Perspectives In Whiplash Associated Disorders



Whiplash has been a subject of controversy between doctors, patients, researchers, and the insurance industry regarding:

• Vehicle damage versus potential for occupant injury
• Mechanisms of injury
• Treatment (including related costs)
• Long term outcome and effects of these injuries on quality of life



Topics discussed:


• Rear impact injury models (energy transfer and abnormal physiologic movement)
• The role of tissue damage and the lesion-based model
• Diagnostic imaging shortcomings (MRI and plain film x-ray)
• Prognosis and long term outcome; chronic pain and pain-related functional deficits
• Clinical Prediction Rules and Recovery Trajectories For WAD
• Physical and psychological factors relating to poor outcome and who suffers chronically?
• Facet capsular ligament injuries, disc injuries, and other common lesions
• Treatment: matched versus non-matched interventions



Injury Models


Currently there are 2 injury models reported by researchers:
Kinetics: the transfer of dynamic loads (energy) to the cervical spine during the collision
Kinematics: refers to 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
“Forward vehicle movement beneath the occupant produces abnormal physiologic motions in the cervical spine which overcome the tissue tensile strength of facet capsular ligaments, intervertebral discs, and multifidus muscles”.
“There is evidence of a lesion-based model in WAD. 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).


1. The role of tissue damage in whiplash associated disorders. Michele Curatolo MD, Nikolai Bogduk MD, et al. Spine. December 2012: S309-S315.



Injury Mechanisms


1. Kinetics
2. Kinematics
• Immediately following rear impact….(milliseconds)
• The occupants head undergoes horizontal shear: head moves slightly rearward towards seatback and torso moves forward as vehicle moves beneath the occupant
• The resultant rapid change from normal convex / C-shape curve to an (abnormal) S-shape curve produces stress loads which exceed physiologic limits of specific tissue sites
• Tears of the facet capsular ligaments, facet capsules, multifidus mm, and attachment of the IVD (intervertebral disc) to the endplates have been verified in post-mortem and cadaver studies as the neck undergoes this abnormal physiologic movement

1Lewert   Perspectives in WAD A Review of the literature booklet
The change from C-shape to S-shape occurs over a fraction of a second and therefore does not allow occupants to “brace” for impact

Vehicle movement beneath the occupant delivers a rapid pulse of energy to the cervical spine. In many cases where injuries occur at lower speeds and without significant vehicle damage, the neck does not undergo extreme flexion or extension.
2Lewert   Perspectives in WAD A Review of the literature booklet
7. Cervical spine curvature during simulated rear crashes with energy-absorbing seat. Ivancic PC, Xiao M, et al. Spine J. 2011;11:224-233.

3Lewert   Perspectives in WAD A Review of the literature booklet
10. Head/neck kinematic re-sponse of human subjects in low speed rear-end collisions. Sieg-mund GP, King j Lawrence JM. 41st Stapp Car Crash Confer-ence;1997. pp357-385.

4Lewert   Perspectives in WAD A Review of the literature booklet
11. Motion analysis of cervical vertebrae during whiplash load-ing.Kaneoka K, Ono K, Inami S, et al. Spine 1999;24:763-769.

Rear impact trauma initiates sustained dysfunction in spinal afferents (pain nerves) with the potential to produce chronic, fibromyalgia-like pain. The goal of treatment should be targeted at specific tissue injury sites; (facet articulations) in order to reduce the local intense inflammatory response.
Inflammation is the body’s natural response to tissue damage. If short in duration, inflammation leads to healing. Pertaining to whiplash, sustained, chronic inflammation leads to chronic pain and cervical spondylosis (osteoarthritis).
TREATMENT should be initiated IMMEDIATELY following rear impact trauma in order to reduce pain and abnormal signaling from spinal afferents, as well as reduce formation of excess collagen (scar tissue).
5Lewert   Perspectives in WAD A Review of the literature booklet
6Lewert   Perspectives in WAD A Review of the literature booklet

7Lewert   Perspectives in WAD A Review of the literature booklet

Facet and disc injuries produce deep pain that radiates to the shoulders. Pain is present with facet loading maneuvers (extreme neck extension-rotation). Symptoms lasting longer than 1-2 weeks post accident are indicative of deep structural injury to intervertebral discs or capsular ligaments. Interestingly, neurologic examination may remain intact and without long tract signs or reflex, sensory, or motor deficit at the 1 month post-accident interval. High field MRI with fat suppression is the imaging modality of choice for evaluation of the facet articulations. Some authors recommend this technique as the new standard for WAD.


