Why Some Patients Take Longer
to Recover from Whiplash Injuries

Pain and the treatment of pain is the biggest health problem in America. In her book, A Nation in Pain, Healing Our Biggest Health Problem, Judy Foreman documents that approximately 50% of American adults suffer from chronic pain (1). A conservative estimate of the direct costs and lost productivity resulting from this pain is up to $635 billion yearly (2).

The body region most likely to suffer from pain is the low back. The third most common body location for pain is headache. The fourth most common location is the neck (3):

Lower-Back Pain - 28.1%
Knee Pain - 19.5%
Severe Headache - 16.1%
Neck Pain - 15.1%
Shoulder Pain - 09.0%

The primary reason patients go to chiropractors is for spinal pain complaints. This was established in the journal Spine two years ago (4). In rounded numbers, 60% go to chiropractors for low back pain and 33% do so for neck pain.

Headaches and neck pain often coexist. Neck problems often manifest in headaches. This is because all headaches synapse in the neck, in a region known as the trigeminal-cervical nucleus (5, 6).

Chiropractic and spinal manipulation are very effective in the treatment of spinal pain syndromes, and levels of patient satisfaction are quite high (4). This is why spinal manipulation has been advocated in official practice guidelines for more than a decade (7, 8, 9, 10, 11).

Pain perception and pain character, in any body location, is linked to inflammatory chemicals. This concept is nicely reviewed in the journal Medical Hypothesis (12):

“Every pain syndrome has an inflammatory profile consisting of the inflammatory mediators that are present in the pain syndrome.”

“The key to treatment of pain syndromes is an understanding of their inflammatory profile.”

“Our unifying theory or law of pain states: the origin of all pain is inflammation and the inflammatory response.”

“Irrespective of the type of pain whether it is acute or chronic pain, peripheral or central pain, nociceptive or neuropathic pain, the underlying origin is inflammation and the inflammatory response.”

“Activation of pain receptors, transmission and modulation of pain signals, neuro-plasticity and central sensitization are all one continuum of inflammation and the inflammatory response.”

“Irrespective of the characteristic of the pain, whether it is sharp, dull, aching, burning, stabbing, numbing or tingling, all pain arises from inflammation and the inflammatory response.”

When discussing inflammation as related to pain, three distinct types of inflammation should be distinguished. This classification is important because they are managed differently:

• Local inflammation
• Systemic inflammation
• A combination of local and systemic inflammation

Local Inflammation

Local inflammation is caused by trauma, prolonged tissue stress, and/or repetitive tissue strain. The local inflammation in the area of tissue stress generates local pain. Causation is established by history and confirmed with examination. The management is local, directed to the painful tissues.

Systemic Inflammation

Systemic inflammation means the entire body is inflamed. The more systemically inflamed a person is, the more likely they will perceive pain secondary to local injury or tissue stress. The best outcome for these individuals requires management of their systemic inflammatory profile.
Systemic inflammation is suspected by history, but often requires lab work for confirmation. There are a number of causes of systemic inflammation. The two most common are:

• Suboptimal levels of omega-3 fatty acids
• A “leaky gut”

The champion of management of chronic spine pain syndromes with omega-3 fatty acids is Joseph Maroon, MD. Dr. Maroon is a neurosurgeon and works with the Pittsburgh Steelers National Football League team (13).

A recent vocal champion of systemic inflammation being caused by “leaky gut” is cardiologist Stephen Gundry, MD. Dr. Gundry’s gut approach to the management of systemic inflammation is well described in his 2017 and 2019 books (14, 15).

A Combination of Local and Systemic Inflammation

A combination of local and systemic inflammation is probably the typical patient suffering with pain. Optimal management requires both local and systemic interventions.

