Whiplash associated disorders pathomechanics, diagnosis, and management (obligatorio)

Blackwell Science, LtdOxford, UKPPRPain Practice1530-70852004 World Institute of Pain43249266MiscellaneousWhiplash Associated DisordersSIZER Et al.

TUTORIAL

Whiplash Associated Disorders: Pathomechanics, Diagnosis, and Management Phillip S. Sizer Jr, PhD, PT*†; Keith Poorbaugh, MPT†‡; Valerie Phelps, PT†‡ *Texas Tech University Health Science Center, Lubbock, Texas; †International Academy of Orthopedic Medicine-U.S., Tucson, Arizona; ‡Advanced Pain Therapeutics of Alaska, Anchorage, Alaska

Abstract: Whiplash has been defined as an injury mechanism, an injury, a medico-legal or social dilemma, and a complex chronic pain syndrome. Whiplash associated disorders are frequent in the cervical spine, especially as a result of a motor vehicle accident. The mechanisms responsible for whiplash-related tissue trauma are complex and a clinician’s understanding of these complexities lends to a more complete appreciation for the anatomical structures and pathological processes that are involved, as well as a comprehensive diagnosis and appropriate management.

While several classification scales have been developed for whiplash associated disorders, a thorough and tissue-specific examination is merited. Management should be directed toward pain reduction and normalization of mechanics.

While conservative measures can address many of clinical sequelae of whiplash, both invasive pain management procedures and surgical interventions may be paramount to a patient’s complete recovery.

Key Words: cervical, disc, trauma, whiplash, WAD, zygapophyseal

INTRODUCTION The incidence of neck trauma related to motor vehicle accidents is on the rise, due to changes in auto construcAddress correspondence and reprint requests to: Phillip S. Sizer Jr, PhD, PT, Texas Tech University Health Science Center, School of Allied Health, Doctorate of Science Program in Physical Therapy, 3601 4th St., Lubbock, TX, 79430, U.S.A. Tel: (806) 743-3902; E-mail: phil.sizer@ttuhsc.edu.

© 2004 World Institute of Pain, 1530-7085/04/$15.00 Pain Practice, Volume 4, Issue 3, 2004 249–266

tion, traffic patterns, and use of seatbelts.1,2 However, the mere existence of neck pain after a motor vehicle accident can conjure doubts regarding the extent of injury and symptom presentation. Patients often develop symptoms of neck pain after the accident and have significant difficulty in portraying a clear picture of their symptoms. Rarely is there a complete description of the forces involved in the accident but the pain can be quite severe, suggesting significant trauma. The lack of any objective findings on plain radiographs, combined with vague presentation upon clinical examination, can leave many questions unanswered in regards to etiology or sources of pain generation. Often it becomes evident to the clinician that the case involves litigation, which could raise suspicion regarding a patient’s intent toward recovery vs. secondary gain. This scenario can divide many practitioners into groups supporting either a nonorganic or organic model for the symptoms associated with whiplash syndrome, presenting little gray area in between the groups.3 This comes as no surprise, because clinicians are frequently eluded when attempting to objectively quantify the diagnosis of this condition.

Whiplash has been defined as an injury mechanism, an injury, a medico-legal and social dilemma, and a complex chronic pain syndrome.4 As a result, the understanding of whiplash sequelae has long been a dilemma for practitioners. The Quebec Task Force on WhiplashAssociated Disorders (WAD) described whiplash in the

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following manner: “Whiplash is an acceleration-deceleration mechanism of energy transfer to the neck. It may result from rear-end or side-impact motor vehicle collision, but can also occur during diving or other mishaps.

The impact may result in bony or soft tissue injuries, which in turn may lead to a variety of clinical manifestations.”2,5 The cervical spine functions as a complex mechanism that responds to sudden loading in a unique manner, due to intricate structure features and kinematics. As a consequence, apparent minor trauma that occurs during impact can result in extensive injuries to the cervical zygapophyseal joints (ZAJs), ligaments, and discs.6–9

PATHOMECHANICS Whiplash remains the most prevalent term used in scientific literature ascribed to neck injuries associated with a motor vehicle accident. However, the pathological mechanisms of the various pain syndromes associated with whiplash remain a contentious area of debate.

No single diagnostic feature can completely describe the atypical presentation of patients involved in motor vehicle accident. To confound this lack of agreement, little consensus can be found in scientific literature regarding the typical injury sequelae imposed on the cervical spine during a motor vehicle accident. According to Barnsley, whiplash involves three components: (1) event; (2) injury; and (3) clinical syndrome.7 The whiplash event is the biomechanical process experienced during a motor vehicle accident resulting in injuries to tissues including the intervertebral disc, ZAJ, supporting musculature, and ligaments. The injury and clinical syndrome are the tissue response and the patient’s clinical presentation, respectively.

Pathomechanical assessment of the whiplash event is not new to the literature. Historic authors described the mechanisms of an acceleration–deceleration injury of the cervical spine and suggested that they result in a “lash-like effect” on the cervical vertebral column.

Additionally, the term “rail spine” was used in early literature to describe the same traumatic cervical injuries specifically induced during a train accident.10 Whiplash biomechanically emerges from the inertial response of the body to the forces delivered to it, in which the head and neck undergo an excursion without being exposed to any direct blow.7 Extensive research has been conducted regarding the pathological mechanisms to which a motor vehicle occupant is exposed during the whiplash event. General consensus suggests that the cervical spine experiences significant stress and

loading during the acceleration and deceleration associated with the sudden impact in a motor vehicle accident.11–19 In response to a rear-end impact, the occupant’s torso is thrusted forward as it is rapidly contacted by the forward moving seat. This causes a transient S-shaped posturing of the cervical spine, forcing the cervical spine into aphysiologic motions of extension in lower segments and flexion in the upper segments. Energy is stored during this event in the elastic components of the cervical spine, followed by a rapid release of this energy that propels the head and neck forward. This energy release produces subsequent rapid flexion and distraction forces in the cervical spine, lending to further trauma. The consequences of these changes could be profound, as the acceleration forces accompanying aphysiological motion could lead to injury from capsular strain, articular compression, or disc trauma. Moreover, it appears that differences in auto seat stiffness may influence these mechanics and subsequent severity of trauma and symptoms.20,21 A whiplash event can be described by assessing the kinematic pattern and inertia loading that occurs in the spine during a simulated impact. Cusick evaluated the response of the human cadaveric head–neck complex during such an impact. Each specimen was tested at a pendulum speed of 2.2 m/second with acceleration of approximately 4 g. The spine initially assumed the previously described S-curve during the whiplash event.

