The hypothesis may help in a better understanding of chronic low back and neck pain patients, and in improved clinical management.
Introduction Low back pain is an important societal problem with significant costs. The total cost of low back pain has been estimated to exceed 50 billion dollars per year in the USA Although neck pain due to whiplash associated disorder is less common and less costly, awareness of this disorder, diagnosis and treatment are equally baffling Further, the term used here refers generally to the entire spine, but in particular to the cervical and lumbar regions.
Back pain is complex. The exact cause of most back low back and neck pain remains unproven The multi-factorial nature of back pain is well recognized with respect to its causes, diagnosis, chronicity, disability and treatment Abnormal mechanics of the spinal column has been hypothesized to lead to back pain via nociceptive sensors The path from abnormal mechanics to nociceptive sensation may go via inflammation 8, 11 , biochemical and nutritional changes 6 , immunological factors 44 , and changes in the structure and material of the endplates 6 and discs 40, 41 , and neural structures, such as nerve ingrowth into diseased intervertebral disc 15, Most likely, the initiating event is some kind of trauma involving the spine.
It may be a single trauma due to an accident or microtrauma caused by repetitive motion over a long time. It is also possible that spinal muscles will fire in an uncoordinated way in response to sudden fear of injury, such as when one misjudges the depth of a step. All these events may cause spinal ligament injury. The research literature on chronic back pain is vast. However, there are some important and common observations.
Chronic low back pain patients have delayed muscle response when asked to perform a task 65 or when the spine is suddenly loaded 35 , or in anticipation of raising an arm to horizontal position 20 , and also delayed muscle shut-off after the external challenge has been withdrawn Further, they show poorer spinal posture control and balance, especially during complex tasks, when compared to subjects without back pain 10, 33, The findings in neck pain patients are similar, although the number of studies is fewer. Patients with whiplash associated disorders have disrupted neck motion 2, 4, 14, 27, 34, 49, 51 and less efficient muscle control 14, 19, 22, 31, A few hypotheses have attempted to explain the clinical observations and research findings in back pain patients.
Others have focused on spinal muscles. The evidence was mixed, and authors suggested that other models, such as spinal instability 46, 47 , may be explored. The role played by the injury to the mechanoreceptors embedded in the ligaments of the spinal column has not been explored by any hypothesis. The spinal column, consisting of ligaments spinal ligaments, discs annulus and facet capsules and vertebrae, is one of the three subsystems of the spinal stabilizing system The other two are the spinal muscles and neuromuscular control unit figure 1. The spinal column has two functions: structural and transducer.
The structural function provides stiffness to the spine. The transducer function provides the information needed to precisely characterize the spinal posture, vertebral motions, spinal loads etc. These mechanical transducers provide information to the neuromuscular control unit which helps to generate muscular spinal stability via the spinal muscle system and neuromuscular control unit The criterion used by the neuromuscular unit is hypothesized to be the need for adequate and overall mechanical stability of the spine.
If the structural function is compromised, due to injury or degeneration, then the muscular stability is increased to compensate the loss. What happens if the transducer function of the ligaments of the spinal column is compromised? This has not been explored. There is evidence from animal studies that the stimulation of the ligaments of the spine disc and facets 21 , and ligaments 59, 62 results in spinal muscle firing. The mechanoreceptor-muscle firing relationships are modulated by several factors, such as ligament fatigue 61 , static flexed posture 60 and cumulative microtrauma The observations from animal studies just mentioned, together with the possibility of transducer dysfunction in back pain patients, form the basis of a new back pain hypothesis.
The purpose is to describe the hypothesis, use the hypothesis to explain the various important research findings and suggest possible treatment options. Single trauma or cumulative microtrauma causes subfailure injury of the spinal ligaments and injury to the mechanoreceptors embedded in the ligaments.
Functional somatic syndromes, somatic symptoms and self-reported whiplash are related to a whole range of socio-demographic and health related factors [ 26 , 27 , 34 , 36 , 39 , 40 , 41 ]. When adjusting for potential covariates, the mean difference in symptom reporting was attenuated to 0. Sing Han has built a world wide business empire, and used the money to finance his grand plan for revenge—manipulate the price of oil, causing debtor nations to default, bringing down the U. Harvey SHM: Physical activity and common mental disorders. Jump To In another part, oil well drilling is explained.
When the injured spine performs a task or it is challenged by an external load, the transducer signals generated by the mechanoreceptors are corrupted. Neuromuscular control unit has difficulty in interpreting the corrupted transducer signals because there is spatial and temporal mismatch between the normally expected and the corrupted signals received.
