Late Whiplash Syndrome: A Clinical Science Approach to Evidence-Based Diagnosis and Management

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1 TUTORIAL Late Whiplash Syndrome: A Clinical Science Approach to Evidence-Based Diagnosis and Management Keith Poorbaugh, PT, ScD, CSCS, FAAOMPT*, ; Jean-Michel Brismée, PT, ScD, OCS, FAAOMPT, ; Valerie Phelps, PT, OCS, FAAOMPT*, ; Phillip S. Sizer Jr, PT, PhD, OCS, FAAOMPT, *Advanced Physical Therapy, Anchorage, AK; International Academy of Orthopedic Medicine, Tucson, Arizona; Texas Tech University Health Science Center, Lubbock, Texas, U.S.A. Abstract: The purpose of this article is to narrow the gap that exists in the clinical application of scientific research and empiric 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 Address correspondence and reprint requests to: Phillip S. Sizer Jr, PT, PhD, OCS, FAAOMPT, Professor and Program Director, ScD Program in PT, Department of Rehabilitation Sciences, School of Allied Health Sciences, Texas Tech University Health Science Center, th St., Lubbock, TX 79430, U.S.A. Submitted: July 5, 2007; Revision Accepted: September 20, World Institute of Pain, /08/$15.00 Pain Practice, Volume 8, Issue 1, among industrialized nations and less developed countries suggests another factor that could influence one s interpretation of symptoms chronicity 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 have 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 purpose 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. Key Words: Facet joint, Injury, Intervertebral disc, Joint instability, Neck, Pain, Spine, Whiplash 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

2 66 poorbaugh et al. 6 months after a whiplash injury. 1,2 Because of the myriad of signs and symptoms with which the patient is capable of presenting, one must consider the many possible different presentations the condition can produce. Whiplash is the most common cause of neck pain associated with chronic musculoligamentous conditions. 2,3 It is estimated that 6.2% of all Americans (approximately 15.5 million) currently suffer from Late Whiplash Syndrome. 2,4,5 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. 2,6 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. 7 9 It is estimated that only 10% of vehicle occupants exposed to a rear-end collision will develop whiplash syndrome. 10 Of these, the incidence of chronic neck pain ranges from 18% to 40%. 10 However, when whiplash symptoms do occur, a delay in symptom onset is expected. Selected studies have demonstrated that the delay in the onset of whiplash symptoms can range from 1 hour to several days after the accident 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. 4,5 However, when presented with chronic symptoms and few causal factors, there is a tendency to suspect underlying nonorganic basis for the patient s symptoms. Structural damage that persists beyond the average healing time for soft-tissue injuries is not common among patients with whiplash. 14 Thus, prolonged disability and limited treatment effectiveness have invoked conflicting views on the role of psychological factors and litigation in a patient s recovery. Various investigators have reported the medico-legal aspects of chronic whiplash and have challenged the organic causes for this disorder, exemplified by the strong association found between retention of a lawyer and delayed recovery from whiplash injury. 14 Even worse, unresolved matters with an insurance provider are strongly associated with a poor outcome from whiplash-associated disorders (WAD) as far out as 3 years after the injury. 21 Thus, it has been contended that Late Whiplash Syndrome should be considered as much a behavioral disorder as a chronic injury. 22 Selected Pathoanatomy and Pathomechanics of Late Whiplash Syndrome Late Whiplash Syndrome involves a myriad of symptoms with considerable overlap between organic and psychosocial origins. 23 A single anatomical site of whiplash injury has yet to be identified. 24 The symbiotic relationship among 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, 25,26 they could serve as primary pain generators in Late Whiplash Syndrome 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. 30 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. 31 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). 32 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. 33 Inertial loading of the trunk and head appears to contribute to the consequences of whiplash injury mechanisms. 6,34,35 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. 36,37 This aphysiological behavior produces pathomechanical tissue responses and potential clinical consequences that have been previously described. 38 For example, trauma may injure cervical facet capsular ligaments that have been shown to suffer injury under combined shear, bending, and compression loads witnessed in a whiplash event. 39 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. 40 Accompanying this response are strain levels in the upper cervical spine ranging from 15% to 26% in the posterior longitudinal ligament and

3 Late Whiplash Syndrome 67 intervertebral discs. Moreover, the order of segmental recruitment during the whiplash even might lend selected segments to more stress than others, especially witnessed at the C5-6 segmental level. 40 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. 41,42 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, 43 where trauma to the cervical spine may accelerate normal age-related disc deterioration. 44,45 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. 46 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 also contribute to the development of pain generators 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 behavior supports the contribution of the zygapophyseal joint to the symptoms associated with Late Whiplash Syndrome. 30 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-end impact causes the diameter of the spinal canal to decrease gradually at C2-3 and C3-4 but remains nearly constant from C4-5 to C Hyperextension of the lower cervical spine occurs in the early phase of whiplash and results in a narrowed spinal canal, because of decreased spinal canal diameter and increased cord diameter. 48 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 vs. a recovered group, especially in those patients with preexisting cervical spondylosis. 49 Any of the structures innervated by the upper cervical segmental nerves can be influenced by a whiplash event, lending to prolonged symptomology. 50 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. 50 Thus, any increased afferent signaling from selected structures innervated by these segmental nerves could trigger cervicogenic headache in this population. 50 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 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 related, in part, 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. 51 The Quebec Task Force on WAD reported that females sustained 60% of all injuries in a cohort of 3014 whiplash patients. 52 Not only are women more likely to sustain a whiplash injury, but they also may be less likely to recover. 53 However, the explanation for these differences is controversial. 49,52 54 Pettersson observed that the spinal canal of female patients was significantly narrower than that of males, 55 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 WAD in comparison to women with idiopathic onset of neck pain, especially in combined rotational and translational hypermobility in the middle cervical spine segments. 56 Similarly, female cadaveric specimens demonstrated significantly greater dorsal shear motion at C4-5 during simulated whiplash when compared to males. 36 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. 29 Simulated rearimpact using human volunteer subjects showed greater degrees of cervical retraction in females who were unaware at time of rear-end impact. 57 This additional

4 68 poorbaugh et al. translation could result in increased strains experienced by restraining structures, such as the facet capsule. Soft-tissue injuries that are common with a rear-end impact could lead to spinal column instability, because of a loss of integrity in the spinal stabilizing system. 41,42 Simulated frontal impacts demonstrated strains in excess of the physiologic limits for supraspinous and interspinous ligaments, as well as ligamentum flavum. 46 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. 58,59 These ligaments have been thoroughly described and can be visualized in a previous article, but a brief description is merited. 60 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. 60 The alar ligaments not only provide the primary restraint to lateral flexion and rotation but also 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. 61 When the head is rotated and flexed, the alar ligaments are maximally stretched and susceptible to injury from sudden acceleration during a vehicle accident. 58,59 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 38 and functional stress radiographic imaging. 62 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 odontoid in place and prevent posterior translation of the process into the spinal canal during cervical flexion. 63 Lesions of the TLA are life-threatening and require immediate referral to a specialist 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. 64 Muscle spasms have the capacity to reduce range of motion (ROM) and to alter IARs. 33 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. 65 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 2 years). Muscles in which transformations had ceased displayed a significantly higher percentage of type IIB fibers than were found in muscles with ongoing transformations. While the stimulus that triggers this transformation is not fully understood, the investigators suggested that it could be the result of factors related to their pathological state, including repeated muscle activity, increased muscular tension, decreased or absent physical activity and/or pain. These factors appear to lend the transitional fibers (type IIC) in the region to transforming into the type IIB fibers. 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 because of reduced neuromuscular control. This may be one of the factors that causes muscle spasms in the presentation of Late Whiplash Syndrome. 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 joint shearing and loading, (4) facet capsular impingement because of local tilting and compression, and (5) dorsal root ganglion (DRG) deformation during transient pressure increases in spinal canal. 66 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. 6