Facet Capsular Injury
Screen shot 2016 07 01 at 1 31 48 PM


Current best-evidence literature


13. Effects of abnormal posture on capsular ligament elongation in a computational model subjected to whiplash loading. Stemper BD, Yoganandan, Pintar FA. J of Biomech. 2005;38:1313-1323.
A large percentage of whiplash injuries lead to chronic pain or disability… “These injuries lead to modification of tissue properties, nociceptive activation, sustained dysfunction in spinal afferents, neuro-plastic changes, phenotypic switching, and central sensitization” (16-19).

16. Capsular ligament involvement in the development of mechanical hyperalgesia after facet joint loading: behavioral and inflammatory outcomes in a rodent model of pain. Lee KE, Davis MB, Winkelstein BA. Journal of Neurotrauma. 2008; 25:1383-1393.
17. Simulated whiplash modulates expression of the glutaminergic system in the spinal cord suggesting spinal plasticity is associated with painful dynamic cervical facet loading. J. Neurotrauma 2011;27:163-174.
18. Structural changes in the cervical facet capsular ligament: potential contributions to pain following sub-failure loading. Quinn KP, Lee KE, et al. StappCar Crash Journal 2007;51:169-187.
19. Painful facet joint injury induces neuronal stress activation in the DRG: implications for cellular mechanisms of pain. Dong L, OdeleyeAO, Jordan-Sciutto KL, et al. NeurosciLett. 2008;433:90-94.
51. The chemistry of discogenic and disc herniation pain: diet and nutri-tional supplement considerations. Seaman D. MS,DC. Anabolic Labs Research Dept. Dec 2012; (1) 1-12.



More evidence


“There is multi-study collaborative evidence of nociceptor (pain nerve) activation, abnormal collagen production, collagen fiber disorganization, axonal swelling, and permanent nociceptor signaling in the spinal cord following forces applied to facet capsular ligaments; and for WAD all lesions to the Z-joints are induced in the absence of grossly observable evidence of rupture or tear. 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).



DEFINITION OF “WHIPLASH”


“The term “whiplash associated disorder” (often trivialized by the insurance industry as “just soft tissue”) 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).
JUST A FEW EXAMPLES OF “SOFT TISSUE” PATHOLOGY

  • HEART ATTACK
  • STROKE
  • BREAST CANCER
  • DEEP VEIN THROMBOSIS

56.) Spitzer WO, Skovron MI, et al. Scientific monograph of the Quebec Task Force on whiplash-associated disorders: Redefining “whiplash” and its man-
1.) The role of tissue damage in whiplash associated disorders. Michele Curatolo MD, Nikolai Bogduk MD, et al. Spine. December 2012: S309-S315.




Microscopic lesions are confirmed but not seen on routine imaging

Screen shot 2016 07 01 at 1 37 35 PM


Tears of the ALL as well as rim lesions (avulsion of the anterior vertebral endplate and annulus fibrosi) have been confirmed in cadaveric and post-mortem studies. Most commonly these lesions occur in the lower cervical spine (6).


6. Injury of the anterior longitudinal ligament during whiplash simulation. Ivancic PC, Pearson AM, Panjabi MM, et al. Euro Spine Journal 2004. 13: 61-68.




Post-traumatic headaches and dizziness


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 (headache or dizziness). 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. Head rotation at the time of impact significantly increases injury risk (23, 24).

9Lewert   Perspectives in WAD A Review of the literature booklet


23. Late sequelae of whiplash injury with dissection of cervical arteries. Hauser V, Zangger P, Winter Y, et al. Eur Neurology 2010;64:214-218.
24. Hemodynamic changes in patients with whiplash injury measured by transcranial doppler sonography. SericV,Blazic-Cop N, Demarin V. CollAnthropol. 2000;24:197-2004.

Other lesions supported by evidence


Multifidus muscle tears

10Lewert   Perspectives in WAD A Review of the literature booklet


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 thereby producing muscular spasm as a protective mechanism (26). This can result in reduced range of motion / abnormal movement patterns which generate pain. Additionally, the multifidi muscles, which insert directly into capsular ligaments of the C4-C7 vertebral levels may also tear and intensify facet capsular 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)
“The fascicular attachment pattern of the multifidus spinae in the cervical region appears to be unique to that region. The direct attachment to cervical facet capsules supports a possible role in neck pain and injury” (25-26).


