Whiplash Associated Disorders: A Review of the Recent Literature





Whiplash Associated Disorders And Mechanisms for Poor Outcome: A Review of the Recent Literature
Ronald L. Lewert, D.C.

Background: Whiplash and Whiplash Associated Disorders (WAD) remain a topic of controversy for patients, treating physicians, and insurers. Auto makers spend billions of dollars yearly in research and design of head restraint and seat belt systems in order to mitigate (increasing) costs relating to cervical spine injuries that result from rear impact collisions. A large segment of patients involved in rear impact collisions,with and without significant vehicle damage, suffer from chronic pain and functional disability. There is consistent evidence that collision dynamics, findings on imaging, neck range of motion, and sensori-motor deficits are not accurate predictors of poor patient outcome following WAD. An understanding of injury mechanisms, patient factors, and clinical findings pertinent to outcome following whiplash are presented.

Objective: The purpose of this article is three-fold: (1) to demonstrate that chronic pain from Whiplash Associated Disorders (WAD) results from specific tissue injury sites that may go undetected on conventional MRI imaging, (2) to provide the clinician with the specific initial patient clinical findings pertinent to poor outcome following whiplash, and (3) provide best-evidence recommendations for formulating a patient-specific (matched-interventional) treatment plan in the prevention of chronic pain following WAD.

Data Sources: The data were accumulated and reviewed over a period of years by reviewing contemporary articles through MEDLINE that are relevant to WAD.

Results and conclusions: There is evidence to support that injury to the cervical zygapophyseal joints is responsible for chronic neck pain following whiplash. Initial presenting pain levels and patient psychological disposition regarding recovery are more pertinent to the development of chronic pain following WAD than are sensori-motor deficits, neck ranges of motion, or collision dynamics. Long-term outcome following WAD is more favorable when treatment is aimed at reducing nociceptive input from the cervical zygapophyseal joints utilizing a combination of matched-interventions such as laser therapy, manual therapies, intermittent traction / decompression therapy, or percutaneous medial-branch ablation. Imaging of the cervical zygapohyseal joints utilizing high-field MRI with fat-suppression technique is recommended as the standard in routine evaluation of WAD. Overall, there is evidence to support 50% of patients involved in rear-impact collisions will never fully recover from WAD.

Introduction

The term Whiplash Associated Disorders (referred to as WAD) has been and continues to be a topic of controversy. The term, whiplash associated disorder (WAD) describes the consequences of a whiplash injury, defined as “bony and soft tissue injuries of the neck” caused by rapid acceleration of the neck and head (56). Patients and physicians are familiar with the (many) symptoms that can result from injuries caused by rear impact collisions…neck-arm-shoulder-upper quadrant pain (50), headaches, dizziness, tinnitus, stiffness, radiating pain; these are some of the more commonly experienced symptoms. However, research also clearly demonstrates that concussion (with or without loss of consciousness), brachial plexus injuries, lower back pain, extremity pain and weakness, disc herniation, rim lesions, zygapophyseal-joint capsular tears, articular pillar fractures, meniscus injuries, rotator cuff tears, depression, anxiety, post-traumatic stress disorder, and central sensitization / central hypersensitivity are among a long list of conditions associated with chronic pain following whiplash (1, 32). Insurers would simply have us believe, however, that WAD is self-limiting and heals without residual pain within six weeks or less (42).

The purpose of this review is to provide factual information from the recent peer reviewed literature regarding WAD so that physicians, patients, and third party payers gain an updated and factual understanding of this potentially disabling condition. Current evidence-based treatment recommendations are reviewed; a treatment-based approach to WAD emphasizing matched interventions that modulate nociceptive central nervous system input produces better outcomes than traditional tissue-based- /-non-matched interventions (50).