5 Late Whiplash Syndrome 69 The zygapophyseal joint appears to be the single most common pain generator associated with chronic neck pain after whiplash. 28,30 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. 30 However, in a study of 318 patients suffering chronic neck pain (symptoms longer than 6 months), Aprill and Bogduk observed a different pattern of zygapophyseal joint involvement determined through provocative discography and cervical zygapophyseal joint blocks. 27 They found that 53% of 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 supports that the zygapophyseal joint is at risk for injury. 67 The mechanism of zygapophyseal joint injuries during whiplash may involve excessive articular compression and/or capsular strain associated with aphysiological translation and loading. 67 This strain easily 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. 68 Mechanoreceptors are present within the joint capsule that may respond to noxious stimuli from excessive capsular loading. 69 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. 36 As a consequence, zygapophyseal capsular strain occurs in the second phase of whiplash because of 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. 70,71 Segmental instability can develop in a whiplash event and complicate zygapophyseal involvement. When present, this segmental compromise can produce excessive segmental translation. Besides creating pain from abnormal loading, this excessive motion at a facet joint that exhibits degenerative articular processes could cause irritation of the medial branch of the dorsal ramus as it courses dorsolaterally around that process. 72 Painful zygapophyseal joints associated with Late Whiplash Syndrome can be challenging to manage. Clinicians can implement joint-specific mobilization to a painful segment 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 of patients may go undiagnosed. 27 The inability of imaging to adequately detect injuries of the zygapophyseal joints after whiplash increases the diagnostic controversy among clinicians. Yet, further evidence for joint pain has been demonstrated using short vs. long lasting diagnostic blocks of the cervical zygapophyseal joints. 28 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. 73 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 disc s annular material. 25 The posterolateral region of the disc contains receptors resembling Pacinian corpuscles and Golgi tendon organs demonstrating a mechanoreceptive function. 25 Disc pathology could potentially produce persistent symptoms after whiplash injury by virtue of irritation to these nerves 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. 47 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. 45 Using whole cervical spine specimens, Panjabi et al. found that the greatest strains occurred at the posterior region of the C5-6 disc during simulated whiplash. 46 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 magnetic resolution imaging (MRI) findings to evaluate 39 whiplash patients within 11 days of injury and at a 2-year follow-up. 43 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. 76 Soft-tissue injuries

6 70 poorbaugh et al. 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. 77 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. 78 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 that the ability to replicate a target position through neck rotation was compromised in chronic whiplash patients. 78 The total range of each rotatory and translatory movement observed in the cervical spine can be divided into neutral and elastic zones. 79 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 neutral and elastic 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. 80 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. 81,82 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 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 multidirectional movement control loss and resultant instability. 82 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. 41,42 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 softtissue trauma. 34 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. 83 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 complemented by the multifidus muscles. 84 Together, these muscles form a sleeve that encloses and stabilizes the cervical spine in all positions of the head. 83 Patients with Late Whiplash Syndrome demonstrate performance deficits during the craniocervical flexion test, indicating dysfunction or impaired ability to activate the deep cervical flexor muscles that include the longus coli. 85 Chronic Whiplash Syndrome can disturb an individual s 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. 24 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 painfree volunteers. 86 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. 87 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 cytokines produces a local sensitization. 88 This chemical sensitization increases the activity of silent nociceptors, producing