The muscle response pattern generated by the neuromuscular control unit is corrupted, affecting the spatial and temporal coordination and activation of each spinal muscle. The corrupted muscle response pattern leads to corrupted feedback to the control unit via tendon organs of muscles and injured mechanoreceptors, further corrupting the muscle response pattern. The corrupted muscle response pattern produces high stresses and strains in spinal components leading to further subfailure injury of the spinal ligaments, mechanoreceptors and muscles, and overload of facet joints.
The abnormal stresses and strains produce inflammation of spinal tissues, which have abundant supply of nociceptive sensors and neural structures. Consequently, over time, chronic back pain may develop. The subfailure injury of the spinal ligament is defined as an injury caused by stretching of the tissue beyond its physiological limit, but less than its failure point Under normal circumstances, to perform a task or to respond to an external challenge, the mechanoreceptors generate a complex and redundant set of transducer signals describing vertebral position, spinal motion, spinal load, and so forth, at each spinal level figure 2.
The signals are transmitted to the neuromuscular control unit for interpretation and action. This is achieved via feedback from the muscle spindles and golgi tendon organs of the muscles as well as the mechanoreceptors of the ligaments. The muscle response pattern includes all the information needed to dynamically orchestrate the muscles: to choose the individual muscles needed, and to activate each muscle in a defined sequence with respect to its onset, activation level and shut-off.
The entire dynamic procedure is relatively quick, non-injurious and leads to no adverse consequences. The injured spine behaves differently figure 3. There is loss of spatial and temporal integrity of the transducer signals received from multiple redundant mechanoreceptors distributed through the spinal column. The neuromuscular control unit, not affected by the injury itself, senses a mismatch between the normally expected and the received transducer signals, and, therefore, has difficulty in choosing the appropriate muscle response pattern. However, it must act. Consequently, the neuromuscular control unit produces a corrupted muscle response pattern, which is the closest match it can determine to the corrupted transducer signals.
The corrupted muscle response pattern affects the choice of the spinal muscles to activate, and the individual muscle activation: force onset, intensity and shut-off. The orchestration of the various spinal muscles responsible for spinal stability, posture and motion is disrupted. Additionally, the feedback to the neuromuscular control unit and mechanoreceptors is also negatively affected, further corrupting the muscle response pattern. This has several adverse effects. Higher stresses, and strains and injuries may develop in the spinal ligaments and mechanoreceptors.
The facet joints may be overloaded, and the spinal muscles may fatigue or be injured. Over time, these injurious stresses and strains can initiate inflammation of neural tissues 12 and accelerate disc 40 and facet joint 9 degeneration. Thus, a vicious cycle is set up, leading to chronic dysfunction of the entire spinal system and resulting in back pain. Discussion The underlying concept of the spinal instability hypothesis was the need for adequate spinal stability provided by vertebrae and ligaments of the spinal column, and augmented by the spinal muscles under the neuromuscular control 46, In the present hypothesis, the focus is on the disruption of the mechanoreceptors due to ligament injury leading to corrupted transducer signals and muscle response pattern, and overall system dysfunction.
What follows is an attempt, using the new hypothesis, to explain some of the observations concerning low back and neck pain patients, and to suggest treatment options. Delayed muscle response is a common observation in low back pain patients. When low back pain patients were challenged by a sudden external load, the delayed muscle onset was observed 35 , and delayed muscle shut-off was seen when the load was removed Similarly, the anticipatory response of the transverse abdominis was delayed These findings can be explained by the hypothesis.
An individual with intact spinal system, when challenged by a sudden change in its load or posture, will produce a quick and normal muscle response pattern, specific to the challenge figure 2. However, when the neuromuscular control unit receives corrupted transducer signals, it may take a longer time to choose a muscle response pattern that most closely matches the corrupted transducer signals, taking into account a multitude of factors such as spinal stability, postural balance, tissue overload and so forth figure 3. Additional factors, such as muscle fatigue, complexity of the task, mental distraction and so forth, may further decrease the efficiency of the neuromuscular control unit leading to the delayed muscle system response.
Balance and postural control are deficient in low back pain patients 10, 33, The balance and postural control includes a three-step process: generation of transducer signals by the mechanoreceptors, selection of appropriate muscle response pattern by the neuromuscular control unit based up mechanoreceptor signals and feedback from the mechanoreceptors and muscle spindles and golgi tendon organs figure 2. Therefore, subfailure injuries of the ligaments disrupt all the three steps involving the mechanoreceptors thereby resulting in poor balance and postural control.