The Role of Tissue Damage in WAD; technological shortcomings

Concerning WAD, current technology does NOT allow for detection of all lesions resulting from rear impact trauma (48).Eventhough high field MRI up to 3.0 Tesla is available for evaluation, micro-tears of the facet joint capsules, capsular ligaments, and multifidus muscles still go undetected on conventional high-field imaging. Patients receivinglow-field MRI evaluation are at risk for false negative interpretation due to lower resolution capabilities compared to high-field scans. The most commonly recognized lesion detected utilizing current high-field MRI is internal disc disruption (IDD or disc herniation). And because these larger, macroscopic injuries are what current technology reveals, this is what we come to believe is the source of pain for patients following rear impact trauma…however this is not always the case. Bogduk et al stated, “There is evidence of a lesion-based model in WAD. The lack of macroscopically identifiable tissue damage does not rule out the presence of painful lesions. Facet joint-/-zygapophyseal joint lesions have been validated and are treatable.These lesions account for a large portion of patients with chronic WAD” (1).

Injury Models

Currently, there are two injury models reported and examined by researchers attempting to quantify whiplash induced injuries to the cervical spine. This has been done in consideration of the latest advances in technology pertaining to injury prevention systems, head restraints, and seat belt systems. The injury models are as follows:

  1. Kinetics- the transfer of dynamic loads (energy) to the cervical spine during the collision.
  2. Kinematics- the (abnormal) inter-vertebral motions that occur as a result of the vehicle moving forward beneath the occupant, resulting in non-physiologic neck motions during collision exposure (1,7,10,11) (See illustration 1)

Whiplash Associated Disorders finished  1


Illustration 1: Forward vehicle movement beneath occupant produces abnormal physiologic motion with transfer of dynamic loads to facet capsular ligaments, inter-vertebral discs, and multifidus muscles.

During a rear impact collision, the cervical spine initially undergoes horizontal shear (or retraction; meaning the head moves slightly rearward towards the seat back) as the vehicle moves forward, beneath the occupant. Forward vehicle movement causes the upper cervical spine to go into slight extension, while the lower cervical spine goes into flexion. The resultant rapid change from the normal convex-/-C-shape curve to an S-shape curve (see illustration1:) produces stress loads beyond physiologic limits (8). Tears of the facet joint capsules and capsular ligaments have been verified as the neck undergoes this abnormal physiologic movement(13, 16).Interestingly, this all occurs within normal ranges of cervical spine motion -contrary to earlier injury models emphasizing hyper-extension of the cervical spine followed by hyper-flexion beyond the normal range.

Complicating Factors Relating To Poor Outcome

The outcome for any given patient involved in the same collision may vary according to age, body, or head position at the time of impact, prior injuries to the neck or back, force vectors / direction of impact, occupant weight and height, occupant gender, use of seat belts, head restraint positioning-geometry, and awareness of the impending collision just to name a few(4, 13, 14, 15, 42). Additional factors affecting occupant outcome include vehicle weight, coefficient of friction between vehicle and road surface, or secondary collisions between occupants and the vehicle interior or other vehicles. However, current evidence-based studies reveal the above factors are not quite as accurate in predicting whether patients will suffer chronically as earlier studies have proposed. Physicians are still encouraged to obtain as many details about the collision and the circumstances involved as this information may be useful in directing their attention to specific body regions during the physical examination.

Collision Dynamics: Is Vehicle Damage an Accurate Predictor of Injury?

There are several factors relating to poor prognosis / less favorable occupant outcome that are not a function of vehicle damage.These factors will be discussed in detail later in this review. In fact, decades of evidence-based research clearly demonstrate occupant outcome or the potential for injury following any given rear impact collision is not related to amount or type of vehicle damage (42). Yet current claims adjusting protocols focus on vehicle damage and suggest the evidence-based research is still being ignored in order to reduce expenses associated with rear-impact collisions. Patients are often required by adjustors to attend “independent” medical evaluations following their whiplash injury; all too often the result of such examinations is premature termination of medical benefits. These examinations often emphasize the absence of any positive root tension signs, sensory, motor, or reflex deficits, or neck ranges of motion within relatively normal limits as a basis for their conclusions.

Further education of claims adjustors and "independent" medical examiners regarding this topic is recommended in order to avoid this highly prejudicial and inappropriate approach to patient case management. Furthermore, based on the current evidence presented in this review, clinicians and emergency medical personnel have a responsibility to thoroughly evaluate all patients following WAD, as well as recommend follow-up treatment in order to mitigate the peripheral and central nociceptive input that results from rear impact trauma.

