Whiplash Injury, Chronic Pain, Non-Pharmacologic Managements Adjuncts


Not everyone injured in a motor vehicle collision recovers completely. A percentage of those injured will suffer for years or sometimes even for decades. Documented examples of this chronic pain syndrome include:


*The author’s study initially included 266 injured patients, but at the follow-up assessment (more then 2 years later) only 145 were evaluated (121 of the original group were not evaluated at the two plus year follow-up). Of the 145 followed patients, 83% were still suffering pain symptoms. The author noted that if he assumed that 100% of the 121 subjects who were not evaluated were completely symptom free, then the incidence of chronic pain in the entire initial 266 patient set fell to 43%.


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In the vast majority of these chronic pain patients, secondary monetary gain does not appear to be the reason for their suffering. If secondary monetary gain were the motivation behind ongoing pain and suffering, such pain and suffering would resolve after receiving the monetary compensation. When an individual continues to complain of post-whiplash pain 2 plus, 7, 7.5, 10.8, 12.5, 15.5, 17, and even 30 years after the initial injury and after all possible monetary compensation has already been awarded, it is difficult to ascribe those chronic complaints to the desire to enhance monetary compensation. Several of the authors of the above studies made comments on this fact, including these:


“If the symptoms resulting from an extension-acceleration injury of the neck are purely the result of litigation neurosis, it is difficult to explain why 45% [minimum, could be as high as 83%] of the patients should still have symptoms two years or more after settlement of their court action.” (1)


“If symptoms were largely due to impending litigation it might be expected that symptoms would improve after settlement of the claim. Our results would seem to discount this theory, with the long-term outcome seeming to be determined before the settlement of compensation.” (2)


The fact that symptoms do not resolve even after a mean 10 years supports the conclusion that litigation does not prolong symptoms. (5)


Symptoms did not improve after settlement of litigation, which is consistent with previous published studies. (6)


“It is not likely that the patients exposed to motor vehicle accidents would over-report or simulate their neck complaint at follow-up 17 years after the accident, as all compensation claims will have been settled.” (7)


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In 1997, a study published in the journal Pain reported that chronic pain whiplash-injured patients have an abnormal psychological profile (9). However, the authors noted that in their review, they were unable to find any evidence that appropriate psychotherapy was able to effectively treat the patient’s pain. Rather, the psychotherapy helped the patient deal with their pain, but it did not remove their pain. In contrast, the authors were able to effectively eliminate the patient’s abnormal psychological profile, essentially 100% of the time, if and only if they were able to establish an organic lesion causing the patient’s pain and effectively treating it. The authors reported that the abnormal psychological profile was the consequence of the chronic pain.


Other studies have also concluded that the whiplash-injured patient’s abnormal psychological profile is secondary to their chronic pain. As an example, in 1996, Squires and colleagues note (6):


Studies have found that patients that were psychologically normal at the time of injury will develop abnormal psychological assessments if their symptoms persisted for three months.


This study showed an “abnormal psychological profile in patients with symptoms after 15 years suggesting that this is both reactive to physical pain and persistent.”


In 2010, Rooker and colleagues note (8):


Whiplash-injured patients with a disability [including chronic pain symptoms] often develop an abnormal psychological profile.


Other studies have also concluded that chronic whiplash pain is not, as a rule, psychometric, but rather it has an organic basis. In 1997, a study published in the Journal of Orthopedic Medicine followed whiplash-injured patients and a matched control population for a period of 10 years (10). Neck pain was 8 times more prevalent in the whiplash group than in the control group. Paraesthesia was 16 times more prevalent in the whiplash group than in the control group. Headaches were 11 times more prevalent in the whiplash group than in the control group. The combination of both back pain and neck pain was 32 times more prevalent in the whiplash group than in the control group. Importantly, objectively, the x-rays showed that radiographic degenerative changes in the cervical spine appeared 10 years earlier in the whiplash group than in the control group. The authors reported:


“The prevalence of degenerative changes in the younger cervical spine [of the whiplash group] suggests that the condition has an organic basis.”


“Degenerative change and its association with neck stiffness support an organic basis for the symptoms that follow soft tissue injuries of the neck.”


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In 2007, a study was published summarizing the basis of all pain, including chronic pain, in the journal Medical Hypothesis (11). The author, from the Division of Inflammation and Pain Research, Los Angeles Pain Clinic, cites studies to support these conclusions:


“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, neuroplasticity 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.”


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In 1975, Stonebrink (12) addresses that the last phase of the pathophysiological response to trauma is tissue fibrosis. Boyd in 1953 (13), Cyriax in 1983 (14), and Majno/Joris in 2004 (15) note that there is tissue fibrosis subsequent to trauma. This fibrosis of repair subsequent to soft tissue trauma creates problems that can adversely affect the tissues and the patient for years, decades, or even forever.


As an example, Cyriax (14):


“Fibrous tissue is capable of maintaining an inflammation, originally traumatic, as a result of a habit continuing long after the initial [cause] has ceased to operate.”