Almost immediately after impact (approximately 60 ms) the cervical retraction occurred while the head maintained its static inertia.22 Kinematic studies of both human cadaveric specimens18,23 and in-vivo volunteers24,25 demonstrate similar kinematic events that occur during relatively low velocity impacts. These studies support the classical notion of extension as a primary factor affecting the cervical spine on a segmental level. Moreover, they suggest that the cervical spine assumes the S shape shortly after impact as lower segments began to extend while the upper segments are still undergoing initial flexion.

Most of this motion remains within the normal range of cervical spine movement and occurs with little restraint from supporting musculature, due to the latencies required to elicit reflexive muscular activity.18 The timing of selected components during the whiplash event illustrates the challenge that such an event poses to the locomotor system about the cervical spine and head. To demonstrate the rapid nature of the event, the use of high-speed photography has depicted the

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excursions of the neck in experiments on normal volunteers undergoing low velocity rear-end impacts.15 During initial impact (0 to 50 ms) there is no kinematic response of the trunk. Instead, a period of preloading is present as the vehicle acceleration precedes that of the trunk. At 50 to 75 ms the cervical spine undergoes a sigmoid deformation as it is compressed by the rising trunk, such that the lower cervical segments undergo extension while the upper cervical segments flex. During this deformation, the lower cervical segments undergo posterior rotation around an abnormally high axis of rotation, resulting in abnormal separation of anterior elements of the cervical spine and impaction of the ZAJs. By 100 ms the subject’s upper trunk moves upward and forward compressing the cervical spine from below. The head rotates backward in response to the forward shift of the trunk and neck beyond the line of gravity of the head. This backward rotation of the head into extension peaks at about 45∞, depending on the position of any vehicular head restraint. By 160 ms after impact the torso pulls the base of the neck forward creating tension sufficient to draw the head forward into flexion.26,27

PATHOANATOMICAL CONSEQUENCES OF THE WHIPLASH EVENT It has been more acceptable to ascribe a diagnosis of whiplash based on the traumatic event rather than diagnose the condition in relation to the patient’s pathology and or symptoms. As a result, difficulty can arise for the clinician in determining a relevant treatment plan and realistic prognosis for recovery. Therefore, an emphasis should be included regarding the identification of those structures that could potentially serve as pain generators in each case of whiplash syndrome, so to better develop an appropriate management strategy best suited for each patient.

Investigators have suggested the involvement of the cervical ZAJ as a pain generator in WAD, including involvement of the articular surface and capsule of the joint complex.18,28,29 The articular surfaces are oriented in an oblique plane coursing dorsal caudal to ventral cranial at approximately 45∞. This orientation considerably contributes to cervical coupling and lends the joint to compressive events during rotatory and translatory movements with trauma.30 In addition, females demonstrate decreased cartilage thickness on the ZAJ surfaces, predisposing them to greater compromise and aphysiological loading of the subchondral bone vs. males under similar traumatic loads.31

The suspicion for ZAJ involvement in WAD is supported by biomechanical evidence for excessive stress on the joint system during whiplash-simulated events. As previously reviewed, impact causes the cervical spine to assume an unnatural double curvature with the impending axial compression, leading to potentially damaging effects on the articular structures. Additionally, the inertial loading of the cervical spine can create the potential for adverse capsular strain. Axial pre-torque of the head and neck increases the magnitude of facet capsular strains that occur during the bending moments typically experienced during a whiplash event.32 Pearson et al. described the tissue events observed in the ZAJ during a whiplash trauma, which include: (1) lower cervical extension and posterior-inferior sliding of the superior ZAJ articular process, accompanied by posterior tipping and the beginning of joint surface compression in the posterior region of the joint compartment; (2) peak joint surface compression and sliding at terminal extension; (3) lower cervical flexion/distraction recoil with joint surface separation and peak anterior capsular tension; and (4) return of the joint surfaces to a neutral starting position, where the capsular fibers are once again perpendicular to the joint surfaces.33 Cusick similarly observed posterior compression of ZAJ surfaces during the extension event, further objectifying the compressive behaviors in the joint with whiplash trauma.22 Whereas pure sagittal motion cannot produce sufficient movement to stress these capsules in the normal cervical spine under typical physiological loading during active motion,34 the stress associated with whiplash rotatory and shear trauma appears to be sufficient to strain the capsule and stress joint surfaces.29 However, these events appear to be segment-specific. Articular surface compression appears to be greatest at C4C5, whereas surface sliding (or shearing) and capsule strain may be greatest at C6C7.29,33 These differences, combined with a compromised protective action of the lower cervical ZAJ surfaces, may lend to varying clinical predispositions and presentations of the different ZAJ afflictions associated with WAD.35 Whiplash trauma does not appear to be solely the consequence of head and cervical motion, but the interaction of those motions with trunk movements during the traumatic event. Yoganandan observed the interaction of the trunk and cervical ZAJ during a whiplash event and attributed whiplash symptoms of neck pain to a pinching mechanism in the ZAJ that resulted of the forward ascent of the trunk impacting the cervical ZAJs. They suggested that this trunk ascent only occurs for a