Restating, inflammation and pain are linked. Successful pain management parallels successful inflammation management. The primary category of drugs to treat pain are non-steroidal anti-inflammatory drugs, or (NSAIDs). NSAIDs work by blocking a series of enzymes that produce an inflammatory hormone-like molecule called prostaglandin E2. The name of this enzyme is cyclo-oxygenase, abbreviated COX. These anti-inflammatory drugs have many serious side effects:

The journal Spine notes in 2003 (16):

“Adverse reactions to non-steroidal anti-inflammatory (NSAID) medication have been well documented.”

“Gastrointestinal toxicity induced by NSAIDs is one of the most common serious adverse drug events in the industrialized world.”

In 2006, the journal Surgical Neurology states (13):

Blockage of the COX enzyme inhibits the conversion of arachidonic acid to the very pro-inflammatory prostaglandins that mediate the classic inflammatory response of pain.

“More than 70 million NSAID prescriptions are written each year, and 30 billion over-the-counter NSAID tablets are sold annually.”

“5% to 10% of the adult US population and approximately 14% of the elderly routinely use NSAIDs for pain control.”

Almost all patients who take the long-term NSAIDs will have gastric hemorrhage, 50% will have dyspepsia, 8% to 20% will have gastric ulceration, 3% of patients develop serious gastrointestinal side effects, which results in more than 100,000 hospitalizations, an estimated 16,500 deaths, and an annual cost to treat the complications that exceeds 1.5 billion dollars.

“NSAIDs are the most common cause of drug-related morbidity and mortality reported to the FDA and other regulatory agencies around the world.”

One author referred to the “chronic systemic use of NSAIDs to ‘carpet-bombing,’ with attendant collateral end-stage damage to human organs.”

NSAIDs always affect the body systemically, resulting in the many diverse multisystem deleterious side effects. For example, taking NSAIDs for a painful sprained ankle will have deleterious influences of the gastrointestinal tract, kidney, liver, and blood vessels. A local treatment that is directed only to the ankle is desired because of the lack of systemic side effects. Such a treatment involves local controlled motion.

Low back pain emanates primarily from the intervertebral disc (17, 18, 19, 20, 21). Neck pain primarily emanates from the facet joint (22, 23, 24, 25).

Chiropractic spinal manipulation primarily helps patients with spinal pain for two reasons:

ONE:

Motion disperses the accumulation of local inflammatory chemicals. This is well-stated in Dr. Vert Mooney’s 1986 Presidential Address of the International Society for the Study of the Lumbar Spine (19). Dr. Mooney notes:

“In the United States in the decade from 1971 to 1981, the numbers of those individuals disabled from low-back pain grew at a rate 14 times that of the population growth. This growth occurred in the very decade when there was an explosion of ergonomic knowledge, labor-saving mechanical assistance devices, and improved diagnostic equipment. We apparently could not find the source of pain.”

“Anatomically the motion segment of the back is made up of two synovial joints and a unique relatively avascular tissue found nowhere else in the body - the intervertebral disc. Is it possible for the disc to obey different rules of damage than the rest of the connective tissue of the musculoskeletal system?”

“Mechanical events can be translated into chemical events related to pain.”

“Mechanical activity has a great deal to do with the exchange of water and oxygen concentration” in the disc.

An important aspect of disc nutrition and health is the mechanical aspects of the disc related to the fluid mechanics.

The pumping action maintains the nutrition and biomechanical function of the intervertebral disc. Thus, “research substantiates the view that unchanging posture, as a result of constant pressure such as standing, sitting or lying, leads to an interruption of pressure-dependent transfer of liquid. Actually, the human intervertebral disc lives because of movement.”

“The fluid content of the disc can be changed by mechanical activity.”

“In summary, what is the answer to the question of where is the pain coming from in the chronic low-back pain patient? I believe its source, ultimately, is in the disc. Basic studies and clinical experience suggest that mechanical therapy is the most rational approach to relief of this painful condition.”