7 Late Whiplash Syndrome 71 clinical hyperpathia that has been observed in patients suffering from chronic WAD. Moreover, gene expression is induced in the DRG because of the peripheral histiochemical response. This leads to increased synthesis of peripheral receptors that equates to increased sensitivity of the nociceptive afferent system. 89 Peripheral sensitization results in an increased nociceptive input to the spinal cord. 90 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 can be interpreted as a central nervous adaptation to the previously described, prolonged peripheral sensitization event, and resulting persistent afferent signaling within various central nervous system locations, including the dorsal horn of the spinal cord. Chronic whiplash patients display pain hypersensitivity because of an alteration of the central processing of sensory input. This condition appears to be more than a simple psychogenic event. 91 A reliance 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 affect the descending modulatory system. 90 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. 92 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. 93 Increased peripheral nociception leads to the increased release of substance P, 88,94 calcitonin gene-related polypeptide, 70,94 and other substances that sensitize the postsynaptic 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. 95 These changes have been observed in patients with chronic neck pain following whiplash, suggesting an appreciable hypersensitivity of the nociceptive system to peripheral stimulation. 91 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 hypersensitivity to a variety of stimuli than those patients with mild symptoms. 96 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. 97 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-end 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. 98 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. 21 Noncompliance or nonadherence should not be surprising to the clinician, especially when a patient is frustrated with being sent to treatments that are less probable to succeed. 99 In this light, malingering is likely not a medical diagnosis, but rather should be considered a clinical opinion. 99 Wallis and Bogduk 100 compared the psychological profiles, as well as patient responses on pain rating scales, of chronic WAD patients vs. 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. 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. 14 Alternately, the response to radiofrequency (RF) medial branch neurotomy was prospectively compared in two groups of whiplash patients (litigant or nonlitigant) with persis-

8 72 poorbaugh et al. tent whiplash symptoms that were refractory to prior conservative treatments. 54 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 Russell 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. 16,101 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. 102,103 For example, in Finland, a poor outcome at 3 years after whiplash injury was significantly related to whether the injured persons had unfinished matters with the insurance company. 21 A number of studies demonstrate convincing evidence of psychological distress as a contributing factor and possibly the determining factor for whiplash outcome. 15,16,101, However, there is no conclusive evidence that an individual s 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 from other types of injuries caused by road traffic injuries. 108 Posttraumatic stress disorder occurs in roughly 10% of car accident survivors during the first year after the accident. 108 Thus, it is important for the clinician to appreciate the interaction of physical and psychological factors in determining the latent outcome of whiplash. 108 It is highly plausible that many conditions have a certain degree of psychological distress that impacts the person s 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. 109 This secondary response can involve fear avoidance behaviors and distress associated with somatization, which can be interpreted as the patient s belief that something is causing pain in the head or neck, thus complicated by the pain-impaired cognitive functioning and subsequent insecurity. Eventually, depression develops as the patient concludes that the pain is permanent. This realization triggers hostility, especially if the accident was not the patient s fault, or when medical science offered no explanation or cure. 109 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 compose the cardinal clinical features and are best predicted based on severity of the initial injury. 107,110 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 patient s 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. 53,87 Minor cervical spine injuries are defined as injuries that do not involve a fracture. 34 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 WAD graded whiplashrelated disorders based on severity and clinical presentation, which has been previously described (Table 1). 38 The risk for WAD at follow-up ranging from 6 to 24 months after injury increases with higher WAD Table 1. Grades of Whiplash-Related Disorders According to the Quebec Task Force on Whiplash Associated Disorders (WAD) Grade Description 0 No neck symptoms or physical signs 1 Neck pain, stiffness, or tenderness only; no physical signs 2 Neck symptoms and musculoskeletal signs 3 Neck symptoms and neurological signs 4 Neck symptoms and fracture or dislocation