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few milliseconds, where the trunk precedes the head in its descent and causes an acceleration pulse.9 The trunk’s forward ascent is significant enough to overload the previously mentioned thin cartilage that covers selected regions of the lower cervical articular facets.31 A synovial-lined capsular envelope surrounds the ZAJs in the cervical spine. Mercer and Bogduk reported possible intra-articular meniscoid projections that extend from the capsule into the cervical synovial joints.36 These projections have the potential for entrapment between articular surfaces notably produced by forceful aphysiological loads witnessed during whiplash trauma. The cervical facet joint capsule is well innervated, receiving its nerve supply from the medial branches of the dorsal rami.37 This nerve supply is comprised of mechanoreceptors and nociceptors, indicating neural input from this spinal structure in proprioception and pain perception. As a consequence of this rich nerve supply, the ZAJ capsule appears to be involved in WAD, as the prevalence of lower cervical facet joint pain in WAD has been reported to be as high as 49%.38 Not withstanding, diagnostic blocks and radiofrequency lesions have been used to suggest the role of the cervical ZAJ as one of the most common source of chronic neck pain after whiplash.11,38–40 Ligaments are frequently injured in response to macrotrauma, and cervical ligaments are particularly vulnerable during the whiplash event. The anterior and posterior longitudinal ligaments are the substantial soft tissue constraints to rotatory and translatory segmental motion in the cervical disc segments. The anterior longitudinal ligament (ALL) demonstrates collagenous layers that course in multiple directions and configurations.36 The ALL is connected to anterior atlantooccipital and atlanto-axial membranes in upper cervical spine, contributing to mechanical continuity between the head and the cervical spine. The ALL is subject to injury during the peak intervertebral extension associated with whiplash trauma, especially in the lower cervical segments.41 In addition, this ligament is site for ossification especially in patients suffering from diabetes.42 This increased ossification contributes to decreased compliance to stress, lending to increased injury potential when ossified.

The posterior longitudinal ligament (PLL) is more developed than the same ligament in the lumbar spine.

Additionally, this cervical ligament provides a more significant biomechanical motion constraint than in the lumbar spine. The PLL is attached to tectorial membrane and demonstrates a very tight connection to the

disc. This ligament possesses a rich population of nociceptive endings, rendering it as a potent pain generator in the context of afflictions to it and the posterior components of the intervertebral disc after tension or shear trauma associated with a whiplash event.

The alar ligaments accompany the transverse ligament of atlas (TLA) in centralizing the dens within the boundaries of C1. Right and left occipital branches of the alar ligament can be observed in all individuals coursing from the posterior tip of the dens to the occiput. These branches are composed of Type I collagen, producing only a 5 to 6% length deformation potential. Right and left atlantal branches of the alar ligament can be observed course only 3 to 4 mm from the anterior dens to the posterior internal surface of the anterior arch of C1 in selected individuals. The alar ligaments are tension loaded with extension, sidebending away from the tested side (contralateral), and rotation toward the involved side (ipsilateral). This ligament system not only helps prevent a tipping of the dens into the brainstem, but it additionally promotes the upper cervical spine coupling behaviors, where any kinetic lateral flexion (sidebending) activity is accompanied by considerable synkinetic rotational motion.

While sitting will accentuate this coupling behavior (due to the gravity loading the facets),43 lesions to the ligaments can increase the range and reduce the control of 3-dimensional coupled movements in the C1C2 motion segment,44 placing the vertebral artery at greater risk for stretching injuries and or sympathetic plexus irritation.45 While the clinical contribution is controversial,4 whiplash trauma can impose permanent damage to the alar ligaments in the ligament bone interface, especially at the condylar insertions to the occiput.46 Whiplash trauma can compromise the TLA in the upper cervical spine.47 The TLA traverses posterior to the dens between lateral masses of C2, prohibiting any separation between C1 and C2. Additionally, this ligament constrains posterior tipping of the dens into the brainstem and spinal cord during forward flexion of the head, which could have potentially serious clinical consequences if allowed after whiplash-induced trauma.48 While demonstrating variation in normal tensile strength, the TLA is the strongest of all ligaments in the upper cervical spine, requiring considerable stress to trigger permanent deformation.49 Injury to the TLA emerges in response to forceful anterior translation and or hyper-flexion of the occiput and C1.47 While injury to this ligament could have life-threatening consequences, its failure is considerably under-diagnosed.50

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The tectorial and posterior atlanto-occipital membranes are vulnerable to permanent deformation in response to the upper cervical hyperflexion and or anterior translation associated with whiplash trauma.51 The tectorial membrane is a strong collagenous structure that serves as a superior continuation of the cervical PLL, connecting the vertebral body of C2 with the basilar groove of the occiput. Selected fibers of this structure are confluent with the dura mater above the level of the dens, as are the fibers of the posterior atlanto-occipital membrane. In a similar fashion, the posterior atlantooccipital membrane functions as an extension of the elastic ligamentum flavum, coursing from the posterior foramen magnum caudally to the posterior atlantal arch. Both membranous structures serve as secondary stabilizers to the craniovertebral junction and failure in either can lend to upper cervical instability.51,52 Moreover, excessive tension loads to these membranes could be transmitted to the dura mater, lending to dural trauma.51 The cervical intervertebral discs are often overlooked as a potential injury site that could cause pain in the acute and chronic phases of WAD.35 The intervertebral discs have limited potential for healing due to relative avascularity. The cervical disc demonstrates distinctive lateral clefts, or “fissures,” associated with the uncovertebral joints (UVJs). These clefts represent the normal physiological adaptation of the cervical disc segment associated with aging.53 The fissures develop over time and eventually communicate, becoming a component of the UVJ as they fill with synovial fluid. The fissures are found in the anular lamellae, where the adjacent collagenous fibers ultimately reorient to course parallel with the fissure.54,55 These clefts are most prominent from C2C3 to C4C5 and less prominent from C5C6 to C7T1.

This prominence is a function of greater translation in the upper cervical disc segments, due to more caudal location of the instantaneous axis of rotation for flexion/extension.

