term health problems after whiplash injury." Spine 29.3 (2004): E47-E51. Mosimann, U. P., et al. "Saccadic eye movement disturbances in whiplash patients with persistent complaints." Brain 123 ( Pt 4) (2000): 828-35. Narayan, P. and R. W. Haid. "Treatment of degenerative cervical disc disease." Neurol.Clin. 19.1 (2001): 217-29. Nederhand, M. J., et al. "Cervical muscle dysfunction in chronic whiplash-associated disorder grade 2: the relevance of the trauma." Spine 27.10 (2002): 1056-61. Nederhand, M. J., et al. "Cervical muscle dysfunction in the chronic whiplash associated disorder grade II (WAD-II)." Spine 25.15 (2000): 1938-43. O'Neill, B., et al. "Automobile head restraints--frequency of neck injury claims in relation to the presence of head restraints." Am.J.Public Health 62.3 (1972): 399-406.

72

Obelieniene, D., et al. "Pain after whiplash: a prospective controlled inception cohort study." J.Neurol.Neurosurg.Psychiatry 66.3 (1999): 279-83. Ommaya, A. K. and A. E. Hirsch. "Tolerances for cerebral concussion from head impact and whiplash in primates." J.Biomech. 4.1 (1971): 13-21. Onan, O. A., M. H. Heggeness, and J. A. Hipp. "A motion analysis of the cervical facet joint." Spine 23.4 (1998): 430-39. Osti OL, Gun RT, and Abraham G. "Potential risk factors for prolonged recovery following whiplash injury." Eur Spine J 14 (2005): 90-94. Oxland, T. R. and M. M. Panjabi. "The onset and progression of spinal injury: a demonstration of neutral zone sensitivity." J.Biomech. 25.10 (1992): 1165-72. Panjabi, M. M. "The stabilizing system of the spine. Part I. Function, dysfunction, adaptation, and enhancement." J.Spinal Disord. 5.4 (1992): 383-89. ---. "The stabilizing system of the spine. Part II. Neutral zone and instability hypothesis." J.Spinal Disord. 5.4 (1992): 390-96. Panjabi, M. M., et al. "Multidirectional instabilities of traumatic cervical spine injuries in a porcine model." Spine 14.10 (1989): 1111-15. Panjabi, M. M., et al. "Injury mechanisms of the cervical intervertebral disc during simulated whiplash." Spine 29.11 (2004): 1217-25. Pearson, A. M., et al. "Facet joint kinematics and injury mechanisms during simulated whiplash." Spine 29.4 (2004): 390-97.
73

Pettersson, K., et al. "Disc pathology after whiplash injury. A prospective magnetic resonance imaging and clinical investigation." Spine 22.3 (1997): 283-87. Pettersson, K., et al. "Decreased width of the spinal canal in patients with chronic symptoms after whiplash injury." Spine 20.15 (1995): 1664-67. Prushansky, T., et al. "Cervical radiofrequency neurotomy in patients with chronic whiplash: a study of multiple outcome measures." J.Neurosurg.Spine 4.5 (2006): 365-73. Radanov, B. P., et al. "Relationship between early somatic, radiological, cognitive and psychosocial findings and outcome during a one-year follow-up in 117 patients suffering from common whiplash." Br.J.Rheumatol. 33.5 (1994): 442-48. Radanov, B. P., M. Sturzenegger, and Stefano G. Di. "Long-term outcome after whiplash injury. A 2-year follow-up considering features of injury mechanism and somatic, radiologic, and psychosocial findings." Medicine (Baltimore) 74.5 (1995): 281-97. Rang, H. P., S. Bevan, and A. Dray. "Chemical activation of nociceptive peripheral neurones." Br.Med.Bull. 47.3 (1991): 534-48. Reid, S. A. and D. A. Rivett. "Manual therapy treatment of cervicogenic dizziness: a systematic review." Man.Ther. 10.1 (2005): 4-13. Reitman, C. A., et al. "Intervertebral motion between flexion and extension in asymptomatic individuals." Spine 29.24 (2004): 2832-43.