Carefully evaluate and monitor progress during the early stages of WAD
Clinicians are recommended to treat and monitor patients for several weeks following their initial injury due to the potential for developing symptoms related to cervical internal disc disruption. The initial examination may reveal subtle signs of injury to the deep neck structures such as the facet articulations or intervertebral discs. These signs include allodynia, painful neck extension-rotation-compression without radiation to the upper extremities, spasm of the anterior scalene muscles, abrasion, hematoma located across the base of the neck consistent with safety belt placement, or mild elevation of the shoulder with spasm of the posterior neck muscles. Patients complaining of worsening neck pain since the date of their collision may indeed have a developing disc herniation in the absence of reflex, sensory, or motor deficits.This is due to the avascular nature of the inner two-thirds of the intervertebral disc. Sensori-motor or reflex deficits will not become apparent on the physical examination until the nucleus pulposus reaches the outer one-third of the annulus.

Rear-impact trauma may injure the vertebral end-plates and initiate an intense inflammatory reaction with sustained production of matrix metallo-proteinases (MMP’s), resulting in eventual migration of the nucleus to the outer layers of the annulus (53). Except in extreme cases of disc extrusion immediately following whiplash, the process of nuclear migration to the outer-third of the annulus may take several weeks to develop. Accordingly, initial clinical presentation may appear benign; patient is diagnosed with cervical strain. A thorough understanding of the biochemical progression of internal disc disruption (IDD) is important in order to avoid failure to accurately diagnose the patient. Classic root tension maneuvers such as the cervical foraminal compression test may give the examining clinician unequivocal results. Taking these factors into consideration, along with a thorough history of the patients pain-related functional disabilities during the early stages following their injury, may provide physicians with enough data to consider MRI evaluation at the four-week post-injury interval.

Emergency room evaluation of WAD

Plain film x-rays taken in the emergency room are routinely absent of gross abnormality. Neurologic abnormalities such as sensorimotor deficit or pathologic reflexes are rare in the initial stages of WAD and may take weeks to develop. This is due to the fact that the inner two-thirds of the annulusisvoid of neuro-vascular tissues. Patients will present with normal sensori-motor exam and deep tendon reflexes until the nucleus pulposus reaches the outer one third of the annulus (51, 53). The absence of neurologic findings and abnormal imaging may give the clinician an inaccurate impression regarding injury severity. In fact, internal disc disruption (IDD / disc herniation / disc protrusion; synonymous terms) following rear impact trauma is more prevalent in patient ages 25-45 years due to presence of active nucleus pulposus as compared to older persons whose discs are desiccated (42,43). This evidence supports reasonable clinical suspicion of a developing disc herniation as a potential source of pain following whiplash, especially in patients 45 years or younger(see illustration 2).
Whiplash Associated Disorders finished 2
Illustration 2: Rear-impact trauma produces horizontal shear across the vertebral endplates resulting in sustained production of MMP’s (matrix metallo-proteinases). Treatment aimed at mitigating this acute inflammatory response may reduce symptoms. Prolonged exposure of MMP’s breaks down proteoglycans and collagen which are responsible for maintaining intact nucleus and annulus, therefore allowing the nucleus to migrate through the annulus to produce disc herniation. The process of nuclear migration to the outer 1/3 of the annulus may take several weeks to develop. Note the inner two thirds of the intervertebral disc is avascular due to high intra-discal pressure gradient.

Lesions

Cadaveric and post mortem studies have revealed many types of tissue lesions that result from forces applied beyond physiologic limits. Structural damage may occur in the following anatomy and may go undetected utilizing current imaging (X-ray, CT, or MRI) (1,18,19):

  • partial or complete rupture of zygapophyseal joint capsules
  • ruptured annulus fibrosi and rim lesions
  • intra-articular fractures and contusions
  • trans-articular synovial fractures
  • partial or complete rupture of capsular ligaments
  • cervical multifidus muscle tears

Whiplash Associated Disorders finished 3Whiplash Associated Disorders finished 4
Illustration 3: Facet / zygapophyseal articulations with associated innervation. Diagnostic facet injection followed by medial branch ablation may be indicated where conservative treatment options fail to reduce chronic pain from WAD. Class 4 laser therapy applied directly to the skin overlying the facets is an effective conservative treatment option in many cases.