Re-positioning error has been consistently found in both low back pain 7, 38, 42 and whiplash 19, 31 patients. The error occurs when the patient is asked, starting from an initial posture, to first bend or twist the spine to a certain posture and then to return to the initial posture. Based upon the hypothesis presented, this is to be expected.
The muscle response pattern generated to bring back the trunk or head to the initial posture makes use of the mechanoreceptor transducer signals, in the three-step process described above. With the ligament injury in back pain patients, the corrupted mechanoreceptor information and the corrupted muscle response pattern will both lead to the re-positioning error. Among chronic whiplash patients, decreased neck motion has been observed in most studies 2, 4, 14, 34, 49, These were active motion studies in which the subject was encouraged to produce the motion.
However, when the subject was relaxed and the motion was produced passively by the examiner, the motion was found to be increased in the whiplash patients compared to the control group How can one explain these contrasting findings? In the active motion studies, corrupted muscle response pattern generated due to corrupted mechanoreceptor signals applies higher muscle forces on the cervical spine. Such forces stiffen the spine and reduce the motion 50, 68, Thus, when the abnormal muscle forces were minimized in the passive examination, the intrinsic injury of the spinal column was exhibited as the increased motion.
Muscle spasm is commonly observed in both low back pain 5, 30 and whiplash patients 39, 55, Muscle coordination may be thought of as an orchestrated activation of various spinal muscles to stabilize the spinal column and accomplish a certain task. The orchestration consists of activation of individual muscles with respect to the onset, magnitude of the force generated, and offset. With the injury of the ligaments, the mechanoreceptors generate corrupted transducer signals, and therefore, there is a mismatch between the expected and the received corrupted transducer signals.
The neuromuscular control unit senses the mismatch and may fire simultaneously both the agonist and antagonist muscles at its command to temporarily stabilize the spine and minimize the intervertebral motions, corrupted transducer signals, and pain. If the situation does not improve with time, then the muscle action may become chronic. Such simultaneous firing of agonistic and antagonist muscles has been observed in low back pain patients. Greater variability has been observed in almost all parameters measured in low back 28, 33, 37, 42, 53 and whiplash 14, 34 patients.
The new hypothesis can explain this increased variability. The subfailure injuries of ligaments are incomplete injuries, which may range between tearing of a few fibers to a nearly complete rupture of a ligament. Importantly, a complex joint, such as a functional spinal unit, includes many ligament structures.
This collection of ligament structures may encompass a wide range of injuries, each structure with different injury severity, depending upon the magnitude and mode of the trauma. The density of the mechanoreceptors imbedded in the various ligament structures may also vary. The result of all these numerous variations can produce a wide spectrum of corrupted muscle response patterns for seemingly similar injury causing events. Further, each low back pain patient is unique, for example with respect to the anatomy, mechanical properties of ligaments and muscle response to the trauma, adding further to the muscle response pattern variability.
There are limitations to the hypothesis. It is recognized that the pain is a subjective experience. Besides affecting the muscle system via the corrupted mechanoreceptor signals, ligament injury may also result in muscle atrophy and weakness due to disuse, thus directly affecting the spinal system function. Additionally, muscle injury, fatigue, atrophy, and so forth may aggravate the spinal system dysfunction.
Whiplash and the compensation hypothesis. Spearing NM(1), Connelly LB. Author information: (1)Australian Centre for Economic Research on. OBJECTIVE: To propose a different hypothesis of whiplash injury mechanism based on a series of experimental studies summarized in this communication.
As the muscles participate in the feedback loop via the mechanoreceptors in the form of muscle spindles and golgi tendon organs figure 3 , their disruption could further corrupt the muscle response pattern. However, an injured muscle may heal relatively quickly due to abundant blood supply, and, therefore, may not be the main cause of chronic back pain.
In contrast, the ligament injuries heal poorly and, therefore, may lead to tissue degeneration over time 40, Thus, the ligament injuries are more likely to be the major cause of the chronic back pain. The corrupted transducer signals may be the result not only of the ligament injury, but also due to ligament fatigue and viscoelastic creep stretch 61 , but such an effect is often reversible given sufficient rest, and, therefore, may not always lead to chronic back pain.
The clinical and research studies presented constitute only a small, but an important and quite representative sample, of the vast literature available on the subject of back pain. It is recognized that there may be other studies whose explanation may or may not fit the new hypothesis.