Connecting the dots, I propose the following model:


Tissue trauma, including whiplash trauma,


heals with varying degrees of fibrous tissue.



Post-traumatic fibrous tissue is capable of maintaining an inflammatory response long after the initial cause has ceased to exist.



This inflammatory fibrous tissue alters the threshold of the pain neurons, increasing the probability of chronic pain perception.


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In 1971, biochemists Sune K. Bergström (Sweden; d.2004), Bengt I. Samuelsson (Sweden) and John R. Vane (United Kingdom; d. 2004) determined that nonsteroidal anti-inflammatory drugs (NSAIDs) could inhibit the synthesis of prostaglandins from the toxic fat arachidonic acid. They subsequently jointly received the 1982 Nobel Prize in Physiology or Medicine for their research on prostaglandins. The official Nobel Prize press release acknowledged:


“Prostaglandins are continuously formed in the stomach, where they prevent the tissue from being damaged by the hydrochloric acid. If the formation of prostaglandins is blocked a peptic ulcer can rapidly be formed.”


As a consequence of the 1982 Nobel Prize in Medicine or Physiology, scientists and healthcare providers have a much better understanding of the mechanisms of how aspirin and other nonsteroidal antiinflammatory drugs reduce pain, but also increase the risk for gastrointestinal bleeding and kidney damage. In an effort to reduce the gastrointestinal bleeding, a new class of NSAIDs, the COX-2 inhibitors, was developed. These drugs are also known as cyclo-oxygenase 2 inhibitors or ‘coxibs’, and the major brand names are Vioxx and Celebrex.


Cox enzymes convert the omega-6 fatty acid arachidonic acid into the pro-inflammatory pain producer prostaglandin E2 (PGE2).




In 2002, a study published in the European Spine Journal reported that of the 55% of whiplash-injured patients with pain 17 years after their injury, 53% of the patients were still using analgesics to manage their pain (7). Of these:


Although non-steroidal anti-inflammatory drugs inhibit the genesis of prostaglandin E2 (PGE2) and subsequently reduce pain, there are problems with habitual consumption of these products in the management of chronic pain syndromes, including the chronic pain that is often observed following whiplash injury (7). Importantly, habitual consumption of NSAIDs for chronic pain conditions has been associated with a number of deleterious health events, including:


In 2003, the journal Spine published a study stating (24):


“Adverse reactions to nonsteroidal antiinflammatory (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.”


“The newer COX-2-selective NSAIDs are less than perfect, so it is imperative that contraindications be respected.”


There is “insufficient evidence for the use of NSAIDs to manage chronic low back pain, although they may be somewhat effective for short-term symptomatic relief.”


In 2006, a study published in Surgical Neurology stated (25):


“The use of NSAID medications is a well-established effective therapy for both acute and chronic nonspecific neck and back pain.”


“Extreme complications, including gastric ulcers, bleeding, myocardial infarction, and even deaths, are associated with their [NSAIDs] use.”


Blockage of the COX enzyme [with NSAIDs] inhibits the conversion of arachidonic acid to the very pro-inflammatory prostaglandins that mediate the classic inflammatory response of pain (dolor), edema (tumor), elevated temperature (calor), and erythema (rubor).


“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.”


COX 2 inhibitors [Celebrex], designed to alleviate the gastric side effects of COX 1 NSAIDs, are “not only associated with an increased incidence of myocardial infarction and stroke but also have no significant improvement in the prevention of gastric ulcers.”


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There are effective nontoxic alternatives to NSAIDs in the management of chronic spinal pain. A well-respected physician who is an advocate of these alternative approaches to chronic pain management is Joseph Charles Maroon, MD. Dr. Maroon is a neurosurgeon from the University of Pittsburgh Medical Center. Dr. Maroon specializes in painful degenerative spinal diseases, and he is also the neurosurgeon for Pro Football’s Pittsburgh Steelers.


Recently (2006 and 2010), Dr. Maroon has published two studies and one book on the efficacy of natural anti-inflammatory agents for pain relief (25, 26, 27). The effective products Dr. Maroon details include:


Omega-3 Essential Fatty Acids (fish oil)


White willow bark


Curcumin (turmeric)


Green tea


Pycnogenol (maritime pine bark)


Boswellia serrata resin (Frankincense)


Resveratrol


Uncaria tomentosa (cat’s claw)


Capsaicin (chili pepper)


In his writings, Dr. Maroon discusses the biological plausibility for the use of each of these products, as well as their therapeutic doses. He particularly emphasizes the viability of omega-3 essential fatty acids, noting that these oils powerfully inhibit the production of both pro-inflammatory prostaglandins and pro-inflammatory leukotrienes. In his 2006 study (25), Dr. Maroon found that he could eliminate pain medication in 59% of his study subjects.


Other studies also support the utilization of omega-3 fatty acids (fish oil) in an effort to achieve an anti-inflammatory state: