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Facet joints are implicated as a major source of neck and low-back pain. Both cervical and lumbar facet syndromes have been described in the medical literature. Biomechanical studies have shown that lumbar and cervical facet-joint capsules can undergo high strains during spine-loading. Neuroanatomic studies have demonstrated free and encapsulated nerve endings in facet joints as well as nerves containing substance P and calcitonin gene-related peptide. Neurophysiologic studies have shown that facet-joint capsules contain low-threshold mechanoreceptors, mechanically sensitive nociceptors, and silent nociceptors. Inflammation leads to decreased thresholds of nerve endings in facet capsules as well as elevated baseline discharge rates. Recent biomechanical studies suggest that rear-end motor-vehicle impacts give rise to excessive deformation of the capsules of lower cervical facet joints. Still unresolved is whether this stretch is sufficient to activate nociceptors in the joint capsule. To answer this question, recent studies indicate that low stretch levels activate proprioceptors in the facet-joint capsule. Excessive capsule stretch activates nociceptors, leads to prolonged neural afterdischarges, and can cause damage to the capsule and to axons in the capsule. In instances in which a whiplash event is severe enough to injure the joint capsule, facet capsule overstretch is a possible cause of persistent neck pain.

Pain generation in lumbar and cervical facet joints.

Neck muscle endurance, self-report, and range of motion data from subjects with treated and untreated neck pain.

Volunteer studies of experimental, low-velocity rear-end collisions have shown a percentage of subjects to report short-lived symptoms, but the cause of these symptoms remains unknown. It is unclear whether the symptoms arise from biomechanical stress causing injury or from psychological stress causing symptom expectation and anxiety. Similarly, the cause of symptoms remains obscure in virtually all “whiplash” patients because it is impossible to identify acute pathology in many cases. In this study subjects were exposed to placebo collisions that almost completely lacked biomechanical stress. It was highly probable that if the symptoms reported following low-velocity collisions were not due to injury but to other factors (including misattribution of symptoms from other sources), then the proportion of subjects reporting symptoms would be similar to that reported for volunteers in true (experimental) low-velocity, rear-end collisions. A total of 51 volunteers (33 males and 18 females, mean age 32.4 years) were recruited through local newspaper advertisements. An experimental set-up for a placebo collision was constructed using two standard European cars. At time T0, prior to the placebo collision, a history and physical examination was performed, including a psychological analysis (Freiburger Personality Inventory). A symptom history and physical examination were also performed at time T1, immediately after the placebo collision, and the subjects completed symptom questionnaires 3 days (time T2) and 4 weeks (time T3) after the placebo collision. Data analysis included a determination of the predictive value of psychological data for the presence of symptoms following exposure to a placebo collision. At time T1, 9 out of 51 participants (17.6%) indicated symptoms. Within 3 days (time T2) after the placebo collision, 10 (19.6%) of the subjects had symptoms, and within 4 weeks (time T3) 5 subjects (9.8%) had symptoms. Of the last group, two of the five did not relate these symptoms to the “collision”. Subjects who endorsed symptoms at time T1 had significantly higher scores on the psychological scale of psychosomatic disorders (measured at time T0). Subjects endorsing symptoms at time T2 had significantly higher scores on emotional instability. There was also a tendency to higher scores on this sub-scale for subjects with whiplash-associated disorders (WAD) at time T3. A discriminant analysis using all four psychological scales from time T0 had a power of 87%, 83% and 92% for correct classification of subjects as symptomatic or asymptomatic at times T1, T2 and T3, respectively. Approximately 20% of subjects exposed to placebo, low-velocity rear-end collisions will thus indicate WAD, even though no biomechanical potential for injury exists. Certain psychological profiles place an individual at higher risk for this phenomenon.

No stress--no whiplash? Prevalence of "whiplash" symptoms following exposure to a placebo rear-end collision.