25. Morphology, architecture and biomechanics of human cervical multifidus. Anderson JS, Hsu AW, Vasavada AN. Spine. 2005;30E86-E91.
26. Central sensitization, referred pain, and deep tissue hyperalgesia in musculoskeletal pain. Graven-Nielsen T, Curatolo M, Mense S. Proceeding of the 11th World Congress on Pain: Seatle IASP Press; 2006. pp217-230.


Neck, shoulder, and arm pain

11Lewert   Perspectives in WAD A Review of the literature booklet


The above illustrates common pain patterns for facet capsular ligament injury as well as injury to the intervertebral disc.
Spinal cord contusions (myelopathy) may result from large disc herniation or extruded disc material. The physical examination of such patients must include cranial nerves, motor strength, deep tendon reflexes, and pathological reflexes: Hoffman’s, Babinski, Chaddock, and clonus...initial physical examination is often absent of sensory-motor deficit, or reflex abnormalities and should be periodically evaluated during the course of treatment.


22. Nerve cell damages in whiplash injuries. Svensson MY, Aldman B, Bosrom O. Orthoped.1998;27:820-826.
23. Late sequelae of whiplash injury with dissection of cervical arteries. Hauser V, Zangger P, Winter Y, et al. Eur Neurology 2010;64:214-218.
24. Hemodynamic changes in patients with whiplash injury measured by transcranial Doppler sonography. SericV,Blazic-Cop N, Demarin V. CollAnthropol. 2000;24:197-2004.



Herniated discs

Screen shot 2016 07 01 at 1 53 23 PM


Patients seen in the emergency room following an accident are often told their x-rays are “normal”. This is because microscopic tears and the resultant inflammatory response do not show on routine imaging. If the trauma was significant enough to produce a sustained intense inflammatory response, MRI imaging will reveal disc pathology. Neck and posterior shoulder pain are the most common symptoms. Intense inflammation may cause the nucleus to migrate to the outer 1/3 of the disc. This will result in pain that continues to worsen over the next several weeks. Some patients may experience neck-shoulder pain...or develop arm pain and weakness. Cell damage occurs at the periosteal attachments of tendons, ligaments, and joint capsules resulting in release of MMP’s (matrix metallo-proteinases). The sustained release of pro-inflammatory cytokines from damaged tissue results in internal disc disruption, breakdown of connective tissue, and sustained nociceptive activation (48, 51).


48. MR Imaging of facet synovitis and facet-related pain in the cervical and lumbar spine: The diagnostic value of fat-saturated magnetic resonance imaging. Czervionke, L,
49. Fenton D, American Society of Spine Radiology, Blog Arch. Res. 2005
51. The chemistry of discogenic and disc herniation pain: diet and nutritional supplement connsiderations. Seaman D. MS, DC. Anabolic Labs Research Dept. Dec 2012; (1):1-12.



12Lewert   Perspectives in WAD A Review of the literature booklet
Vascular vertebral endplate “bleeds” MMP’s into disc (intense inflammatory response to trauma)
Rear impact trauma initiates an intense inflammation at the periosteal attachments of the disc. Normal diffusion of nutrients occurs through the vertebral endplate and outer 1/3 of the disc. The inner 2/3 of the disc is a high pressure zone and is therefore, avascular. Chondrocytes and fibroblasts synthesize and maintain the collagen and proteoglycans which comprise the nucleus and annulus. There is removal and replacement of old cells by a family of connective tissue degrading enzymes called matrix metallo-proteinases (MMP’s). Collagenase, gelatinase, stromelysin, and elastase are commonly recognized MMP’s. Tissue inhibitor metalloproteinases (TIMP’S) function to modulate MMP activity, therefore creating a homeostasis between the two as it pertains to connective tissue remodeling and maintenance.

Disc degeneration, disc herniation, and disco-genic pain involves an imbalance between TIMP’s and MMP’s; favoring MMP’s over activity. The process of disc herniation / degeneration usually begins with damage to the weakest structure; the vertebral endplate. Endplate damage disrupts the delicate homeostatic environment, reducing nutrient and oxygen supply to the disc; favoring MMP degradation of proteoglycans within the nucleus. As MMP activation continues, the cohesive structure of the nucleus becomes compromised and is unable to resist and evenly distribute compressive loads...axial loading is transferred to the annulus fibrosis and facet articulations. This causes the nucleus to migrate from the center of the disc, through the annulus fibrosis (producing annular tears). This process may take several days or weeks to develop into what we see on MRI imaging: herniated disc, bulging disc, annular tear, annular fissure.
13Lewert   Perspectives in WAD A Review of the literature booklet
Trauma induced nuclear migration to outer 1/3 of annulus with nerve root compression (view from top)

Technological Shortcomings


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 patients 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).


"High field strength MRI units provide better spatial and contrast resolution and allow more accurate interpretations than low field strength units; these findings may affect clinical treatment" (44).
•Taking into consideration the limitations of “open”/low field MRI, this author considers the use of same inappropriate for evaluation of WAD
•With low field MRI the clinician must consider the possibility of false negatives
•Some studies suggest low field /“open” MRI should be used only in cases of extreme claustrophobia (44).
•Some major insurers recommend the use of high field MRI as the standard of choice for imaging of the spine
•Neurologists, neurosurgeons, and pain management physicians almost NEVER utilize “open” MRI for evaluation of the central nervous system (brain and spinal cord)


48. MR Imaging of facet synovitis and facet-related pain in the cervical and lumbar spine: The diagnostic value of fat-saturated magnetic resonance imaging. Czervionke, L, Fenton D, American Society of Spine Radiology, Blog Arch. Res. 2005
44. Comparison of high-field-strength versus low field strength MRI of the shoulder. Magee T, Shapiro M, et al. American J Roentgenology. 2003 Nov; 181(5):1211-1215.


Best-evidence regarding course and prognosis following WAD


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 time period (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-modelling analysis (34-38). Patients who experience mild to moderate symptoms follow an initial reduction of symptoms within the first few months following the initial injury with @ 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 12 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).


34. Course and prognostic factors of whiplash: a systematic review and meta analysis. Kemper S, Rebbeck T, Maher C, McAuley J, Sterling M. Pain. 2008;138:617-629.
35. Assessment and validation of prognostic models for poor functional recovery 12 months after whiplash injury: a multicenter inception cohort study. Sterling M, Hendrikz J, Kenardy J, Kristjansson, et al.Pain. 2012:153;1727-1734.
36. Risk factors for persistent problems following whiplash injury: results of a systematic review and meta-analysis. Walton d, Pretty J, Macdermid, J, Teasel R. J of Orthop Sports PhysTher. 2009:39;334-350.
37. Recovery in whiplash associated disorders: do you get what you expect. Carroll L, Holm L, et al. J of Rheumatology. 2009:39:1063-1070.
38. Expectations for recovery important in the prognosis of whiplash injuries. Holm L, Carroll L, Cassidy D, et al. PLoS Med. 2008:5:e105.



Best-evidence regarding course and prognosis following WAD




Research has identified 3 recovery trajectories based on patient’s initial symptom presentation:
• Mild to moderate initial symptoms with mild to moderate pain-related disability reported at 12 months
• Moderate to severe initial symptoms with moderate to severe pain-related disability reported at 12 months
• Severe initial symptoms with severe pain-related disability reported at 12 monthsScreen shot 2016 07 01 at 2 20 42 PM

5. Physiotherapy management of whiplash associated disorders (WAD). Sterling M. 2014 Journal of Physiotherapy 60:5-12.


Recovery Trajectories For WAD


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 reported disability (functional losses) at 12 months


CPR (Clinical Prediction Rule)

Lewert   Perspectives in WAD A Review of the literature booklet
***Supported by current evidence-based research
***refer to page 21

Recovery Trajectories For WAD


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 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)

CPR (Clinical Prediction Rule)

Lewert   Perspectives in WAD A Review of the literature booklet
***Supported by current evidence-based research
***refer to page 21



Recovery Trajectories For WAD


Severe group:
• @ 16 percent of patients will present with initial severe complaints (functional losses / 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 symptoms, 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

CPR (Clinical Prediction Rule)

Lewert   Perspectives in WAD A Review of the literature booklet
***Supported by current evidence-based research
***refer to page 21



What Else Does Research Say Regarding Outcome?