In general, hypotheses and models are extremely difficult, if not impossible, to fully validate They can only attempt to explain the available findings, and may be used to predict outcomes in specific situations.
The symptoms reported by individuals with functional somatic syndromes are prevalent in healthy populations [ 29 , 30 ] and characterized by diffuse and non-specific symptoms emerging from different organs and body parts [ 26 , 28 , 30 , 31 , 32 ]. Furthermore, the symptoms of functional somatic syndromes are very similar to somatization disorder, and the two conditions are thought to be closely related [ 26 , 33 , 34 ]. There are alternative models and explanations for increased symptoms beyond those expected according to the organic model for whiplash.
One alternative explanation can be called the recall bias hypothesis. This hypothesis suggests that the generally increased symptom load in self-reported whiplash is a memory, response style or attention bias seen in some individuals, producing positive responses to questions regarding both past injuries and recent symptoms.
By way of anxiety, personality, the belief that one is sick, negative expectations about the future course of the disease and stressful events, diffuse symptoms present in the general population might by some individuals be perceived as more noxious and troublesome [ 26 ]. Also, individuals experiencing increased symptom load are more likely to think about what could cause their symptoms — and will therefore to a greater extent recall and report injuries of all sorts.
This hypothesis can, however, be tested by exploring whether symptoms as seen in somatization disorder are elevated in a self-reported past non-functional disorder, i. The purpose of this study was to investigate whether self-reported whiplash injuries are associated with increased prevalence of a broad range of somatic symptoms not readily related to a neck injury. To explore if our finding is merely a result of recall bias, we also explored if the same somatic symptoms are equally increased in self-reported past fractures of hand or wrist.
Finally, we aimed to examine if the proportion of the population self-reporting whiplash diminishes with time, and how the symptom burden changes with time since the whiplash injury. This joint epidemiological research project was conducted in cooperation between the National Norwegian Health Screening Services, the University of Bergen and local health services.
Of these, 18, 8, men and 9, women accepted the invitation, filled in the questionnaires and attended clinical examinations including measures of blood pressure, height, weight, waist- and hip circumference. In correspondence with previous work [ 21 ], we defined our group of chronic whiplash sufferers as individuals having experienced the trauma no sooner than one year prior to the survey and reporting neck pain for at least three consecutive months during the last year.
In the same section and wording as for whiplash, participants were also asked whether they have ever fractured their hand or wrist. The frequencies of common somatic symptoms arising from different body parts and organ systems were investigated. The list contains 13 items from the ICD research criteria for somatization disorder F45 [ 33 ] and 4 other symptoms related to somatization and functional somatic syndromes [ 26 , 28 , 36 ].
It has previously been used when exploring somatization [ 37 , 38 ]. The two latter possibilities were truncated to one, yielding a symptom load ranging from 1—4. The mean frequency of complaints was calculated across symptoms for each individual. As in previous studies [ 37 , 38 ], this mean score was used as an indication of somatization tendency. Functional somatic syndromes, somatic symptoms and self-reported whiplash are related to a whole range of socio-demographic and health related factors [ 26 , 27 , 34 , 36 , 39 , 40 , 41 ].
We have therefore adjusted the association for the following factors:. Summary of the variables included in the analysis, and differences between individuals reporting chronic whiplash and individuals not reporting chronic whiplash.
As somatic diagnoses can affect the symptom profile, we are investigating the number of somatic illnesses each individual was suffering from at participation time, or had suffered from earlier. The number of diagnoses was recorded as participants ticked off the following: heart infarction, angina pectoris, stroke, asthma, diabetes or multiple sclerosis. The responses from 18 participants reporting 3 or more somatic diagnosis were truncated to 3. HADS is a widely used self-report questionnaire considered reliable for patients in psychiatric and non-psychiatric settings, and for the general population [ 43 , 44 , 45 ].
Somatic symptoms commonly seen in anxiety and depression are excluded, making the scale useful in populations with somatic illness and symptoms. Each item has four alternative responses ranging from symptom not present 0 to maximum reported level of symptom 3 , giving a sum score range from 0 to 21 for both subscales. Health-related behavior was evaluated in line with previous studies [ 47 , 48 ]. Physical activity was evaluated by asking how often and for how long the participants engaged in both light and intense leisure-time physical activity.
Light activity was defined as activity that did not lead to being sweaty or out of breath, while intense activity was activity that did result in sweating or breathlessness. After the first questionnaire and the clinical examination, a second questionnaire was distributed to a random subsample and completed by 8, individuals [ 49 ]. This questionnaire contained a question on sleep which was included as a covariate in this subsample. Participants answering one of the two first were considered as having good sleep, participants answering one of the two latter were considered as having bad sleep.