9 Late Whiplash Syndrome 73 grade classification. 111 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 patient s 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. 52 Muscle dysfunction is suspected in many Late Whiplash Syndrome patients but remains difficult to quantify, as the use of palpation to assess point tenderness or muscle spasm is questionable in context with poor interexaminer reliability. 112 Muscle dysfunction was used to distinguish patients with chronic Grade II WAD from healthy controls in a study using surface electromyogram (EMG) to assess upper trapezius muscle function. 113 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 if upper trapezius EMG activity could be used to differentiate between patients with chronic Grade II WAD and those with nonspecific neck pain. 114 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. 114 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 with chronic whiplash suffers 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. 34 Even today s 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 While cervical spine imaging can give an appreciation of age-related changes that have the same prevalence in asymptomatic individuals, 49,120,121 it is possible for lesions to exist in the cervical spine and escape detection on conventional radiography, 74, MRI, 74, or computed tomography (CT) scanning. 125,127,128 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 because of internal disc disruption (IDD) that can occur in response to a whiplash. 49 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 patient s 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 patient s position at time of impact, type of impact, and the level of the patient s 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 W s that include Who? What? Where? When? and Why? The question of Who? refers to the patient s 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 if there are any patterns of symptom aggravation or alleviation. Lastly and most important in the history 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. 21 Headaches are often the unexplained side effect of Late Whiplash Syndrome, while they can occasionally serve as the primary complaint. 129

10 74 poorbaugh et al. 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 patient s 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 a physician 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. 130 Examination testing is initiated by instructing the patient to perform neck motions in all cardinal planes to assess quantity and quality of movement. Symptom behavior is noted throughout the movements to establish a motion limitation and/or provocation pattern that indicate one or more particular lesions (see Clinical 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. 131 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 singlelevel intervertebral rotation is a suggested criterion for identifying abnormal cervical spinal motion, 132 radiographically appreciable cervical spine instability is not present in all patients suffering with cervical segmental instability. 133 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. 134 Thus, objectifying whiplash-associated segmental instability becomes a clinical challenge. 46,62 Clinical testing of the alar ligament and TLA ligaments has been previously described. 60 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. 133 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 occupant s head in relation to the torso during a rearend collision has been investigated. A study conducted soon after the introduction of head restraints demonstrated that 29% of drivers without head restraints reported neck injuries during a rear-end impact, compared with 24% of drivers with head restraints. 135 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, 136 the distance between the head and headrest should not exceed 10 cm. 137 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

11 Late Whiplash Syndrome 75 restraint. 136 If adjustable headrests were placed in the up-position, there would be a 28.3% reduction in whiplash injury risk. 138 Prognostic indicators The prognostic factors for a poor recovery from whiplash involve pretraumatic neck pain, female gender, low education level, a WAD grade of II or III, 139 work disability, high levels of somatization, sleep difficulties, 140 and high initial neck pain intensity. 21,140 The Fear Avoidance Behavior Questionnaire 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 patients with chronic lumbar pain. 141 The patient s individual coping style will significantly influence treatment outcomes. Obvious patterns of avoiding daily activities and nonharmful functions indicate a tendency to avoid, rather than confront, behaviors that the patient fears could result in pain. Conservative Management The primary role of intervention must be centered on patient education, so as to improve the patient s 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, as 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 explanations regarding the underlying factors that sustain the patient s 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. 142 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). 143 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 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 patient s individual coping style could significantly influence treatment outcomes. Obvious patterns of avoiding daily activities and nonharmful 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, as they are often based on unsubstantiated concerns. According to consensus-based recommendations from the Quebec Task Force on WAD, ROM exercises should be immediately implemented. 52 A number of studies point to the importance of early activation as a preferred treatment program for acute whiplash patients 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. 106 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. 147 However, when these treatment procedures were combined with exercise, the effects are beneficial for persistent mechanical neck disorders with or without headaches. 148 A 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 ROM. These results suggested that an active intervention was more effective in reducing pain intensity and sick leave, as well as in retaining/ regaining total ROM vs. the standard intervention for chronic whiplash patients. 149 The careful application of manual skills 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 patient s history to rule out the presence of any red flags or contraindi-

12 76 poorbaugh et al. cations to mobilization. This pretreatment screening should include a thorough assessment of ligamentous instability and vertebral artery insufficiency, which have been previously described. 60 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, then 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 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 includes neck pain and stiffness, persistent headache, dizziness, upper limb paresthesia, and psychological emotional symptoms. These symptom characteristics can be further delineated into subcategories that are described in the following case profiles aimed at assisting the clinician in proper diagnosis and management (Figure 1). For 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. These subcategories are based on symptom location, including Local Cervical Syndrome, Cervico Cephalic Syndrome, and Cervico Brachial Syndrome. 150 Figure 1. Diagnosis and Treatment Algorithm of Late Whiplash Syndrome. ROM, range of motion; RFTC, radio frequency thermal coagulation.