TWO:

Motion initiates a neurological sequence of events that “closes” the pain gate. This is well-stated by orthopedic surgeon WH Kirkaldy-Willis, MD, in 1985 (26):

“Spinal manipulation is essentially an assisted passive motion applied to the spinal apophyseal [facet] and sacroiliac joints.”

Melzack and Wall proposed the Gate Theory of Pain in 1965, and this theory has “withstood rigorous scientific scrutiny.”

“The central transmission of pain can be blocked by increased proprioceptive input.” Pain is facilitated by “lack of proprioceptive input.” This is why it is important for “early mobilization to control pain after musculoskeletal injury.”

The facet capsules are densely populated with mechanoreceptors. “Increased proprioceptive input in the form of spinal mobility tends to decrease the central transmission of pain from adjacent spinal structures by closing the gate. Any therapy which induces motion into articular structures will help inhibit pain transmission by this means.”

Stretching of facet joint capsules will fire capsular mechanoreceptors which will reflexively “inhibit facilitated motoneuron pools” which are responsible for the muscle spasms that commonly accompany low back pain.

Why Do Some Whiplash-Injured
Patients Take Longer to Recover?

When a traumatic soft tissue injury does not recover as expected, there are two classic explanations:

• One was discussed above, systemic inflammation. An injury superimposed on a patient already suffering from systemic inflammation is often treatment resistant until the systemic inflammation is addressed.
• The second explanation is pre-accident degenerative spinal disease. This includes intervertebral disc degeneration, facet arthrosis, and/or uncinate joint arthrosis. Collectively they are often referred to as degenerative joint disease and/or spondylosis.

•••

In 1964, whiplash injury expert and pioneer, Ruth Jackson, MD, published an article titled “The Positive Findings in Neck Injuries” in the American Journal of Orthopedics. Dr. Jackson’s conclusions in this article were based on her evaluation of 5,000 injured patients. She notes (27):

Pre-existing pathological conditions of the cervical spine, when injured, “result in more damage than would be anticipated in a so-called ‘normal’ cervical spine.”

•••

In 1977, Samuel Turek, MD, clinical professor from the Department of Orthopedics and Rehabilitation at the University of Miami School of Medicine, and author of the reference text, Orthopaedic Principles and Their Applications, states (28):

“The injury may be compounded by the presence of degenerative disease of the spine.”

“With advancing age, especially in the presence of degenerative disease, the tissues become inelastic and are easily torn.”

•••

In 1981, Rene Cailliet, MD, professor and rehabilitation specialist from the University of Southern California, and author of the book Neck and Arm Pain, states (29):

“The pre-existence of degeneration may have been quiescent in that no symptoms were noted, but now minor trauma may ‘decompensate’ the safety margin and symptoms occur.”

•••

In 1983, Norris and Watt followed 61 whiplash-injured patients for a minimum of six months in order to establish factors that were prognostic for recovery. Their conclusions include (30):

“Factors which adversely affect prognosis include the presence of objective neurological signs, stiffness of the neck, [loss of cervical lordosis], and pre-existing degenerative spondylosis.”

Degenerative spondylosis was detected in 26% of patients with no objective findings, 33% of patients with reduced cervical range of motion, and 40% of patients with neurological loss, indicating that cervical spine degenerative changes are associated with greater injury and worse prognosis for recovery.

This “study suggests that prognosis is predictable on the basis of the initial presentation of the patient.” “Two features on plain radiographs seem relevant.”

1) “Pre-existing degenerative changes in the cervical spine, no matter how slight, do appear to affect the prognosis adversely.”

2) Abnormal curves in the cervical spine “are more common in patients with a poor outcome.”

“The prognosis may be modified by the presence or absence of degenerative changes, by an abnormality [degeneration] of the cervical spine on the initial radiograph, or by both.”

•••

In 1985, Webb in his article titled “Mechanisms and Patterns of Tissue Injury” notes (31):

“Degenerative joint disease is recognized as a major influence on subsequent tissue damage both in severity and pattern.”

“In any individual where changes consistent with degenerative joint disease are present, one can expect the injury to be more severe or a very minor injury to produce severe symptoms requiring prolonged treatment.”

•••

In 1986, Arthur Ameis, MD, from the University of Toronto, notes (32):

“For the elderly, neck injury can be very serious. The degenerative spine is biomechanically ‘stiffer’, behaving more like a single long bone than like a set of articulating structures. Deforming forces are less evenly dissipated, and more damage is done.”

•••

In 1987, physicians Edward Dunn and Steven Blazar authored “Soft-Tissue Injuries of the Lower Cervical Spine” for the American Academy of Orthopedic Surgeons. In this publication they note (33):

“If present, degenerative changes should be duly noted as they may affect the prognosis.”

“...pre-existing degenerative changes adversely affected the outcome.”

•••

In 1988, Maimaris and colleagues published a study titled “Whiplash Injuries of the Neck.” They reviewed 102 whiplash-injured patients 2 years after injury. They concluded (34):

“The analysis of the radiological results showed that pre-existing degenerative changes in the cervical spine are strongly indicative of a poor prognosis.”

•••

In October of 1988, physician Hirsch and colleagues published a paper titled “Whiplash Syndrome, Fact or Fiction?” in Orthopedic Clinics of North America. These authors note (35):

Pre-existing structural changes and degenerative changes are “frequently associated with a more difficult, more prolonged, and less complete recovery.”

“The films should be inspected especially for evidence of pre-existing structural changes or for alteration, which are frequently associated with a more difficult, more prolonged, and less complete recovery.”

•••

In their 1988 reference text on whiplash injuries titled Whiplash Injuries, The Acceleration/Deceleration Syndrome, Steve Foreman and Arthur Croft note (36):

“...the presence of preexisting degenerative changes, no matter how slight, appears to alter the prognosis adversely.”

•••

In 1989, physician Porter published an article in the British Medical Journal titled “Neck Sprains After Car Accidents.” He noted (37):

“Pre-existing degenerative changes may worsen the prognosis.”

•••

In 1991, Watkinson, along with Gargan and Bannister, radiographically reviewed 35 whiplash-injured patients 10.8 years after injury. They concluded (38):

“Patients with degenerative change initially have more symptoms after 2 years than those with normal radiographs at the time of injury.”

“Degenerative changes occurred significantly more frequently in patients who had sustained soft tissue injuries than in a control population.”

Also in 1991, the reference text Painful Cervical Trauma, Diagnosis and Rehabilitative Treatment of Neuromusculoskeletal Injuries, notes (39):

“The elasticity of tissues decreases with an increase in age. The range of motion in the cervical spine also decreases. In both cases, the potential for injury is increased because the neck is less resilient.”

•••

In 1995, physician Jerome Schofferman and colleague Dr. S. Wasserman published in Spine an article titled: “Successful treatment of low back pain and neck pain after a motor vehicle accident despite litigation.” These authors also noted (40):

“Pre-existing degenerative changes on initial x-rays, no matter how slight, had a worse prognosis.”

•••

In 1996, Squires, along with Drs. Martin Gargan and Gordon Bannister, published a 15.5-year follow-up evaluation of 40 patients who had been injured in a motor vehicle collision. They published their results once again in the prestigious British Journal of Bone and Joint Surgery, titled “Soft-tissue Injuries of the Cervical Spine: 15-year Follow-up.” In this article, these authors note (41):

“The patients who had deteriorated were on average five years older than the rest of the group.”

“80% of the patients who had deteriorated in the last five years had degenerative changes.”

“100% of patients with severe ongoing problems had cervical degeneration at 11 years after injury.”

•••

In 1999, the reference text Whiplash and Related Headaches, by neurologist Bernard Swerdlow, MD, makes the following point (42):

Risk factors that may lead to chronicity include “pre-existing degenerative osteoarthritic changes.”

“Other conditions that may pre-exist the accident that may contribute to a chronic state following the accident are osteoarthritis, degeneration of vertebral body joints, disc degeneration and inflammatory processes.”

“Studies indicate that pre-existing osteoarthritic changes contributed to alter the prognosis adversely.”

•••

In 2002, in their reference text titled Whiplash, Gerard Malanga, MD and Scott Nadler, DO, state (43):

“Several researchers have associated poor clinical outcomes with spondylosis, reporting a higher prevalence of spondylosis in patients with continued symptoms.”

“It is certainly theoretically possible that symptoms from a previously asymptomatic cervical spondylosis are precipitated by trauma and are responsible for the continuing pain.”

•••

In 2005, physician Schenardi published a study titled “Whiplash injury, TOS and double crush syndrome, Forensic medical aspects.” In this article he addresses the issue of pre-injury cervical spine degeneration by stating (44):

A substantial percentage of people will have whiplash symptoms for more than a few months, “especially the elderly or those with pre-existing neck problems who may develop chronic long-term problems which may never resolve.”

•••

In his 2005 reference text titled Motor Vehicle Collision Injuries, Lawrence Nordhoff notes (45):

“Patients who have clinically significant pre-existing medical conditions may have more severe injuries, slower recoveries and poorer prognoses.”

Dr. Nordhoff clearly lists “spinal degeneration” as one such pre-existing medical factor.

•••

In 2019, a study published in The Spine Journal followed 121 whiplash-injured subjects prospectively for six months with CT scan. They noted (46):

“This study demonstrates an increased risk for non-recovery after whiplash trauma for patients with moderate facet joint degeneration as demonstrated on CT scans performed shortly after trauma.”

“We suggest that one of the underlying mechanisms of WAD may be that trauma triggers a painful clinical manifestation of underlying, previously asymptomatic, cervical facet joint degeneration.”

In conclusion, pre-existing degenerative joint disease renders those joints less capable of adequately handling and dispersing the forces of a new injury; therefore, injury to these articulations and the surrounding soft tissues is greater; the amount of treatment required for maximum improvement is greater, and there are more long-term subjective, objective, and functional residuals.

REFERENCES:

1. 
   Foreman J; A Nation in Pain, Healing Our Biggest Health Problem; Oxford University Press; 2014.
2. Pho K; USA TODAY, The Forum; September 19, 2011; pg. 9A.
3. Wang S; Why Does Chronic Pain Hurt Some People More?; Wall Street Journal; October 7, 2013.
4. Adams J, Peng W, Cramer H, Sundberg T, Moore C; The Prevalence, Patterns, and Predictors of Chiropractic Use Among US Adults: Results From the 2012 National Health Interview Survey; Spine; December 1, 2017; Vol. 42; No. 23; pp. 1810–1816.
5. Seletz E; Headache of Extracranial Origin; California Medicine; November 1958; Vol. 89; No. 5; pp. 314-317.
6. Bogduk N; Anatomy and Physiology of Headache; Biomedicine and Pharmacotherapy; 1995; Vol. 49; No. 10; pp. 435-445.
7. Chou R, Qaseem A, Snow V, Casey D, Cross JT, Shekelle P, Owens DK; Diagnosis and Treatment of Low Back Pain; Annals of Internal Medicine; Vol. 147; No. 7; October 2007; pp. 478-491.
8. Chou R, Huffman LH; Non-pharmacologic Therapies for Acute and Chronic Low Back Pain; Annals of Internal Medicine; October 2007; Vol. 147; No. 7; pp. 492-504.
9. Globe G, Farabaugh RJ, Hawk C, Morris CE, Baker G, DC, Whalen WM, Walters S, Kaeser M, Dehen M, DC, Augat T; Clinical Practice Guideline: Chiropractic Care for Low Back Pain; Journal of Manipulative and Physiological Therapeutics; January 2016; Vol. 39; No. 1; pp. 1-22.
10. Wong JJ, Cote P, Sutton DA, Randhawa K, Yu H, Varatharajan S, Goldgrub R, Nordin M, Gross DP, Shearer HM, Carroll LJ, Stern PJ, Ameis A, Southerst D, Mior S, Stupar M, Varatharajan T, Taylor-Vaisey A; Clinical practice guidelines for the noninvasive management of low back pain: A systematic review by the Ontario Protocol for Traffic Injury Management (OPTIMa) Collaboration; European Journal of Pain; Vol. 21; No. 2 (February); 2017; pp. 201-216.
11. Qaseem A, Wilt TJ, McLean RM, Forciea MA; Noninvasive Treatments for Acute, Subacute, and Chronic Low Back Pain: A Clinical Practice Guideline from the American College of Physicians; For the Clinical Guidelines Committee of the American College of Physicians; Annals of Internal Medicine; April 4, 2017; Vol. 166; No. 7; pp. 514-530.
12. Omoigui S; The biochemical origin of pain: The origin of all pain is inflammation and the inflammatory response: Inflammatory profile of pain syndromes; Medical Hypothesis; 2007; Vol. 69; pp. 1169–1178.
13. Maroon JC, Bost JW; Omega-3 Fatty acids (fish oil) as an anti-inflammatory: An alternative to nonsteroidal anti-inflammatory drugs for discogenic pain; Surgical Neurology; April 2006; Vol. 65; pp. 326– 331.
14. Gundry S; The Plant Paradox: The Hidden Dangers in “Healthy” Foods that Cause Disease and Weight Gain; 2017.
15. Gundry S; The Longevity Paradox: How to Die Young at a Ripe Old Age; 2019.
16. Giles LGF, Muller R; Chronic Spinal Pain: A Randomized Clinical Trial Comparing Medication, Acupuncture, and Spinal Manipulation; Spine; July 15, 2003; Vol. 28; No. 14; pp.1490-1502.
17. Smyth MJ, Wright V, Sciatica and the intervertebral disc. An experimental study; Journal of Bone and Joint Surgery [American]; December 1958; Vol. 40; No. A-6; pp. 1401-1408.
18. Nachemson AL; The Lumbar Spine: An Orthopedic Challenge; Spine; Vol. 1; No. 1; March 1976; pp. 59-71.
19. Mooney V; Where Is the Pain Coming From?; Spine; Vol. 12; No. 8; October 1987; pp. 754-759.
20. Kuslich S, Ulstrom C, Michael C; The Tissue Origin of Low Back Pain and Sciatica: A Report of Pain Response to Tissue Stimulation During Operations on the Lumbar Spine Using Local Anesthesia; Orthopedic Clinics of North America; Vol. 22; No. 2; April 1991; pp.181-187.
21. Izzo R, Popolizio T, D’Aprile P, Muto M; Spine Pain; European Journal of Radiology; May 2015; Vol. 84; pp. 746–756.
22. Bogduk N, Aprill C; On the nature of neck pain, discography and cervical zygapophysial joint blocks; Pain; August 1993; Vol. 54; No. 2; pp. 213-217.