Indicators of Poor Functional Recovery
Factors that are consistent with poor recovery (consistent evidence)


• Initial pain levels of >5.5/10
• Initial NDI score >29%
• Symptoms of post-traumatic stress
• Negative expectations of recovery
• Pain catastrophizing
• Cold hyperalgesia


Factors that do not predict poor recovery (consistent evidence)


• Accident-related features; vehicle damage, collision aware-ness, speed of accident, or position in vehicle
• Findings on imaging
• Motor deficit / dysfunction


Factors with inconsistent evidence


• Older age
• Female gender
• Neck range of movement
• Compensation-related factors



Best evidence regarding recovery trajectories and poor outcome***


CPR (Clinical Prediction Rules)


1. The role of tissue damage in whiplash associated disorders. Michele Curatolo, M.D., Nikolai Bogduk, M.D., Beth Winkelstein, PhD. Spine December 2012: S309-S315.
5. Physiotherapy management of whiplash associated disorders WAD. Sterling M. 2014 Journal of Physiotherapy 60: 5-12.
34. Course and prognostic factors of whiplash: a systematic review and meta analysis. Kemper S, Rebbeck T, Maher C, McAuley J, Sterling M. Pain. 2008;138:617-629.
35. Assessment and validation of prognostic models for poor function-al recovery 12 months after whiplash injury: a multicenter inception cohort study. Sterling M, Hendrikz J, Kenardy J, Kristjansson, etal.Pain. 2012:153;1727-1734.
36. Risk factors for persistent problems following whiplash injury: re-sults of a systematic review and meta-analysis. Walton d, Pretty J, Mac-dermid, J, Teasel R. J of Orthop Sports PhysTher. 2009:39;334-350.
37. Recovery in whiplash associated disorders: do you get what you expect. Carroll L, Holm L, et al. J of Rheumatology. 2009:39:1063-1070.
38. Expectations for recovery important in the prognosis of whiplash injuries. Holm L, Carroll L, Cassidy D, et al. PLoS Med. 2008:5:e105.
40. Cold hyperalgesia as a prognostic factor in whiplash associated dis-orders: a systematic review. Goldsmith R, Wright C, Bell S, et al. Manu-al Therapy m2012:17;402-410.
41. Sensory hypersensitivity occurs soon after whiplash injury and is associated with poor recovery. Sterling M, Jull G, Vicenzino B et al. Pain. 2003:104;509-517.



Treatment of WAD

14Lewert   Perspectives in WAD A Review of the literature booklet
PROGRESSION OF CERVICAL DISC DEGENERATION FOLLOWING WHIPLASH
Early treatment following WAD is directed at reducing the acute inflammatory response to trauma. It is equally important to remember to consult your doctor regarding upper back and shoulder strengthening exercises to help prevent progression of disc degeneration, which leads to forward head carry and other postural abnormalities such as kyphosis (pictured above).



Treatment of WAD


Matched Interventions
The clinical goal in the use of matched interventions aims at reducing the acute inflammatory response created by local tissue damage as well as reducing peripheral and central nociceptive input


• Class 4 Therapeutic Laser (not cold laser)
• Manual therapies; including trigger point therapy, manual spinal manipulation, joint mobilization
• Intermittent traction / decompression therapy
• Neuro-dynamic techniques; active and passive range of motion, resistive exercise
• Acupuncture
• Facet injection / Percutaneous medial-branch ablation therapy


Non-matched Interventions
Currently lack support in the literature. However, these modalities are commonly used in the treatment of WAD


• Electrical stimulation, interferential current, and ultra-sound
• Heat or cold packs
• Superficial massage techniques
• OTC or prescription analgesics
• Muscle relaxers


“The current state of evidence favors acupuncture, intermittent traction, and laser therapy. Some electrical therapies show little benefit for chronic pain” (49, 52).


49. An ICON overview on physical modalities for neck pain and associated disorders. Graham N, Gross AR, et al. Open Orthop. J. 2013;20;7:440-460.
52. Multidimensional associative factors for improvement in pain, function, and working capacity after rehabilitation of whiplash associated disorder; a prognostic prospective outcome study. Felix Angst, Andreas R Gantenbein et al. BMC Musculoskeletal Disord. 2014; 15:130.