Trauma of the cervical spine may accelerate normal age-related disc degeneration and investigators have identified a high incidence of discoligamentous injuries in whiplash-type distortions.8,56 Moreover, whiplash trauma imposes excessive shear strain and axial deformation on the disc, potentially producing injury and pain generation.57 Clinically, disc lesions have been identified as a contributing factor in the development of chronic neck pain after whiplash injury in 33% of the patients presenting with grade 2 to 3 WAD.58

SENSORY-MOTOR CONTROL STRATEGIES AND WHIPLASH The quality of an individual’s pre-whiplash motor control appears to influence the severity of consequences associated with whiplash trauma. Siegmund was able to demonstrate significant differences in kinematic and muscle response between alert and unaware subjects exposed to sudden perturbation. The investigators concluded that there is a greater potential for injury due to increased capsular strain in females that were unaware of the impending traumatic event at time of perturbation. This is reasonable, considering the previously discussed short latencies involved in the traumatic whiplash event.59 Considering the short event latencies involved in the whiplash event, one would surmise that any automatic reflexive muscle activity during those time intervals could reduce the tissue injury sequelae. To test this, Stemper et al. evaluated the influence of reflexive muscle contraction in unaware whiplash victims through modeling. While reflexive muscle contraction reduced segmental angulations and overall capsular ligament distractions, the reduction was less than 10% and 16%, respectively. In addition, capsular ligament distractions were increased significantly at C5C6 and C6C7 by the same contractions, leading the investigators to suggest that automatic reflexive muscle contractions would unlikely alter cervical kinematics or reduce subsequent tissue injury during a whiplash event.60 While the quality of pre-morbid motor control appears to influence the nature and degree of injuryproducing mechanical events, the nature of posttraumatic control strategies appears to be influenced by whiplash trauma as well. Distorted joint position error, motor recruitment, and motor system function are all consequences of whiplash trauma. Joint position sense and error detection can be altered in concert with distorted sensory information arriving from injured ZAJs. Additionally, muscle group recruitment patterns can be changed in the attempt to reorganize movement strategies after whiplash trauma. As a consequence, range of motion can be reduced as much as 40% in specific directions and motor control can be appreciably distorted. Moreover, distorted control can delay recovery and render the cervical spine vulnerable to further injury.61,62 Investigators have frequently used dynamic posturography to appraise the integrity of advanced control mechanisms associated with the locomotor system and

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balance alterations have been observed in concert with whiplash syndrome.63–65 Whiplash syndrome can compromise automatic postural adjustment responses, producing increased postural sway as result of compromised cervical proprioceptive information. The accelerated muscular fatigue that accompanies the whiplash condition may compound this effect,66 as can the visual disturbances that frequently accompany whiplash syndrome.62 With these control issues in mind, the clinician is encouraged to identify altered control strategies that whiplash patients may demonstrate and incorporate management components that help the patient improve the control of the cervical spine and neck after whiplash trauma.

CLINICAL HISTORY AND THE WHIPLASH PATIENT The Quebec Task Force on Whiplash Associated Disorders has classified the WAD into five different categories based on pathoanatomical changes in response to trauma (see Table 1).2,5,67 In addition, an abbreviated injury scale has been used for judging the severity of an injury (see Table 2) and a more recent classification system has been proposed based on the site of functional impairment and disability (see Table 3).67 While these scales serve to offer objectivity in classifying each patient’s condition after whiplash trauma, they do not negate the importance of a complete account of patient Table 1. The Quebec Task Force on Whiplash Associated Disorders Classification System for WAD Grade 0 1 2 3 4

Table 3. New Whiplash Classification System Based on the Site of Functional Impairment and Disability

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

Table 2. Abbreviated Injury Scale Used for Judging the Severity of an Injury Grade 0 1 2 3 4 5 6

history and functional examination to assist the clinician with identifying the various pain generators present in the patient suffering from WAD. The clinical profile of whiplash associate disorders appears to be multifactorial. The incidence of acute WAD appears to be most frequent in male drivers between 20 and 24 years old, while passengers in the same event are most frequently between 15 and 19 years of age.68 Conversely, female gender, older age, neck pain on palpation, and muscle pain appear to be independently associated with a slower recovery from whiplash, as are pain or numbness radiating from the neck to arms, hands or shoulders, and headache.20,69 Similarly, Hartling et al. suggested that increased age, number of initial physical symptoms, and early development of upper back pain, upper extremity numbness or weakness, and or disturbances in vision all can contribute to increased risk for developing persistent WAD.70 Clinical examination of the whiplash patient begins with a thorough history to include a detailed description of the accident. An understanding of the mechanism of injury would require knowledge of the direction of forces, nature of impact, and general position of the head, neck and body at the point of impact. It is apparent that the traumatic loading of the cervical column during a whiplash event causes significant compression of the articular surfaces and intervertebral discs, due to inertial loading and aphysiological motion. There is adverse capsuloligamentous strain and articular com-

Description No injury Minor injury Moderate injury Serious injury Severe injury Critical injury Virtually unsurvivable injury

Adapted from Tenenbaum A, Rivano-Fischer M, Tjell C, Edblom M, Sunnerhagen KS. The Quebec classification and a new Swedish classification for whiplash-associated disorders in relation to life satisfaction in patients at high risk of chronic functional impairment and disability. J Rehabil Medical. 2002;34:114–118.

Step 1. Determination of area(s) of impairment Area Code Head/neck/shoulders a Arm b Neuropsychological* c Step 2. Categorization of condition based on area of impairment according to step 1 Category Code a A a+b B a+c C a+b+c D Step 3. Time course. A grouping is made based on time after the trauma Definition Term Abbreviation Acute <12 weeks X weeks Xv Chronic >12 weeks Y months Ym *Intensive, frequent or widespread neuropsychological problems such as dizziness, cognitive problems (attention and memory), stress-sensibility, irritability, sound- and light-sensitivity. As understood from the parts above, patients with obvious brain damage are excluded.

Adapted from Tenenbaum A, Rivano-Fischer M, Tjell C, Edblom M, Sunnerhagen KS. The Quebec classification and a new Swedish classification for whiplash-associated disorders in relation to life satisfaction in patients at high risk of chronic functional impairment and disability. J Rehabil Medical. 2002;34:114–118.

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pression due to delayed response of the supporting musculature and high velocity “lash-like” movements of the head.

The whiplash syndrome is comprised of a constellation of symptoms attributed to the injury. The profile of whiplash syndrome remains difficult to define, as each occupant of a particular vehicle may report altogether different symptoms, although they all experienced the same whiplash-producing event. There is no lack of anecdotal evidence that a variety of symptoms could be considered possible components of whiplash syndrome, including cervical pain, headaches, cognitive difficulties, visual obscuration, and dizziness.22,65,67,71 Additionally, patients can present after whiplash trauma with a host of symptoms associated with true neurogenic thoracic outlet syndrome.72 However, the principal constituents of whiplash syndrome are cervical pain and headaches,22 as neck pain is the most commonly reported symptom at the emergency room after a motor vehicle accident.73,74 Dvorak found through a survey of 11 000 cervical injury cases that the symptoms of headache and neck pain were present in 25% of the cases at 4 to 7 years after the motor vehicle accident.75 Hence, clinicians are faced with a pain syndrome that is poorly defined with a high propensity for chronicity.

Headache accompanies neck pain in many patients after whiplash trauma.13,76 Females appear to be at greater risk for this whiplash sequel and a pre-trauma headache history appears to predispose them for headache after whiplash trauma.77 Whiplash-related headaches are typically unilateral in location (but can occasionally present bilaterally), moderate to severe in nature, and last 4 to 72 hours. They are commonly precipitated by physical activity, such as cervical movement or prolonged posturing. However, these headaches can demonstrate unprecipitated attacks that could increase in frequency over time and finally merge into a pattern of chronic, fluctuating persistent headache symptoms. They can be dull and diffused, as well as throbbing in nature. They can be accompanied by photo- and phonophobia, as well as nausea and vomiting. Adjacent interscapular and upper trapezial pain is frequent, along with cervical motion limitations.78–80 Although whiplash-related symptoms may not be localized to a specific region soon after an accident, it is worth noting the pain intensity and general region of involvement. Reports of severe pain intensity soon after an accident are predictive of a poor outcome and increased risk for chronicity.81,82 The location of symptoms may suggest the structures affected, as the disc and

facet joints maintain some predictable elements related to symptom presentation. It is well documented that most pain localized to the neck region is referred from the ZAJs or intervertebral discs.83,84 Symptoms related to ZAJ injury rarely cross the midline or extend beyond the clavicle anteriorly and scapula posteriorly.85 However, discogenic lesions can be quite diffuse presenting centrally along the cervical spine. Additionally, pain can refer cranially to regions of the head, thoracic spine, and upper extremity, in concert with autoimmune and enzymatic activities in the disc and surrounding neural tissues.3,83,86–88 Chronicity associated with WAD can produce symptoms that are more widespread. The propensity for developing chronic symptoms in whiplash syndrome is considerable, with 12% to 40% of patients reporting symptoms that persist as long as a 1 year after the accident.89–91 The tendency for chronicity among a high number of WAD patients has led to the use of the term “late whiplash syndrome” to identify the long-lasting complaints associated with traumatic injury to the neck following an accident. While the persistence of this condition is variable,89,92 late whiplash syndrome is considered a disorder characterized by a constellation of symptoms including headache, neck pain, neck stiffness, dizziness, upper limb parasthesia, temporal-mandibular symptoms, and psychological-emotional disturbances that develop or persist more than 6 months after an injury.93,94 The development of late whiplash syndrome appears to be multifactorial, suggesting a contribution from neurophysiological, cognitive, psychosocial, and emotional components of the neural matrix.95 Hypersensitivity of neural tissues and subsequent hyperalgesia are often observed in patients exhibiting late whiplash syndrome.96–98 For example, Curatolo et al. found that the cutaneous stimulus intensity required to evoke pain is significantly lower in chronic whiplash patients than in healthy subjects. This hypersensitivity to peripheral stimulation in whiplash patients appears to indicate alterations in the central processing of sensory stimuli in late whiplash syndrome.99 Along with hypersensitivity, chronic whiplash symptoms can be confounded by variable involvement of the sympathetic nervous system.100,101 The consequences of sympathetic coupling with the somatic system can range from somatosensory changes, such as persistent neuropathic pain,102,103 to severe vasomotor changes, such as Raynaud-like symptoms in the upper extremity.104 Finally, cervico-trigeminal relay can contribute to late

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whiplash symptoms, involving irritation of the trigeminal nerve nuclei in the cervical spinal cord. For this condition, chemical substances are released in the spinal cord and new interneuronal connections are constructed between the incoming afferent pathways and the trigeminal nuclei.105–107 As a consequence, chronic symptoms can emerge in the head, face, neck, mouth, and ears.

Many cognitive, psychosocial, neuropsychological, and emotional factors should be considered when examining the clinical picture in a patient after whiplash trauma. Cognitive symptoms associated with WAD include exhaustion, lack of concentration, and forgetfulness, while brainstem involvement can produce neuropsychological symptoms, including dizziness, visual and oculomotor disturbances, nausea/emesis, hyperacusis, tinnitus, and dysphagia. Conversely, depressive symptoms include sleep disturbances, irritation, and anxiety.89,91,108 Conclusively, Schmand et al. suggested that these symptoms are inter-related, where patients frequently present with increases in selected symptoms that influence the intensity of others.109 The early emotional aspects of the whiplash injury seem to play a contributory role to the development of late whiplash syndrome. For example, the coping style exhibited during the first few weeks after a car accident has been associated with the development of late whiplash syndrome.110 In a first of its kind, Buitenhuis et al. determined that patients who sought palliative treatment and failed to share their concerns or fear with others were at risk for the further development of late whiplash syndrome.

The influence of biopsychological factors on late whiplash syndrome is complicated by the effect of cultural expectations that generate symptom amplification and attribution.111 Patient profiles can be influenced by impending litigation and or possible gains from malingering behaviors, but the influence is not fully understood. Schmand et al. found that the prevalence of malingering in late whiplash patients is considerable, particularly in context with ongoing litigation.109 Osti et al. reported that the degree of damage to the vehicle was not a predictor of late legal settlement in whiplashrelated litigation. Conversely, they observed a weak association between late settlement and a concurrent workers’ compensation claim, prior neck disability, and or the claimant undergoing physiotherapy and or chiropractic care. Most informative was the strong association they observed between late settlement and the claimant consulting a legal solicitor (producing fourfold increase in time-to-settlement).112

IMAGING Computerize tomography (CT) and magnetic resonance imaging (MRI) could be considered diagnostic for injuries typically associated with neck pain, but linking positive findings to the presence of neck pain is controversial. MRI can be helpful in identifying partial or complete lesions to the alar ligaments after whiplash trauma providing a moderately reliable test for clinical identification of this lesion.45,46,113 Similarly, MRI has been used to accurately identify traumatic failure of the TLA114,115 after whiplash trauma.47 Magnetic resonance can be useful for establishing the limits of failure in the tectorial and posterior atlanto-occipital membranes.51 Finally, MRI has been used to find secondary cervical spondylosis associated with whiplash.116 Putting these more obvious sequelae aside, the use of imaging may be problematic for the diagnosis of WAD.35 Zhu noted that even without bony injury (producing negative plain-film and CT imaging), the cervical spine could become unstable after high-speed trauma involving axial compression, resulting in an enlarged segmental neutral zone.117 As a consequence, the utility of the CT may be isolated to the identification of bony architectural compromise such as fracture, but not useful when evaluating minor whiplash-related injuries.

Minor injuries of the cervical spine are defined as injuries that do not involve a fracture and many whiplash injuries are archetypical of minor injury.27 In the simplest of terms, the minor injuries that do not involve bony trauma can be classified as soft-tissue injuries.

However, if whiplash is nothing more than a muscular injury with no evidence of segmental disturbance, difficulty may arise in explaining Dvorak’s finding that 25% of patients that sustained cervical injuries continued to have symptoms for up to 7 years after the accident.75 Post mortem dissections and operative findings indicate that these injuries can be significant yet remain poorly defined with plain X-ray, CT, or MRI.118 As previously mentioned, any number of soft-tissue injuries can occur including tears to the ZAJ capsule, intervertebral disc lesions, ligamentous rupture and muscular lesions. As the cardinal tool for screening the cervical spine for injury after trauma, plain radiographs cannot identify soft-tissue injuries, leaving the diagnosis as one of clinical exclusion. The problem then lies in the limited ability of radiographic assessment to accurately objectify injuries in the cervical spine. It is a common expectation that any long-standing medical condition can be isolated or further objectified through advanced tests such as an

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X-ray, MRI, or CT. The limits of this notion are that scientific literature has yet to confirm the validity of any specific imaging evaluation for diagnosis of neck pain.

Therefore, it is crucial that the findings of a complete functional examination are given significant weight in determining the potential pain generator rather than solely relying on often erroneous or limited imaging studies.

CLINICAL EXAMINATION AND DIAGNOSIS OF WAD A summation of findings from a complete functional examination is required to gain an accurate diagnosis explaining the majority of physical symptoms and limitations related to WAD. The functional examination of the cervical spine has been previously described,119 but in summary it can be divided into 5 basic areas that focus on an assessment of impairment and pain provocation. The interpretation of the examination results can identify the underlying structures that serve as pain generators in the whiplash clinical profile.

The first part of the examination includes inspection and palpation. Observation of the patient’s posture is important to identify early signs of impaired head positioning. A slightly laterally flexed (sidebent) or rotated position of the head could indicate impaired proprioception or could be typical of an antalgic posture. Normally, the supraclavicular region in the area of the upper trapezius should appear concave as it contours up to the neck. A complete view of the neck and shoulder girdle region could identify the atypical convexity of this area that can indicate an elevated first rib. While palpation at this stage of the examination is used merely to assess skin condition and the presence of swelling, further confirmation could be made by palpation and gentle rib springing to assess first and second rib joint stiffness.

However, any extensive palpation for the localization of specific tenderness will only serve to misguide the examiner to associate areas of tenderness with injury.

Next, the clinician should observe the patient performing cervical range of motion in each of the cardinal planes. The primary goal is to assess quantity and quality of motion, as well as provocation of symptoms. The most common disturbance in function after a whiplash injury is limitation in active range of movement.13,81,120,121 Not only is the range of motion limited, but also it often involves irregular or abnormal movement patterns with marked guarding from supportive musculature. It is possible that significant guarding and apprehension could contribute to marked limits in

range of motion. Therefore, the actual sequence of motion limitations must be assessed to identify a true capsular pattern vs. a noncapsular pattern. Capsular pattern is a specific sequence of limitations of motion in relation to the function and structure of the supporting joint. In the cervical spine it would be represented by a limitation of extension that is worse than the limitation of bilateral rotation and sidebending, followed by even less limits in flexion. The presence of a capsular pattern in the cervical spine after trauma could indicate a fracture or traumatic arthritis of a ZAJ. Conversely, a noncapsular pattern of limitation is any pattern of limitation other than the capsular pattern, where each different noncapsular pattern suggests a particular paingenerating affliction. For example, pain from an internal disc disruption is often midline and diffuse, being most provoked and limited in the sagittal plane due to increased intradiscal pressure.122,123 On the other hand, an injury of the ZAJ will be characterized by smaller asymmetrical limits in rotation and or sidebending.

Moreover, the most provocative motion for zygapophyseal injuries is 3-dimensional rotation either toward or away from the site of pain, based on the commanding influence that the joint system has on rotational movement in the transverse plane.32,124 Finally, while the role of the UVJ in whiplash-related disorders has not been thoroughly discussed in the literature, it has been examined in terms of its role in cervical mechanics and discussed in terms of its impact on local cervical symptomology. In response, one can begin to understand the pain produced by this joint system after whiplash. Therefore, WAD afflictions of the UVJ will typically be most provoked and asymmetrically limited during cervical lateral flexion (sidebending), due to that joint’s constraint on that movement.30,125 A complete neurological assessment should include myotome testing, as well as assessment of sensory functions and reflexes that includes the scapulohumeral reflex, which examines the neurological integrity of the upper cervical cord levels.126 The inclusion of Babinski and Hoffmann reflexes is crucial in the examination of the whiplash patient, as the integrity of the spinal cord could be compromised with cervical trauma in patients with premorbid canal narrowing. Ito et al. found that the spinal cord narrowed with simulated whiplash trauma, especially at C5C6. However, the investigators suggested that the narrowing would not likely injure the spinal cord during whiplash, unless the individual possessed previous narrowing.127 Even so, clinicians should screen whiplash patients for this possibility.

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The basic resistive test screening of the shoulder girdle and upper extremity is sufficient to clear the myotomes for C2-T1. The cervical spine motions can be tested to assess myotome for C1 during cervical flexion and to potentially rule out significant injury. It is crucial to provide adequate support and prevent any motion during isometric resistive testing, so to avoid exacerbation of symptoms that do not relate to the actual test of musculotendinous function.

Cervical motion limits observed in whiplash patients can be accompanied by disturbed motion patterns in specific cervical segments. As a consequence, segments can be hyper- or hypomobile, depending on the level and extent of involvement. To understand these segmental disturbances, investigators have evaluated the normal behaviors of the instantaneous axes of rotation (IAR) for cervical spine segments and potential alterations of those behaviors with pathology.17,128,129 For example, Dimnet et al. identified normal distributions of the IAR at each cervical segmental level in patients with neck pain. Their results suggested that abnormal patterns of segmental movement present in the patient group could be reflected by deviations of the IAR away from accepted normative behaviors. Moreover, they supported the notion that it is possible for distorted segmental motion in an injured cervical segment to produce altered IAR in an adjacent segment.130,131 This provides an explanation to the propensity for the cervical spine to compensate in the presence of injury. After whiplash injury the presence of impaired and limited motion may be due to an injury at one segment leading to an altered IAR at segment typically cranial to the injured segment.

While representing a segment with a motion disturbance, the level of abnormal IAR (instantaneous axis of rotation; see “Biomechanics”) does not appear to correspond with the level of pain generation. Amevo et al. found that abnormal IAR significantly correlated with the presence of chronic neck pain in 109 patients but the location of an abnormal axis did not correlate with the segmental source of pain determined by provocative discography or ZAJ blocks.131 Thus, because the pain-producing segment in the cervical spine may not correspond with the segment demonstrating altered mechanics and mobility, it is paramount that the clinician distinguishes between those segmental levels that are pain generators and those that are mechanically altered. For example, a whiplash-related disc lesion at C6C7 could be accompanied by an altered IAR and restricted motion at C2C3 or C3C4, while C1C2 and

or C0C1 can demonstrate laxity associated with ligament injury.

There are special tests to provide the clinician with an indication of instability in the atlanto-occipital region, including tests that appraise the alar ligament complex and transverse ligament of the atlas (TLA).

These tests are indicated in the presence of the cardinal signs of upper cervical instability, which include complaints of dizziness, confusion, blurred vision, or drop-attacks. Alar ligament integrity can be assessed by stabilizing the spinous process of C2 and then attempting to manually sidenod the cranium.44,132,133 If the ligament is intact, the movement is arrested, while a disrupted ligament allows the movement in spite of attempts to stabilize the C2 vertebra. The TLA can be assessed by stabilizing C2 on C3 followed by manually translating the occiput and C1 vertebra in an anterior direction. If the ligament is intact then the test is asymptomatic, while testing a disrupted ligament results in the production of previously mentioned symptoms.

Segmental rotation and translation disturbances can emerge as a consequence of late whiplash syndrome.133 Amevo et al. observed the segment most frequently identified with abnormal IAR was C2C3, while the most positive responses to zygapophyseal blocks and provocation discography occurred at C5C6. In addition, only 2 out of 109 patients were identified with positive provocation testing at C2C3 and only 1 was identified with abnormal IAR at C6C7.131 While it is helpful to understand the influence of pain on the IAR and subsequent segmental motion disturbances, it is impossible to determine the IAR in the clinical setting. This merits the clinician’s evaluation of the consequences of a disturbed IAR in the cervical disc segments, which includes the manual assessment of segmental pain provocation and motion limits through segmental end-feel testing that has been previously described.132 Once identified, those segments found to be hypomobile can be best treated with joint-specific mobilization that emphasizes collagen remodeling, while pain-producing segments can be best treated with pain modulating techniques. Finally, the decision for appropriate management of whiplash syndrome must take into account the nature and severity of symptoms.

Even in the acute stages, certain factors such as generalized hypersensitivity and psychological distress can be heightened by severity of reported symptoms.61 The patient’s pain intensity reported soon after the accident carries strong predictive ability for poor treatment outcome.81,82

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MANAGEMENT OF WHIPLASH ASSOCIATED DISORDERS The management of local cervical, cervicocephalic, and cervical brachial syndromes has been previously described.118,132 However, the literature offers selected strategies that have been specifically incorporated and evaluated with respect to the management of WAD. While caution should be exercised when estimating the efficacy of conservative treatments in patients with whiplash injury, active interventions appear to be more effective vs. passive management strategies in patients with whiplash injury.135 Conservative management of whiplash patients can serve as a valuable concomitant to invasive pain management procedures that are aimed at reducing inflammation about a ZAJ or controlling sympathetic activity associated with a chronic disc lesion. Conservative management of whiplash can involve activity counseling with encouragement return to activity, gentle traction, axial separation, joint specific treatment to limited zygapophyseal and UVJs, stabilization exercises, and generalized cardiovascular conditioning (re-activation). Activity counseling with encouragement to return to activity is crucial to the recovery of whiplash patients.2 The use of a cervical collar is frequently recommended, particularly in the acute stages of whiplash.

The symptoms of neck pain and headache may not develop until 24 hours after the accident, thus creating a gradual crescendo of pain. The cardinal provocative gesture is cervical motion causing most patients to selflimit their activity and motion. The cervical collar can be useful in giving the patient a tactile cue to protect the end range of various movements, thus reducing the muscle guarding associated with the compensatory movement patterns that are often present in the acute stage.136 However, early active exercise proved to be statistically superior to traditional, conservative soft collar use over a 6-month period in terms of pain and self-reported disability after whiplash injury.137 Therefore, there is no evidence that cervical collars provide any long-lasting benefits and their use should be limited to the acute stage of symptoms.138 The restoration of movement in the whiplash patient is essential to insuring recovery. Movement restoration can be achieved through a combination of manual therapy and active exercise. Manual therapy utilizes passive movement techniques or mobilization and manipulation to restore joint mobility and reduce pain. For the treatment of acute whiplash syndrome, joint specific mobili-

zation treatment combined with exercise provides a significantly better outcome than exercise alone.139 Early patient participation in an active physiotherapy program that emphasizes active mobilization has been proven to achieve improved pain reduction and increased cervical mobility compared with control groups prescribed with 2 weeks rest and a soft cervical collar.140,141 The use of therapeutic exercise should focus on restoring normal function of the cervical spine through coordination and activation exercises. The whiplash patient often presents with limited range of movement and significant apprehension due to fearavoidance behavior. The avoidance of normal neck movement can result in the “disuse syndrome” contributing to muscle atrophy and impaired motor pool firing.

The application of active treatments has been related to reduction of neck pain and self-experienced benefits for patients with chronic neck pain.142,143 In addition to segmentally-appropriate manual therapy and active exercise therapy, the physical therapist can emphasize cervicothoracic stabilization and proprioceptive training through the use of exercises geared toward restoring cervicothoracic muscle endurance and coordination. This may include relaxation training, behavioral support, eye fixation exercises, and posture re-education. Additionally, a whiplash patient’s symptom profile may be influenced by individual beliefs and psychological distress. In response, clinicians should give attention to patients’ beliefs, coping strategies, locus of control, and disability in activities of daily living to insure complete management.135 As a consequence, patients can demonstrate improvements in physical symptoms, disability, and mental well-being even when plagued with persistent WAD lasting as long as 6 years.144 For many patients suffering from WAD, the benefits of conservative management can be maximized through invasive pain control measures. These strategies can include various block measures to the ZAJs,6,145 including radiofrequency cervical medial branch neurotomy.146,147 Moreover, secondary muscle spasms related to the WAD can be effectively treated with botulinum toxin injections.148,149 Selected sequelae from whiplash trauma may merit surgical intervention. For example, while limited cases of traumatic atlanto-occipital dislocation can be treated with long-duration halo ring cervical traction, surgical stabilization is typically incorporated in the management of this potentially fatal consequence of whiplash trauma.150 Additionally, surgical stabilization may be

260 • sizer et al.

indicated in the case of the occasional vertebral fracture and or dislocation in the cervical disc segments after significant whiplash macrotrauma.

SUMMARY Whiplash associated disorders are frequent in the cervical spine, especially as a result of a motor vehicle accident. The term “whiplash” describes an event that lends to numerous clinical disorders. The mechanisms responsible for tissue trauma are complex and a clinician’s understanding of these complexities lends to a more complete appreciation for the anatomical structures and pathological processes that are involved. From this understanding, a comprehensive diagnosis and appropriate management can emerge. While several classification scales have been developed for whiplash associated disorders, a thorough and tissue-specific examination is merited so to maximize the potential for tissue-specific management. Management should be directed toward pain reduction and normalization of mechanics. While conservative measures can address many of clinical sequelae of whiplash, both invasive pain management procedures and surgical interventions may be paramount to a patient’s complete recovery.

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Instructions: For each question, please select the most appropriate answer.

1. Which of the following describes the initial endrange position of the cervical spine once a sudden rear-end impact is encountered in a motor vehicle accident? a. C-shaped posture, convex anteriorly b. C-shaped posture, convex posteriorly c. Rigid erect posture d. S-shaped posture 2. Which of the following specific cervical postures occurs initially in an individual upon sudden rear-end impact in a motor vehicle accident? a. Upper and lower cervical extension b. Upper and lower cervical flexion c. Upper cervical extension and lower cervical flexion d. Upper cervical flexion and lower cervical extension

Whiplash Associated Disorders â&#x20AC;˘ 265

3. Which of the following cervical levels first demonstrates an expansion of extension neutral zone flexibility after a whiplash extension trauma? a. C3C4 b. C4C5 c. C5C6 d. C6C7 4. Which of the following remains relatively stationary during the initial impact of the whiplash traumatic event? a. Cervical spine b. Cervicothoracic junction c. Head d. Thoracic torso 5. In the event that sidebending is the most provocative movement in the patientâ&#x20AC;&#x2122;s functional examination, you would first suspect which of the following structures as the pain generator? a. Anterior longitudinal ligament b. Intervertebral disc c. Uncovertebral joint d. Zygapophyseal joint 6. At which of the following motion segmental levels would one experience the greatest zygapophyseal joint surface compression during a whiplash traumatic event? a. C3C4 b. C4C5 c. C5C6 d. C6C7 7. The capsule of the cervical zygapophyseal joint is best stressed with which of the following cardinal movements, suggesting its involvement in the clinical WAD when most provocative of the movements? a. Axial rotation b. Extension c. Flexion d. Sidebending 8. The occipital alar ligaments are tension loaded with a combination of all of the following movements, EXCEPT FOR: a. Contralateral sidebending b. Extension c. Flexion d. Ipsilateral rotation 9. All of the following components of the psychomotor system have been reported to be reduced by whiplash trauma, EXCEPT FOR:

10.

11.

12.

13.

14.

15.

a. Error detection b. Joint position sense c. Locomotor coordination d. Postural sway All of the following appear to contribute to delayed recovery from whiplash, EXCEPT FOR: a. Male gender b. Muscle pain c. Neck pain on palpation d. Older age Which of the following is considered the principle clinical constituent of WAD? a. Cognitive difficulties b. Dizziness c. Pain d. Visual obscuration All of the following are frequently observed in whiplash patients suffering from headache that arose out of the whiplash trauma history, EXCEPT FOR: a. Bilateral in location b. Female c. Last 4 to 72 hours d. Moderate to severe in nature Diffused, vague pain that crosses the cervical midline and is most provoked with cervical flexion, is most likely generated by an affliction of which structure? a. Anterior longitudinal ligament b. Intervertebral disc c. Uncovertebral joint d. Zygapophyseal joint Stabilization to C2 spinous process while attempting to sidenod the head best assess the integrity of which structure? a. Alar ligament b. Anterior longitudinal ligament c. Posterior tectorial membrane d. Transverse ligament of atlas All of the following are recommended for the management of WAD, EXCEPT FOR: a. Joint specific mobilization b. Long-term soft-collar use c. RF medial branch neurotomy d. Stabilization exercises

266 â&#x20AC;˘ sizer et al.

Question 1 2 3 4 5 6 7 8 9 10 11 12 13 14 15

Answer d d c c c b a c d a c a b a b