All of the lesions listed above lead to modification of tissue properties, nociceptive activation, sustaineddysfunction in spinal afferents, neuro-plastic changes, phenotypic switching, and central sensitization(16-19). Once damage to the capsular ligaments occurs, the resultant abnormal spinal motion initiates an inflammatory cascade resulting in prolonged depolarization of group four spinal afferents (pain nerves). The sustained aberrant joint motion which is a direct result of tissue damage, perpetuates the pain cycle with continued release of pro-inflammatory cytokines such as H+ ions, bradykinin, prostaglandins, MMP's and substance P. Chronic cervical spine pain will persist until the inflammatory cascade is either interrupted or eliminated. Effective treatment of such lesions has been and continues to remain the focus of current research pertaining to reducing symptoms associated with chronic WAD.

Currently, the greatest body of literature relating to treatment of chronic neck pain focuses on zygapophyseal joint injuries and the resultant cervical instability (53). There is multi-study collaborative evidence of nociceptor (pain nerve) activation, abnormal collagen production, collagen fiber disorganization, axonal swelling, and permanent abnormal nociceptor signaling in the spinal cord following forces applied to facet capsular ligaments. Unfortunately, whiplash-induced lesions to the Z-joints occur in the absence of grossly observable evidence of rupture or tear on plain film x-ray or conventional high-field MRI. Despite imaging shortcomings, clinical, post-mortem, and cadaveric studies continue to provide consistent proof that whiplash trauma produces Z-joint injury with chronic pain. In a 2012 study pertaining to tissue damage and chronic neck pain resultant from whiplash, Curatolo et al stated, "These observations provide pivotal basic scientific evidence that cervical zygapophyseal joints can be damaged by whiplash injury and become the source of (chronic) pain" (1).Furthermore, capsular ligament injury initiates chronic activation of mechanoreceptors (Pacinian corpuscles, Raffini endings, and golgi tendon organs) termed, ligamento-muscular reflex (53). Although the ligamento-muscular reflex acts as a protective mechanism to add stability and restrict movement of the injured cervical spine, the resultant muscular spasm can cause intense chronic pain.


In one double blind controlled study, 60%of patients source of pain following whiplash was determined to be facetogenic (pain originating from injury to facet joints) and was able to be confirmed by diagnostic medial branch block injection (20). In other words, treatment directed at the facet articulations in particular has the potential for reducing a significant amount of pain for patients suffering from chronic WAD. Interestingly, intense symptoms resulting from acute disc herniation are often the focus of clinical treatment in the early stages of WAD (based on MRI findings). Accordingly, the appropriate application of epidural steroid injection often reduces disco-genic pain in its early stages. However, over time, as the disc desiccates and thetransfer of mechanical stress loads to the posterior elements (facet joints) progresses, the application of facet injection or medial branch ablation may be more appropriate in the reduction of chronic pain.

Treatment Options: Invasive and Non-invasive Approaches

The invasive approach to treatment of the facet articulations involves injection, applied by pain management physicians and is performed under anesthesia.If relief is obtained by percutaneous zygapophyseal facet injection, a medial-branch ablation / radio-frequency neurotomy may be recommended. Results, however, may vary from patient to patient depending on the individual’s physical and psychological health status (52).

Studies using double-blind controlled medial branch blocks found that the prevalence of pain stemming from one or more zygapophyseal joints was at60% among patients with chronic neck pain after whiplash. The most commonly injured facet articulations producing headache and chronic neck pain following whiplash were determined to be C2-3, C5-6, and C6-7. Once the diagnosis of facet-/-zygapophyseal joint injury is confirmed, injection of these structures reduced chronic pain in up to 70% of patients in one study (20-22).

Best evidence regarding non-invasive treatment of chronic WAD favors acupuncture, manual therapies ( including spinal manipulation and neuro-dynamic techniques), intermittent traction, and (Class 4) laser therapy. The following quote was taken from a 2011 review of the research on chronic cervical spine and upper quadrant pain entitled, Clinical presentation and manual therapy for upper quadrant musculo-skeletal conditions-

"The current state of evidence favours acupuncture, laser, and intermittent traction for chronic neck pain.Some electro-therapies show little benefit for chronic neck pain" (50).

Regarding Class 4 therapeutic laser and intermittent traction (including spinal decompression-traction); these modalities have the ability to reduce chronic nociceptive input from injured facet articular structures in part due to their ability to penetrate deeper than the older technologies (30). Modalities such as electric stimulation, interferential current, and ultrasound do not have the capability of penetrating deep enough to provide any lasting therapeutic benefit for zygapophyseal joint injuries, although many therapy clinics currently utilize these modalities routinely in the treatment of WAD. Education of practitioners regarding the use of appropriate modalities for the treatment of facet articulations and treatment of WAD is lacking.


To that end, best-evidence supersedes individual physician preference for treatment modalities relating to treatment of WAD. Class 4 laser therapy, spinal decompression / traction therapy, and manual therapies (-including a combination of matched interventions; manual spinal manipulation, trigger point therapy, joint mobilization, active and passive range of motion, resisted exercises), and neuro-dynamic techniques are appropriate in reducing peripheral and central nociceptive input resultant from chronic WAD. The use of (outdated technologies or non-matched interventions) electrical stimulation, ultrasound, hot and cold packs, soft collars, superficial massage techniques, or prescription analgesics is neither recommended nor supported in the current literature. Physicians and attorneys have a responsibility to their patients-/-clients when making recommendations for care in order that they utilize or refer to practitioners who are current and up-to-date with research and best-evidence treatment recommendations.

Other Lesions

  • Anterior longitudinal ligament- tears of the anterior longitudinal ligament and rim lesions of the anterior annulus have been confirmed in cadaveric and post-mortem studies. Most commonly, these lesions occur in the lower cervical spine (5,6). These lesions are not routinely visible on plain film x-ray or MRI. Cervical instability / hypermobility created by injury to the ALL may contribute to chronic abnormal motion patterns that result in perpetuation of chronic neck pain.
  • Dorsal root ganglion-aside from direct DRG impingement, which is rare, the cervical nerve roots are at risk for injury due to rapid changes in canal pressure that is created by rapid head and neck motions during whiplash. Although the vasculature surrounding the vertebral column regulates blood volume to accommodate for changes in spinal canal size, during rapid head / neck motions, resistance to blood flow can generate pressure gradients which have been shown to induce plasma membrane breakdown of spinal ganglia nerve cells and damage to neuron cell bodies (22). Since cervical nerve roots occupy up to 70% or more of the intervertebral foramen, compression or tractioning of the nerve roots (from whiplash) may be a source of chronic radicular pain (54).
  • Vertebral artery dissection- a retrospective analysis of 500 whiplash patients indicated that cervical arterial dissections were significantly higher in this group than in the general population. In fact, onset of cerebro-vascular symptoms may occur 4 to 12 months following the automobile collision. Trauma to the cervical spine causing altered blood flow rates in the vertebral arteries may produce chronic symptoms of vertebrobasilar insufficiency (VBAI): persistent dizziness or vertigo after whiplash, headache, neck pain, migraines, speech difficulty, dysphagia, syncope, auditory, and visual disturbances. The presence of cervical spondylosis or cervical instability may contribute to obstruction of blood flow, especially in patients that have their head rotated at the time of impact. Advanced age, severe cervical spondylosis with hyperlordosis, and athersclerosis are also factors which may contribute to VBAI (vertebrobasilar artery insufficency syndrome). Vertebral artery injuries may originate from intimal tears, most commonly seen at C1-2 due to extension-rotation of the neck at the time of impact. Transient vascular compromise may be due to pinching of the vessel along its course through the transverse foramen and around the superior articular process of C1 (23, 24,55).
  • Muscles- whiplash may produce injury to muscles as a result of imposed lengthening during the crash (25). Trauma introduced to the zygapophyseal joints may induce abnormal signaling from mechanoreceptors (Pacinian corpuscles, Raffini endings, and golgi tendon organs) thereby producing muscular spasm as a protective mechanism (26, 53).Additionally, the multifidi muscles, which insert directly into capsular ligaments of the C4-C7 vertebral levels may also tear and intensifyfacetcapsular injury.Interestingly, to date there is no validated diagnostic tool to accurately identify muscles as a primary source of nociception in WAD. However, muscles can be areas of referred pain, the primary nociceptive focus being another structure in the neck such as Z-joint, joint capsule, or annulus fibrosi (1)(See illustration 4).
    Many authors recommend against the use of soft collars and muscle relaxers following whiplash as this may promote stasis of inflammatory metabolites and formation of scar tissue in deep muscle groups such as the mutifidus (53).

10Lewert   Perspectives in WAD A Review of the literature booklet Illustration 4: Location of the cervicalmultifidus muscles. These muscles may produce intense neck pain following whiplash injury due to signaling from Pacinian corpuscles, Ruffini endings, and golgi tendon organs;ligamento-muscular reflex.

Severity of pain reported and any associated disability; functional or otherwise, following WAD, is not exclusively a product of tissue damage (31,32). Additional factors such as psychology and social context of the patient, how the compensation system treats them, (28,29) and central neuroplastic changes leading to hyperalgesia and allodynia play a role in outcome following whiplash (26).
There is evidence supporting a lesion-based model in Whiplash Associated Disorders. Zygapophyseal joint pain is the one entity that has been fully validated, for which there is a valid diagnostic test, and for which there is a proven treatment that can reduce or abolish chronic pain from WAD. Failure to demonstrate these lesions due to limitations in scanner resolution should not imply absence of that or other lesions. Currently many of the lesions demonstrated in cadaver models are still too small for detection utilizing today's MRI scanners. However, the prospect of improving MRI resolution is promising in that lesions to the zygapophyseal joints, joint capsules and capsular ligaments will be visualized with greater clarity and accuracy. From a clinical perspective, more detailed MRI visualization of Z-joint pathology is necessary and may help to further illustrate the specific location and extent of damage to these structures.

MRI Evaluation of Acute and Chronic WAD

Some studies suggest frequency selected fat-saturation technique with or without contrast as a means by which to detect facet capsular injuries.

"Detection of active inflammation within and surrounding the facet joints (facet synovitis) is possible using MR imaging using a frequency selective fat saturation technique with or without the use of paramagnetic contrast agent. It is not possible to reliably detect active inflammation in the facets on routine MR imaging, without the use of fat suppression. The characteristic MR appearance correlates with the patient’s pain. MR imaging with fat saturation is a valuable tool in choosing the appropriate level or levels for facet injection. It is recommended that MR imaging sequences with fat suppression be implemented in the routine protocol for MR imaging of the spine" (48).

Important Note Regarding Open MRI:

The use of low field or “open MRI” is inappropriate for accurate diagnosis following whiplash. The peer-reviewed literature suggests physicians utilize high-field MRI for assessment of neuro-musculo-skeletal injuries (especially for imaging of the central nervous system; brain and spinal cord) due to superior quality and resolution compared to low field (open MRI).

"High field strength MRI units provide better spatial and contrast resolution and allows more accurate interpretations than low field strength units; these findings may affect clinical treatment" (46-48).

Low field / open MRI may be used in cases of extreme claustrophobia or in some cases, for intra-articular operative purposes.

A Large Percentage of Patients Do Not Recover Completely: Recovery Trajectories

Many of the old insurance funded studies reported full recovery from whiplash within four to six weeks with minimal to no permanent-/-long term effects. However, the recent peer reviewed research does not agree with this and, in fact, continues to validate chronic WAD due to significant medical costs associated with long term disability following rear impact trauma (4,31-32).

Cohort studies have demonstrated that recovery, if it occurs, takes place in the first two to three months following the injury with a plateau in symptoms following this timeperiod(34). A significant number of patients, however, remain symptomatic for significantly longer periods of time due to injuries which occur to the deep anatomical structures mentioned earlier in this paper (zygapophyseal joint injuries, capsular ligament injuries, disc herniations, cervical multifidus injuries, rim lesions, etc.).

"Recovery following whiplash is dependent on several factors which were recently established using trajectory-modeling analysis (34-38). Patients who experience mild-to-moderate symptoms follow an initial reduction of symptoms in the first few months following the initial injury with at 45% progressing to good recovery in less than six months. However, those patients who experience moderate-to-severe symptoms initially follow a much different pathway- to partial recovery-/-moderate functional disability still present at the twelve month interval. Almost 40% of patients are predicted to follow this pathway. Another 16% of patients whose initial symptoms are severe are predicted to experience partial recovery to moderate-to-severe disability". (34)

Overall, 50% of patients involved in a rear impact collision will report ongoing pain and disability after 12 months (34-38).
Recovery Trajectories Summarized
Mild to moderate group:

  • @ 45 percent of patients will present with initial mild to moderate complaints
  • This group is expected to follow a relatively good path to “recovery” with treatment
  • Course of treatment is expected to last 6 months or less with a reduction and plateau in symptoms in 2-3 months
  • NDI (Neck disability index) scores 0-28% (< 29%)
  • Visual Analogue Scale (VAS) / self-reported pain levels <5.5
  • No report of post-traumatic stress, depression, or pain-catastrophizing
  • Quebec Task Force (QTF) classification II
    -Clinical signs: neck pain, decreased range of movement, and point tenderness
  • “Recovery”: patients still report mild levels of pain and pain-related functional disability reported at 12 months

Moderate to Severe group:

  • @ 39 percent of patients will present with initial moderate to severe complaints
  • This group is expected to follow a significantly different path to only partial “recovery” with treatment
  • Course of treatment is expected to last longer than mild to moderate group with moderate levels of pain and pain-related functional disability still present at 12 months
  • NDI (Neck disability index) scores (> 29%)
  • Visual Analogue Scale (VAS) / self-reported pain levels >5.5
  • Some reports of post-traumatic stress, depression, or pain-catastrophizing
  • Quebec Task Force (QTF) classification II /III
  • -Clinical signs: neck pain, decreased range of movement, point tenderness, neurologic findings (decreased or absent DTR’s, sensory, and/or motor deficit)

Severe group:

  • @ 16 percent of patients will present with initial severe complaints (severe pain-related functional disability)
  • This group is expected to follow a significantly different path to only some “recovery” with treatment
  • Course of treatment is expected to last longer than moderate to severe group with moderate levels of pain and moderate or severe functional disability still present at 12 months
  • NDI (Neck disability index) scores @50-68%
  • Visual Analogue Scale (VAS) / self-reported pain levels >5.5
  • Common reports of post-traumatic stress, depression, and pain-catastrophizing
  • Quebec Task Force (QTF) classification III
  • Clinical signs: neck pain, decreased range of movement, point tenderness, neurologic findings (decreased or absent DTR’s, sensory, and/or motor deficit)
  • -For QTF classification IV; fracture or dislocation

Cold Hyper-algesia, Pain Catastrophizing, and Central Sensitization

Other factors which have been shown to predict poor outcome following whiplash have been identified, including psychological factors of initial moderate post-traumatic stress symptoms, pain catastrophizing, and symptoms of depressed mood(31,32).A person’s lower expectations of recovery have also been shown to predict poor functional recovery.



"There is evidence that addressing negative pain beliefs in the management of persistent pain can affect treatment outcomes. Negative pain beliefs can contribute to the transition from acute pain to persistent pain" (5, 51).

Clearly, psychological factors are an important part of the recovery process as patients who do not expect to recover well may indeed not recover fully.

