Strengths and limitations
The main strength of this study is the population-based design enabling a comparison between a group of chronic whiplash sufferers and a healthy population. Clinical data would not be appropriate for a study like this due to selection bias. Individuals with a heavy symptom load would to a greater extent seek medical help after a whiplash injury than others, resulting in an exaggerated symptom reporting in the chronic whiplash group. Using a population-based design, we were able to compare all individuals reporting a whiplash injury and neck pain, including individuals not in contact with health services.
The large number of participants and the relatively high participation rate should also be noted as advantages. Furthermore, the dataset contains information on many co-variables, making adjustments for multiple confounders possible. The richness of variables also enabled us to explore if the recall bias hypothesis by comparing our results to that of self-reported fractures.
Both participants in the health study and the staff collecting the data were blinded to the specific hypothesis of this study. Also, the study was conducted in no relation to any litigation, compensation or insurance process. This is important, as such processes have been found to lead to increased symptom reporting and delayed recovery [52
The study also has some notable limitations. Firstly, the study is cross-sectional, making it impossible to conclude on causal inference. For instance, somatic symptoms and symptoms of anxiety and depression might have been present before the accident. Increased pre-injury levels of symptoms of anxiety and depression have been found [35
], and reporting low pre-injury physical and mental health predicts whiplash [54
All data used are self-reported with no objective confirmation. This applies both to self-report of whiplash and fracture of hand or wrist. We do not know if chronic whiplash developed after the whiplash accident: Some individuals in our chronic whiplash group might be recovered from the accident but reporting neck pain with an etiology different from whiplash.
Information based on self-report make the study design vulnerable to possible recall bias; hence increased tendency in some individuals for whatever reason to remember both past injuries and recent symptoms. We aimed to explore the relevance of this bias by repeating all analyses for fractures of the hand or wrist. As symptoms were only slightly increased in individuals self-reporting fractures, we conclude the recall bias problem might be relevant, but cannot entirely explain the increased symptom report in chronic whiplash.
Previous studies have used self-reported data and similar methods of classification when investigating chronic whiplash [13
]. A recent study found self-reported whiplash to strongly predict a subsequent allowance of disability benefits [35
], indicating clinical relevance of self-reported whiplash, whether it is picking up true whiplash sufferers or not. The lack of a medical confirmation is truly a limitation if to be regarded a study of true whiplash victims. We do believe the overlap between self-reported whiplash and sufferers of whiplash injuries who could be clinically verified to be far from perfect, including both false negatives and false positives (i.e. self-diagnosed whiplash). We do, however, also believe that the group self-reporting whiplash is clinically relevant with the highly increased prevalence of somatic symptoms and increased risk of future disability benefits.
Somatic symptoms are also self-reported. The questions related to somatic symptoms were not linked to whiplash in the questionnaire used in HUSK. This could reduce the risk of attribution and symptom accentuating in relation to data collection.
Participants report their symptoms unrelated to any medical condition. We do not know whether the particular participant has an organic explanation for the reported symptoms. Though a broad symptom profile can be difficult to explain within chronic whiplash [55
], some of the symptoms seen might have an organic etiology related to the accident. Our study design, did not, however, allow for evaluation of whether or not each symptom was organic in origin.
Also, other somatic diagnoses could lead to increased load of somatic symptoms. Participants were asked if they suffered from heart infarction, angina pectoris, stroke, asthma, diabetes or multiple sclerosis. The association between somatic symptoms and chronic whiplash was adjusted for these comorbid diagnoses. The mean difference in symptom reporting was changed by only 3.4% (from 0.58 to 0.56 SD) when adjusting for these comorbid diagnoses. Whether more of the association could have been explained by inclusion of somatic diagnoses beyond those available in this study remains an open question.
Another limitation is the narrow age span. The base-population for the Hordaland Health Study was 29,400 individuals living in Hordaland County, born between 1953 and 1957. Some researchers find age to hold no prognostic importance after a whiplash accident [56
], while others claim older age to increase the risk of poor recovery [57
]. A review from 2008 claims conflicting results [58
]. Consequently, we cannot exclude the possibility that the narrow age range of our study limits the generalizability of findings.
Interpretation of findings
Our findings of increased reporting of diffuse symptoms from all body parts among chronic whiplash sufferers and the positive linear association between time since whiplash injury and frequency of somatic symptoms are hard to explain within the organic model. The findings are more compatible with, and indicative evidence of, a functional element within chronic whiplash. However, other explanations may also be relevant.
In line with previous studies [4
], the most frequent symptoms amongst chronic whiplash sufferers were headache, dizziness and neck pain/joint-muscle pain. Somatic symptoms beyond headache, dizziness and joint/muscle pain have not previously been as thoroughly explored in the literature. Some studies have found increased levels of gastrointestinal symptoms, palpitations, shortness of breath and sleep disturbances [15
], but to the best of our knowledge, this is the first study showing that the entire range of somatic symptoms included in the ICD-10 criteria for somatization disorder are increased in individuals self-reporting whiplash.
Different theories aim to explain increased symptom reporting in chronic whiplash: For instance, changes in zygapophysial joints seem to cause neck pain and headache in some individuals after whiplash injuries [24
]. In contrast, it is claimed that no MRI changes can be found after whiplash injuries, not for acute [64
], nor chronic cases [7
Stress system responses including catecholaminergic systems, serotonin systems and the hypothalamic-pituitary-adrenocortical systems also appear capable of producing hyperalgesia and allodynia [25
As in other chronic pain conditions, sensitization might be of importance [25
]. The sensitization model explains pain as having a physical cause related to changes in the nervous system [70
]: After repetitive activation of nociceptors, specific neurons within the spinal cord become sensitized. Also, new connections are made between neurons and inhibitory neurons die. Following this, non-nociceptive stimuli from the periphery may now be misinterpreted as pain. The model further stresses that psychological, behavioral and social problems are related to the existence and persistence of sensitization.
Headache, dizziness and neck pain/joint-muscle pain arise from the neck- and head-area and are therefore the symptoms most easily explained by a whiplash neck injury. As these symptoms are important among individuals suffering from chronic whiplash, we included them in our study. But as they in relation to chronic whiplash cannot be regarded as unexplained diffuse somatic symptoms, they are set aside from the other symptoms in tables/figures.
In our study we cannot explore the cause or origin of symptoms; we solely investigate the symptom load in chronic whiplash. Also, regardless of whether some symptoms are caused by physical injury, other processes might also be of great importance in the development and maintenance of chronic suffering after a whiplash accident.
For instance, theories on symptom amplification and re-attribution [26
] are useful in explaining our findings. We will consider neck pain as an example. Neck pain is common in the general population, and an individual experiencing a whiplash injury might have had neck pain before the incident. After the accident, however, he/she becomes more aware of the neck pain, and considers the neck pain a result of the injury. The importance of attribution of pre-existing symptoms to the trauma has been emphasized in previous studies [35
]. In line with this, a tendency to underestimate experienced symptoms such as back pain, neck pain and psychological distress experienced before the accident [72
] has been found.
After a whiplash accident, neck pain might also lead to fear of serious damage and chronicity. This again leads to amplification [26
]; neck pain will be more noticed and appear more troublesome.
Looking at this the other way around, individuals experiencing an increased load of somatic symptoms are more likely to spend time thinking about what causes their symptoms. These individuals are therefore more likely than others to remember and report all types of injuries and accidents, which for this purpose can be labeled the recall bias hypothesis. Exploring if somatic symptoms were equally increased in individuals self-reporting a past fracture of hand or wrist, we found at best limited support for this recall bias hypothesis. There was only a very modest increase in the overall somatic symptom score in individuals self-reporting fractures, and limited to only six symptoms.
A declining number of self-reported injuries was found with increasing time since accident. Alongside this, the association between a reported whiplash injury and somatic symptoms got slightly stronger. This finding is contrary to the organic model for chronic whiplash and coherent with several other explanations including the functional model, recall bias, and other explanations.
Anxiety, depression and benefit receipt were the covariates separately attenuating the association between chronic whiplash and somatic symptoms the most. The increased load of symptoms of anxiety and depression found among individuals reporting a whiplash injury, is in line with previous studies [3
]. Two explanations have been given for the increased level of anxiety and depression seen in chronic whiplash: It has been considered a psychological response to the injury, like in post-traumatic stress disorder, or as a response to physical pain resulting from the injury [74
]. Recent findings do, however, suggest reverse causality, namely that: anxiety and depression at baseline increases the risk of reporting whiplash at follow-up [35
]. This debate of cause or effect in the association between whiplash and anxiety/depression does have consequences for whether anxiety/depression is to be regarded a mediating, confounding or even moderating factor in this association. However, our cross sectional design precludes further exploration of the temporal alignment of chronic whiplash and symptoms of anxiety/depression.
The increased symptom reporting, the broad symptom profile and the importance of amplification and attribution, indicate that chronic whiplash cannot merely be considered an organic disorder caused by a neck injury. In previous studies, also other aspects by chronic whiplash have been explored, supporting this.
First, there is a drastically varying prevalence of chronic whiplash in different cultures with similar traffic pattern [40
]. Also, the outcome after a whiplash trauma is more affected by cultural expectations [2
] and cultural factors that generate symptom amplification and attribution [40
], than by the actual speed, forces or tissue damage [2
]. This is in accordance with the functional model for whiplash, but more difficult to incorporate in relation to the organic model.
Thoughts and emotions in relation to the accident are also of importance for prognosis [78
]. For instance, the feeling of not being responsible for the accident, and being angry or worried, predict a worse outcome [53
]. Pain-related fear and avoidance appear to be essential in developing chronic pain and disability [73
]. Also, poor expectations for recovery are tightly associated with poor recovery [83
People experiencing whiplash accidents in relation to sports stand out from other whiplash victims with their absence of chronic symptoms and disability [27
]. At the same time, even a placebo rear-end collision without biomechanical potential for injury might give rice to head and neck pain [85
]. Finally, individuals self-reporting whiplash have increased risk of being awarded disability pension, also in the absence of neck-pain, and medico-legally for a whole range of diagnoses [35
The debate over whiplash being a functional or organic disorder is by far settled by this study. But the broad symptom profile found among sufferers of chronic whiplash strongly resembles the diffuse and non-specific profile presented by individuals suffering from functional somatic syndromes [26
], and our findings support the repeated suggestions that chronic whiplash is best understood and treated as a functional somatic syndrome [21
One attempt to settle or calm the debate over whether chronic whiplash best is regarded an organic disorder or functional somatic syndrome is to introduce alternative perspectives and models. For example, chronic whiplash has been described with a biopsychosocial approach [40
]. This alternative model dismisses both the organic and the functional model for whiplash, and suggests that chronic whiplash is a result of cultural expectations, and that symptom reattribution and amplification is of importance. At the same time the possibility of coexisting physical or psychological causes for symptoms is kept open. The biopsychosocial model is broader than the functional somatic model and therefore less readily testable. Though we in our study aimed to investigate the functional somatic syndrome model, our results are also in line with the biopsychosocial model.