74

Richmond, F. J. and D. A. Bakker. "Anatomical organization and sensory receptor content of soft tissues surrounding upper cervical vertebrae in the cat." J.Neurophysiol. 48.1 (1982): 49-61. Ronnen, H. R., et al. "Acute whiplash injury: is there a role for MR imaging?--a prospective study of 100 patients." Radiology 201.1 (1996): 93-96. Rosenfeld, M., et al. "Active intervention in patients with whiplash-associated disorders improves long-term prognosis: a randomized controlled clinical trial." Spine 28.22 (2003): 2491-98. Samad, T. A., et al. "Interleukin-1beta-mediated induction of Cox-2 in the CNS contributes to inflammatory pain hypersensitivity." Nature 410.6827 (2001): 47175. Sapir, D. A. and J. M. Gorup. "Radiofrequency medial branch neurotomy in litigant and nonlitigant patients with cervical whiplash: a prospective study." Spine 26.12 (2001): E268-E273. Schellhas, K. P., et al. "Cervical discogenic pain. Prospective correlation of magnetic resonance imaging and discography in asymptomatic subjects and pain sufferers." Spine 21.3 (1996): 300-11. Scholten-Peeters, G. G., et al. "Clinical practice guideline for the physiotherapy of patients with whiplash-associated disorders." Spine 27.4 (2002): 412-22.

75

Schrader, H., et al. "Natural evolution of late whiplash syndrome outside the medicolegal context." Lancet 347.9010 (1996): 1207-11. Schwarzer, A. C., et al. "The prevalence and clinical features of internal disc disruption in patients with chronic low back pain." Spine 20.17 (1995): 1878-83. Scott, D., G. Jull, and M. Sterling. "Widespread sensory hypersensitivity is a feature of chronic whiplash-associated disorder but not chronic idiopathic neck pain." Clin.J.Pain 21.2 (2005): 175-81. Seffinger, M. A., et al. "Reliability of spinal palpation for diagnosis of back and neck pain: a systematic review of the literature." Spine 29.19 (2004): E413-E425. Siegmund, G. P., et al. "Mechanical evidence of cervical facet capsule injury during whiplash: a cadaveric study using combined shear, compression, and extension loading." Spine 26.19 (2001): 2095-101. Siegmund, G. P., et al. "Awareness affects the response of human subjects exposed to a single whiplash-like perturbation." Spine 28.7 (2003): 671-79. Sizer P, Phelps V, and Brisme JM. "Differential diagnosis of local cervical syndrome as compared to cervico-brachial syndrome." Pain Practice 1 (2001): 21-35. ---. "Diagnosis and management of cervicogenic headache and local cervical syndrome with multiple pain generators." J Man Manip Ther. 10 (2002): 136-52. Sizer P, Poorbaugh K, and Phelps V. "Whiplash associated disorders: pathomechanics, diagnosis, and management." Pain Practice 4 (2004): 249-66.

76

Sjostrom, H., et al. "Trunk sway measures of postural stability during clinical balance tests in patients with chronic whiplash injury symptoms." Spine 28.15 (2003): 1725-34. Slipman, C. W., et al. "Therapeutic selective nerve root block in the nonsurgical treatment of traumatically induced cervical spondylotic radicular pain." Am.J Phys.Med.Rehabil. 83.6 (2004): 446-54. Slipman, C. W., et al. "Outcomes of therapeutic selective nerve root blocks for whiplash induced cervical radicular pain." Pain Physician 4.2 (2001): 167-74. Slipman, C. W., et al. "Provocative cervical discography symptom mapping." Spine J 5.4 (2005): 381-88. Spitzer, W. O., et al. "Scientific monograph of the Quebec Task Force on WhiplashAssociated Disorders: redefining "whiplash" and its management." Spine 20.8 Suppl (1995): 1S-73S. Stemper, B. D., N. Yoganandan, and F. A. Pintar. "Gender- and region-dependent local facet joint kinematics in rear impact: implications in whiplash injury." Spine 29.16 (2004): 1764-71. Sterling, M., et al. "Characterization of acute whiplash-associated disorders." Spine 29.2 (2004): 182-88. Sterner, Y., et al. "The incidence of whiplash trauma and the effects of different factors on recovery." J Spinal Disord.Tech. 16.2 (2003): 195-99.

77

Streitwieser, D. R., et al. "Accuracy of standard radiographic views in detecting cervical spine fractures." Ann.Emerg.Med 12.9 (1983): 538-42. Svensson, M. Y., et al. "The influence of seat-back and head-restraint properties on the head-neck motion during rear-impact." Accid.Anal.Prev. 28.2 (1996): 221-27. Taylor, J. R. and L. T. Twomey. "Acute injuries to cervical joints. An autopsy study of neck sprain." Spine 18.9 (1993): 1115-22. Tencer, A. F., S. Mirza, and K. Bensel. "The response of human volunteers to rear-end impacts: the effect of head restraint properties." Spine 26.22 (2001): 2432-40. ---. "Internal loads in the cervical spine during motor vehicle rear-end impacts: the effect of acceleration and head-to-head restraint proximity." Spine 27.1 (2002): 34-42. Treleaven, J., G. Jull, and N. Lowchoy. "Standing balance in persistent whiplash: a comparison between subjects with and without dizziness." J Rehabil.Med 37.4 (2005): 224-29. Treleaven, J., G. Jull, and M. Sterling. "Dizziness and unsteadiness following whiplash injury: characteristic features and relationship with cervical joint position error." J Rehabil.Med 35.1 (2003): 36-43. Tropiano, P., et al. "Using a finite element model to evaluate human injuries application to the HUMOS model in whiplash situation." Spine 29.16 (2004): 1709-16. Uhlig, Y., et al. "Fiber composition and fiber transformations in neck muscles of patients with dysfunction of the cervical spine." J Orthop.Res. 13.2 (1995): 240-49.

78

Uitvlugt, G. and S. Indenbaum. "Clinical assessment of atlantoaxial instability using the Sharp-Purser test." Arthritis Rheum. 31.7 (1988): 918-22. Vendrig, A. A., P. F. van Akkerveeken, and K. R. McWhorter. "Results of a multimodal treatment program for patients with chronic symptoms after a whiplash injury of the neck." Spine 25.2 (2000): 238-44. Viano, D. C. and M. F. Gargan. "Headrest position during normal driving: implication to neck injury risk in rear crashes." Accid.Anal.Prev. 28.6 (1996): 665-74. Viikari-Juntura E. "Interexaminer reliability of observations in physical examination of the neck." Phys.Ther. 67 (1983): 1526-32. Waldrop, M. A. "Diagnosis and treatment of cervical radiculopathy using a clinical prediction rule and a multimodal intervention approach: a case series." J Orthop.Sports Phys.Ther. 36.3 (2006): 152-59. Wallis, B. J. and N. Bogduk. "Faking a profile: can naive subjects simulate whiplash responses?" Pain 66.2-3 (1996): 223-27. Wallis, B. J., et al. "The psychological profiles of patients with whiplash-associated headache." Cephalalgia 18.2 (1998): 101-05. Wallis, B. J., S. M. Lord, and N. Bogduk. "Resolution of psychological distress of whiplash patients following treatment by radiofrequency neurotomy: a randomised, double-blind, placebo-controlled trial." Pain 73.1 (1997): 15-22.

79

Watkinson, A., M. F. Gargan, and G. C. Bannister. "Prognostic factors in soft tissue injuries of the cervical spine." Injury 22.4 (1991): 307-09. White AA III, Panjabi MM. Clinical Biomechanics of the Spine. 2nd ed. Philadelphia: Lippincott, 1990. Willauschus, W. G., et al. "Lesions of the alar ligaments. In vivo and in vitro studies with magnetic resonance imaging." Spine 20.23 (1995): 2493-98. Winkel D, et al. Diagnosis and Treatment of the Spine. Nonoperative Orthopaedic Medicine and Manual Therapy. Gaithersburg: Aspen Publishers, Inc., 1996. Winkelstein, B. A., et al. "The cervical facet capsule and its role in whiplash injury: a biomechanical investigation." Spine 25.10 (2000): 1238-46. Woolf, C. J. and M. W. Salter. "Neuronal plasticity: increasing the gain in pain." Science 288.5472 (2000): 1765-69. Yoganandan, N., et al. "Whiplash injury determination with conventional spine imaging and cryomicrotomy." Spine 26.22 (2001): 2443-48. Yoganandan, N., et al. "Anatomic study of the morphology of human cervical facet joint." Spine 28.20 (2003): 2317-23. Zhang, J., et al. "Surgical anatomy of the nerves and muscles in the posterior cervical spine: a guide for avoiding inadvertent nerve injuries during the posterior approach." Spine 28.13 (2003): 1379-84.

80

Zhu, Q., et al. "Traumatic instabilities of the cervical spine caused by high-speed axial compression in a human model. An in vitro biomechanical study." Spine 24.5 (1999): 440-44.

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