Study Design: A systematic review of the literature. Objectives: To assess the efficacy of conservative treatment in patients with whiplash injuries. Summary of Background Data: Many treatments are available for patients with whiplash injury, but there continues to be no evidence for their accepted use. Methods: A computerized literature search of Medline, Embase, Cinahl, Psychlit, and the Cochrane Controlled Trial Register was performed. Studies were selected if the design was a (randomized) clinical trial; if all patients had sustained a whiplash injury; if the type of intervention was a conservative one; if pain, global perceived effect, and participation in daily activities were used as one of the outcome measures, and if the publication was written in English, French, German, or Dutch. The methodologic quality was independently assessed by two reviewers by using the Maastricht‐Amsterdam list. Three quality scores were calculated using this criteria list: the Overall Methodologic Quality Score, the Internal Validity Score, and the Delphi Quality Score. The conclusion of the review was based on articles that scored a quality score of at least 50% of the maximum available score on two of three quality scores. Results: Eleven studies met the inclusion criteria. Only three studies satisfied at least 50% on two of three ways of calculating a quality score, indicating overall poor methodology. There was a high rank correlation among the three ways of calculating a quality score. No statistical pooling was performed because of the heterogeneity of the interventions. This review indicates that active treatments show a beneficial long-term effect on at least one of the primary outcome measures. Conclusion: Caution is needed when drawing a valid conclusion on the efficacy of conservative treatments in patients with whiplash injury. It appears that “rest makes rusty,” whereas active interventions have a tendency to be more effective in patients with whiplash injury. [Key Words: conservative treatment, efficacy, neck sprain, physiotherapy, randomized clinical trial, systematic review, whiplash] Spine 2001;26:E64 ‐E73 For a long time there has been no consensus on the definition of whiplash. The term whiplash was used to describe a mechanism of injury, the injury itself, the various clinical manifestations as a consequence of the injury, and signs and symptoms designated as the whiplash syndrome. In 1995 the Quebec Task Force on WhiplashAssociated Disorders (WAD) adopted the following definition of whiplash: Whiplash is an acceleration‐ deceleration mechanism of energy transfer to the neck. It may result from rear-end or side-impact motor vehicle collisions, but can also occur during diving or other mishaps. The impact may result in bony or soft tissue injuries (whiplash injury), which in turn may lead to a variety of clinical manifestations called WAD. 33 By using WAD, patients with whiplash injury can be classified according to severity in signs and symptoms and duration. Nevertheless, there’s still potential vagueness in the definition. 7 Research 19,27,30 has shown that the most common symptoms observed after an acute motor vehicle collision are neck pain (88 ‐100%) and headache (54 ‐ 66%). Other symptoms are neck stiffness, shoulder pain, arm pain and numbness, paraesthesia, weakness, dysphagia, visual

The Efficacy of Conservative Treatment in Patients With Whiplash Injury

The validity of whiplash syndrome has been a source of debate in the medical literature for many years. Some authors have published articles suggesting that whiplash injuries are impossible at certain collision speeds; others have stated that the problem is psychological, or is feigned as a means to obtain secondary financial gain. These articles contradict the majority of the literature, which shows that whiplash injuries and their sequelae are a highly prevalent problem that affects a significant proportion of the population. The authors of the current literature critique reviewed the biomedical and engineering literature relating to whiplash syndrome, searching for articles that refuted the validity of whiplash injuries. Twenty articles containing nine distinct statements refuting the validity of whiplash syndrome were found that fit the inclusion criteria. The methodology described in these articles was evaluated critically to determine if the authors' observations regarding the validity of whiplash syndrome were scientifically sound. The authors of the current critique found that all of the articles contained significant methodologic flaws with regard to their respective authors' statements refuting the validity of whiplash syndrome. The most frequently found flaws were inadequate study size, nonrepresentative study sample, nonrepresentative crash conditions (for crash tests), and inappropriate study design. As a result of the current literature review, it was determined that there is no epidemiologic or scientific basis in the literature for the following statements: whiplash injuries do not lead to chronic pain, rear impact collisions that do not result in vehicle damage are unlikely to cause injury, and whiplash trauma is biomechanically comparable with common movements of daily living. Language: en

A review and methodologic critique of the literature refuting whiplash syndrome.

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A review and methodologic critique of the literature refuting whiplash syndrome.