13 Late Whiplash Syndrome 77 Thus, in order for clinicians to understand the variety of ways in which Late Whiplash Syndrome can present, they should give consideration to the various different clinical profiles below. Late Whiplash Syndrome Clinical Profile 1: Local Cervical Syndrome Local Cervical Syndrome is a disorder that involves local neck complaints, such as neck pain and stiffness. The primary pain generator may be associated with a discrelated or joint-related disorder. In the case of Late Whiplash Syndrome, the symptoms may arise because of a combination of these etiologies. Local Cervical Syndrome involves complaints of neck pain and stiffness that are local and referred in a nonradicular distribution. For example, cervical IDD has been shown to cause local and referred symptoms. 151 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 a disc lesion. The most frequent spinal segments to present as Local Cervical Syndrome are C5-6 and C6-7; 30,152 however, a whiplash injury may cause disc lesions at more cranial disc levels (C2-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 occur from an IDD 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. Conversely, painful limits in the transverse plane are more predictive of a zygapophyseal lesion, particularly if the symptoms are aggravated with three-dimensional movements to stress the capsule or cartilage. 153,154 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 three-dimensional movement of retraction (producing upper cervical flexion) or protraction (producing upper cervical extension) with rotation or sidenodding. The capsuloligamentous structures of the C0-C1 would be best stressed through protraction or retraction and sidenodding. Conversely, C1-C2 is most stressed when rotation is added to the same sagittal movements. 60 Consistent three-dimensional behaviors in the cervical disc segments (C2-3 through C7-T1) allow for predictable stress of the articular vs. capsuloligamentous structures in those levels (Appendix A). 133,155 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 threedimensional patterns would emphasize the side contralateral to the direction of rotation during flexion vs. 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 away from the rotation. 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 uncovertebral joint surface is best stressed with sidebending accompanied by contralateral rotation. 155 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. 60,150 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 conditions 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 threedimensional movements that stress the joint structures (contralateral sidebending and rotation). The painful segments should be treated with gentle pain-relieving techniques such as segmental traction. The stiff or restricted cervical segments can be mobilized to improve rotation or sidebending. The patient s home exercise

14 78 poorbaugh et al. 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 extraocular 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. 156 Intervention offered by pain specialists may be indicated to address persistent symptoms related to Late Whiplash Syndrome. The prevalence of cervical facet joints being the painful structure in chronic neck pain has been determined to be as high as 60%. 30 Randomized clinical trials offer limited evidence that RF denervation can afford relief of chronic neck pain of zygapophyseal joint origin. 30,54,157 In a prospective, double-blind, placebo-controlled study, the effectiveness of RF ablation of the cervical medial branch nerves afforded patients a median of 263 days of adequate pain relief, 30 while acceptable pain relieve was reported 1 year following cervical RF neurotomy in patients with chronic whiplash. 158 Late Whiplash Syndrome Clinical Profile 2: Cervicogenic Headache Postwhiplash cervicogenic headache has the typical characteristics of a benign headache with moderate intensity and a chronic course. 159 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. 159 Chronic cervicogenic headaches may be associated with reduced cervical ROM (especially extension), dizziness, and ipsilateral shoulder pain. IDD may be an underlying cause of persistent neck pain and headaches. 160 The pathological features of IDD are radial fissures extending from the nucleus pulposus (NP) to the innervated outer third of the annulus fibrosis that allows the nerve endings to be exposed to the noxious 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. 161 A normal MRI 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. 160 The cervical zygapophyseal joint is a likely culprit for the symptoms associated with cervicogenic headache. Innervation of the joint by the medial branches of the segmental nerve s dorsal ramus lends to producing cervicogenic headache 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. 129 As 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, then surgical intervention may be indicated. However, when it is not radiographically appreciable and the upper cervical ligaments are intact, then the patient is 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. 162 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. 162 Late Whiplash Syndrome Clinical Profile 3: Cervicogenic Vertigo Cervicogenic vertigo has only recently been recognized in the clinical and scientific domain as a pathological condition that may result because of 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