23. Barnsley L, Lord SM, Wallis BJ; Bogduk N; The prevalence of chronic cervical zygapophysial joint pain after whiplash; Spine; January 1, 1995; Vol. 20; No. 1; pp. 20-25.
24. Lord SM, Barnsley L, Wallis BJ; Bogduk N; Chronic cervical zygapophysial joint pain after whiplash. A placebo-controlled prevalence study; Spine; August 1, 1996; Vol. 21; No. 15; pp. 1737-1744.
25. Bogduk N; On Cervical Zygapophysial Joint Pain After Whiplash; Spine
    December 1, 2011; Vol. 36; No. 25S; pp. S194–S199.
26. Kirkaldy-Willis WH, Cassidy JD; Spinal Manipulation in the Treatment of Low back Pain; Canadian Family Physician; March 1985; Vol. 31; pp. 535-540.
27. Jackson R; The Positive Findings in Neck Injuries; American Journal of Orthopedics; August-September 1964; pp. 178-187.
28. Turek S; Orthopaedics Principles and their Applications; Lippincott; 1977; p. 740.
29. Cailliet R; Neck and Arm Pain; F. A. Davis Company; 1981; p. 103.
30. Norris SH, Watt I; The Prognosis of Neck Injuries Resulting From Rear-end Vehicle Collisions; The Journal Of Bone And Joint Surgery (British); November 1983; Vol. 65-B.
31. Webb; Whiplash: Mechanisms and Patterns of Tissue Injury; Journal of the Australian Chiropractors’ Association; June 1985.
32. Ameis A; Cervical Whiplash: Considerations in the Rehabilitation of Cervical Myofascial Injury; Canadian Family Physician; September 1986.
33. Dunn EJ, Blazar S; Soft-tissue injuries of the lower cervical spine; Instructional course lectures; 1987;Vol. 36; pp. 499-512.
    Maimaris C, Barnes MR, Allen MJ; ‘Whiplash injuries’ of the neck: A retrospective study; Injury; November 1988; Vol. 19; No. 6; pp; 393-396.
34. Hirsch SA, Hirsch PJ, Hiramoto H, Weiss A; Whiplash syndrome: Fact or fiction? Orthopedics Clinics of North America; October 1988; Vol. 19; No. 4; pp. 791-795.
35. Foreman S and Croft A; Whiplash Injuries, The Acceleration/Deceleration Syndrome; Williams & Wilkins; 1988; p. 389 and p. 395.
36. Porter KM; Neck sprains after car accidents; British Medical Journal; April 15, 1989; 298(6679); pp. 973-974.
37. Watkinson A, Gargan M, Bannister G; Prognostic factors in soft tissue injuries of the cervical spine; Injury: the British Journal of Accident Surgery; July 1991; pp. 307-309.
38. Friedmann L, Marin E, Padula P; “Biomechanics of Cervical Trauma” in Painful Cervical Trauma, Diagnosis and Rehabilitative Treatment of Neuromusculoskeletal Injuries; Edited by C. David Tollison and John R. Satterthwaite; Williams and Wilkins; 1991, p. 17.
39. Schofferman J, Wasserman S; Successful treatment of low back pain and neck pain after a motor vehicle accident despite litigation; Spine; May 1, 1994; Vol. 19; No. 9; pp. 1007-1010.
40. Squires B, Gargan M, Bannister G; Soft-tissue Injuries of the Cervical Spine, 15-year Follow-up; Journal of Bone and Joint Surgery (British); November 1996, Vol. 78-B, No. 6, pp. 955-7.
41. Swerdlow B; Whiplash and Related Headaches; CRC press; 1999; p. 1040.
42. Malanga G and Nadler S; Whiplash; Hanley & Belfus; 2002; p. 91.
43. Schenardi C; Whiplash Injury, TOS and double crush syndrome, Forensic medical aspects; Acta Neurochirurgica; supplement, Vol. 92; 2005; pp. 25-27.
44. Nordhoff L; Motor Vehicle Collision Injuries, Biomechanics, Diagnosis, and Management; Second Edition; Jones and Bartlett; 2005, pp. 537-538.
45. Rydman E, Kasina P, Ponzer S, Jarnbert-Pettersson H; Association Between Cervical Degeneration and Self-perceived Non-recovery After Whiplash Injury; The Spine Journal; December 2019; Vol. 19; No. 12; pp. 1986−1994.

“Authored by Dan Murphy, D.C.. Published by ChiroTrust® – This publication is not meant to offer treatment advice or protocols. Cited material is not necessarily the opinion of the author or publisher.”