Summary and Conclusions


• Research supports 2 injury models for WAD:


-Kinetic (transfer of energy to specific tissue sites)
-Kinematic (rapid change from C-shaped curve to S-shaped curve)


• Research supports a lesion-based model for WAD; specifically disc herniation, facet joint capsular tears and facet capsular ligament tears
• These lesions are validated and supported by evidence and are responsible for chronic pain
• Research supports the presence of other lesions such as trans-synovial articular fractures, internal disc disruption, injuries to DRG, vertebral artery dissection, and multifidus muscle tears
• WAD leads to modification of tissue properties, nociceptive activation, sustained dysfunction in spinal afferents, neuro-plastic changes, phenotypic switching, and central sensitization
• Technological shortcomings in MRI currently do not allow for detection of some painful lesions on routine imaging; fat suppression technique is recommended as a standard method (high-field MRI)
• Low-field / “open” MRI is not recommended in the evaluation of WAD due to inferior image quality and low resolution compared to high-field
• There is evidence to support chronic pain based on the specific tissue lesions discussed. Other factors which contribute to chronicity include initial pain levels reported by patient, post-traumatic stress symptoms, negative pain-beliefs, pain-catastrophizing, and cold hyper-algesia
• There is consistent evidence to support that vehicle damage, occupant position in vehicle, collision dynamics, findings on imaging, or sensori-motor deficit are NOT indicators of patient outcome following WAD. Additionally, female gender, advanced age, neck range of motion, or whether patients have an attorney are NOT accurate indicators of poor prognosis
• Research supports the use of matched-interventions; specifically manual therapies (including manual spinal manipulation), laser therapy, neuro-muscular therapies, and acupuncture to reduce peripheral and central nociceptive input from WAD



Important things to keep in mind if you are involved in a traffic accident…the basics:

• Florida law requires that you see a physician within 14 days from the date of the accident. Should you fail to do so, your insurance WILL NOT cover your medical expenses
• YOUR Florida No-Fault insurance pays for up to $10,000. in medical treatment per incident; Florida is a “no fault” state. Therefore, regardless of who caused the collision, your insurance covers you, and the other person’s insurance covers them
• If you were a passenger in someone else’s vehicle, YOUR insurance covers you for your injuries; unless you are a non-driver. In such a case, you are either covered under the policy (or policies) which are registered to your address of residence, or you will be covered under the driver’s policy
• If you were involved in an accident with an un-insured or under-insured person, your insurance covers you regardless of who is at fault for the collision
• No referrals are needed with Florida no-fault; you can see any physician of your choice
• Regarding your insurance claim; you must call your auto insurance carrier to report the collision as well as obtain a claim number in order for your doctor to process claims for treatment...give the claim number and date of accident to your doctor at the time of your first visit



Child Safety and Seatbelts


• Always wear your seatbelt...even when riding in the rear of the vehicle
• Teach your children to buckle their seatbelt
• Never wear (or allow a child to) wear the seatbelt under the arm or around / over the neck or abdomen...serious or fatal injuries can occur
• REAR FACING SEAT (infants) - children weighing up to 20 lbs. Head must be at least an inch from top of seat back. Children should remain rear facing for as long as possible (minimum 1 year old)
• FORWARD-FACING SEAT- children over 1 year old and weighing 20 to 40 lbs. may ride in a forward-facing CRS (child restraint system)
• BOOSTER SEAT - kids no longer able to fit in a 5-point harness; generally ages 4 to 8, should ride in a booster seat WITH HIGH BACK AND HEAD RESTRAINT (not just booster) until they are at least 57” tall
• NEVER PLACE A CHILD UNDER 57” TALL IN THE FRONT SEAT
• NEVER PLACE THE CRS IN THE FRONT OF ANY VEHICLE...EVER
For more information regarding Child Safety go to nhtsa.gov

Each year thousands of people are injured in traffic related accidents, many of whom seek medical care and / or legal representation. A common practice in the insurance industry is to assess the severity of injury based on the severity of vehicle damage. However, the current evidence-based scientific research demonstrates this method to be grossly inaccurate and consistently unreliable in determining injury potential or outcome following whiplash.
This provides a detailed review of evaluation and assessment of long term outcome following WAD (whiplash associated disorders). Furthermore, a thorough review of our current understanding pertaining to mechanism of injury to specific tissue sites responsible for chronic pain is presented.
Lastly, it is my intent to provide patients, physicians, counsel, and third parties with a credible, accurate, scientific approach to WAD. To that end, all of the references to scientific publications utilized in the production of this booklet are available online at www.Pubmed.gov. or by request.

The information presented in this booklet is intended to provide the reader with factual information, including references to the peer reviewed literature. All of the materials contained herein are copyright protected. Diagrams are presented with written permission from the source / author where available. The original author and presenter of this material is, Ronald Lewert D.C. This booklet is neither for sale, reproduction, or distribution without the express written consent of Dr. Lewert. Final copy February 2016.