15 Late Whiplash Syndrome 79 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 because of the high neck muscle afference in concert with eye movements coordination. Any conflict or incongruity of input could result in dizziness, imbalance, or nausea. 163 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 also affect spatial orientation and control of posture. 164 The complaint of dizziness in the whiplash patient s 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 patient s 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 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. 165 When stemming from proprioceptive disturbances, the clinical management approach includes gentle mobilization, exercise, and instruction in proper posture and use of the neck. 2 In some patients, the cause of the dizziness is pathology or dysfunction of upper cervical vertebral segments that can be treated with manual therapy. 166 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 suggested) 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 observed with lower cervical segment, the neck complaints associated with Cervico-Brachial segment typically involve aching pain that extends from the midcervical region to the mid-thoracic level. The radicular symptoms may be described as sharp and shooting in nature indicating irritation of the DRG. 150 The DRG is mechanosensitive and it lies in close proximity to its bony borders. 167 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. 168 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 patient s 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. In this case, the patient will present with a capsular pattern of limitation that includes restricted extension, bilateral sidebending, and rotation. 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 five out of six Cervico Brachial syndrome patients. 169 General or local cervical traction can be utilized to reduce mechani-

16 80 poorbaugh et al. cal irritation of the nerve root or dorsal root ganglion. Over-the-door traction has been shown to be an effective treatment for chronic radiculopathy because of disc herniation. 170 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. 171 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. 172 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. 114 A prospective cohort study of car accident victims who filed compensation claims demonstrated that the patient s coping style played a role in recovery during the first few weeks after the accident. 173 Those claimants that sought palliative relief of symptoms, experienced fear, annoyance, and anger as well as those who sought palliative relief of symptoms, 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. 9 The biopsychosocial model involves three systems (behavioral, cognitive, and psychophysiologic) that could be triggered in response to the trauma associated with the acceleration-deceleration injury. 114 In essence, the actual injuries suspected to be caused by the trauma could have little influence on the symptom presentation under this model. The biopsychosocial model views the patient as a system integrating biological, psychological, and social dimensions. The role of psychological and social factors has the most bearing on the patient s recovery in this model. A cornerstone of any treatment regime prescribed to patients with fear avoidance behaviors is active interventions and cognitive-behavioral training to reduce fear of re-injury. Patient education and encouragement are vital components of a treatment program aimed at restoring function and reducing chronicity. 174 However, a 3-year follow-up of a prospective randomized trial in 97 patients with acute WAD found that active intervention was more effective than a standard intervention for restoring ROM and reducing pain intensity and sick leave. 149 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 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 symptoms with which patients present 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. A successful treatment regime involves a multidisciplinary approach. As expected in any instance of chronic pain, there are factors related to psychosocial and behavior that have some impact on symptom presentation. Notwithstanding 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. REFERENCES 1. Kasch H, Stengaard-Pedersen K, Arendt-Nielsen L, Staehelin JT. Headache, neck pain, and neck mobility after acute whiplash injury: a prospective study. Spine. 2001;26: Karlberg M, Magnusson M, Malmstrom EM, Melander A, Moritz U. Postural and symptomatic improvement after physiotherapy in patients with dizziness of suspected cervical origin. Arch Phys Med Rehabil. 1996;77: Narayan P, Haid RW. Treatment of degenerative cervical disc disease. Neurol Clin. 2001;19: Freeman MD. A Study of Chronic Neck Pain Following Whiplash Injury. Ann Arbor: UMI Dissertation Services; 1998.

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