To enable a comparison between the whiplash-group and the no whiplash-group in relation to somatic symptom profiles, the reported frequency of each symptom was standardized z-scored with a mean of 0 and a standard deviation of 1 [ 50 ]. This standardization enables a straightforward interpretation of reported frequency across the different somatic symptoms. Independent t-tests were then employed to each of the standardized symptoms and the standardized mean frequency of the reported symptoms somatization.
In order to adjust for covariates, a multiple linear regression model was employed. Each covariate was adjusted for separately, but all regressions included gender. A fully adjusted model was computed. Also a separate regression analysis was conducted, adjusting each symptom for all covariates. These analyses were then repeated for individual self-reporting a past fracture of the hand or wrist. To investigate the unadjusted association between the standardized mean frequency of reported symptoms and time since whiplash-accident, a linear regression model was employed.
All the participants in this study gave their written consent upon inclusion. The individuals in the whiplash group reported more symptoms of anxiety and depression and were more likely to be benefit recipients than those in the comparison group. They also reported a higher number of somatic diagnoses and worse sleep Table 1. Mean difference of reported somatic symptoms compared between individuals reporting chronic whiplash and individuals not reporting chronic whiplash, and between individuals reporting a past fractured hand or wrist and no previous fractured hand or wrist.
Mean difference in the association between those reporting chronic whiplash and somatic symptoms compared to those not reporting chronic whiplash. Mean difference of reported frequency of 17 somatic symptoms compared between individuals reporting chronic whiplash and individuals not reporting chronic whiplash and individuals reporting a past fractured hand or wrist and no past fractured hand or wrist, unadjusted, adjusted for gender and fully adjusted.
Somatic symptoms, frequency of participants reporting whiplash and time since accident. The mean difference of symptom reporting between those reporting fracture and those reporting no fracture was 0. Adjusting for possible confounders changed the mean difference to 0. Self-report of chronic whiplash was associated with increased frequency of all somatic symptoms examined. Adjusting for potential confounding variables only partly accounted for this difference.
A memory or response style bias only cannot explain all of the increased symptom reporting: self-reporting fractures of the wrist or hand was associated with only a few somatic symptoms and only weakly so. Finally, a declining number of self-reported whiplash injuries were found with increasing time since the accident. Older whiplash injuries were associated with more somatic symptoms reported at participation in HUSK. 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 , 53 ]. 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 , 21 ].
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.
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. 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, individuals living in Hordaland County, born between and 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 claims conflicting results [ 58 ].
Consequently, we cannot exclude the possibility that the narrow age range of our study limits the generalizability 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. Some studies have found increased levels of gastrointestinal symptoms, palpitations, shortness of breath and sleep disturbances [ 15 , 21 ], but to the best of our knowledge, this is the first study showing that the entire range of somatic symptoms included in the ICD 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 , 55 , 62 , 63 ]. In contrast, it is claimed that no MRI changes can be found after whiplash injuries, not for acute [ 64 ], nor chronic cases [ 7 , 65 , 66 , 67 ]. Stress system responses including catecholaminergic systems, serotonin systems and the hypothalamic-pituitary-adrenocortical systems also appear capable of producing hyperalgesia and allodynia [ 25 , 68 ].
As in other chronic pain conditions, sensitization might be of importance [ 25 , 69 ]. 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.
As these symptoms are important among individuals suffering from chronic whiplash, we included them in our study. 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 , 40 ] 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. The importance of attribution of pre-existing symptoms to the trauma has been emphasized in previous studies [ 35 , 71 ]. 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 , 40 , 73 ]; 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 , 13 , 15 , 21 ]. 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 ]. 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 , 75 ] and cultural factors that generate symptom amplification and attribution [ 40 ], than by the actual speed, forces or tissue damage [ 2 , 18 , 76 , 77 , 78 ]. 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 , 79 ].
For instance, the feeling of not being responsible for the accident, and being angry or worried, predict a worse outcome [ 53 , 80 , 81 ]. Pain-related fear and avoidance appear to be essential in developing chronic pain and disability [ 73 , 82 ]. Also, poor expectations for recovery are tightly associated with poor recovery [ 83 , 84 ]. 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 , 28 , 31 , 32 ], and our findings support the repeated suggestions that chronic whiplash is best understood and treated as a functional somatic syndrome [ 21 , 26 , 27 ].
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.