Cold hyper-algesia(decreased cold-pain tolerance) has been shown to predict disability as well as poor mental health outcomes following whiplash(39-40).A recent systematic review concluded that there is moderate evidence available to support cold hyper-algesia as a poor prognostic indicator(41).Some studies suggest mechanical hyper-algesia, or low pressure-pain thresholds (sensitivity to light touch at a distal extremity) is not as a reliable predictor of poor outcome. The exact mechanisms underlying the hyperalgesic responses are not clearly understood and are an ongoing topic of research. The exaggerated responses to light touch and movement are generally acknowledged, however, to reflectaugmented nociceptive processing in the central nervous system. Another recognized term for these responsesiscentral hypersensitivity / central sensitization. It is important to recognize the above factors as being more reliable according to research in predicting poor outcome as compared to certain aspects of the clinical assessment or physical examination. For example decreased range of neck movement and sensorimotor abnormalities are not consistent predictors of poor outcome (5).This is not to say that these factors should not be considered in the evaluation of patients, however, they should not be used to gauge prognosis of WAD. (See illustration 6 below)

Illustration 6: There is consistent evidence throughout the literature pertaining to reliability of factors that are accurate / consistent with poor recovery. Likewise, there is consistent evidence pertaining to those factors which do not predict poor outcome from WAD.Whiplash Associated Disorders finished 6

Is There A Correlation Between Vehicle Damage And Occupant Injury?

Auto insurers have employed a number of strategies to control their losses when it concerns WAD. One such technique that has been widely accepted by the public, physicians, and personal injury attorneys alike is the MIST strategy, or “minimal impact soft tissue” protocol(42).Since the mid-1990’s major insurers utilizing this protocol dictated that all injury claims resulting from property damage of $1000 or less will be segmented / “adjusted” for minimal compensation.

“Claims adjustors were instructed as a general precept, crashes with minimal damage are unlikely to or cannot cause significant or permanent injury. Thus any claim for injury in the presence of minimal vehicle or property damage was to be handled as a type of fraudulent claim and claims adjustors were instructed that regardless of medical evidence of injury, the injury should not or could not have occurred because of the nature of the crash and the claim goal was to close without payment”(42).

Despite decades of research and evidence disproving the above strategy, insurers continue to take a hard line regarding rear-impact crashes. -Simply stated, “Property damage is an unreliable predictor of injury risk or outcome following low velocity crashes. According to a number of databases, a significant number of injuries occur as a result of low velocity rear impact collisions. The MIST protocol for prediction of injury does not appear to be valid”(42).

Conclusions

Research supports two injury models for WAD. There is good evidence to demonstrate specific injury mechanisms for acute as well as chronic pain resulting from whiplash. In particular, intervertebral disc and facet capsular injuries as well as other lesions are responsible for chronic pain following WAD. Damage to specific tissue sites leads to modification of tissue properties, sustained dysfunction in spinal afferents, and peripheral and central sensitization. Chronic neck pain may result from cervical instability despite current technological shortcomings in MRI imaging.

Technological shortcomings in standard imaging of whiplash does not allow for visualization of facet synovitis and related anatomy involved in the production of chronic symptoms. High-field MRI with fat-suppression technique is recommended as the standard in the evaluation of patients with WAD.
Initial presenting symptom severity and patient psychological factors such as pain-catastrophizing and negative pain beliefs are more accurate predictors of patient outcome than vehicle damage, collision dynamics, neck range of motion, findings on imaging, or sensori-motor deficit. Physician utilization of the Visual Analogue Scale (VAS) and Neck Disability Index (NDI) are recommended as part of the initial evaluation process for WAD. These tools have been identified as accurate predictors of outcome following whiplash.

Treatment of WAD and the reduction of chronic pain resultant from same are best achieved utilizing evidence-supported matched-interventions aimed at reducing nociceptive input from tissue damage sites; namely the cervical zygapophyseal joints and the related anatomy.

Whiplash is not a self-limiting condition. A large portion of patients involved in rear-impact collisions suffer chronically. Further education of the public and physicians regarding the potential long-term consequences of WAD is needed. Vehicle damage and collision dynamics are not accurate predictors of injury potential or long-term outcome following whiplash injury.

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Submitted for publication Dec. 2014 Copyright R. Lewert, D.C.