Attempts to classify whiplash (WL) patients in order to predict chronicity and long-term disability following trauma have been unsuccessful. Treatment studies applying the existing classification or grading systems even with individualized therapy have been unable to improve the outcome after WL injuries [30, 38].

Twenty years ago, The Quebec Task Force introduced the whiplash-associated disorders (WAD) grading system, with grades from 0 to IV based on encountered symptoms and neurological findings after exposure to a WL trauma. More recent WL literature rules out the WAD [34] grades 0 and IV as being WL injuries [3]. However, restricting the application of the WAD grading system to grades I-III has shown limited power as a tool for predicting the transition toward chronicity [25]. Recent research has emphasized the importance of both psychological and social factors in combination with the apparent biological features presented by the patient at first examination [1, 4, 5, 12, 31, 32].

Nociceptive sensitization is present in both acute and chronic WL patients. Nonrecovery is probably related to the initial pain barrage and to previous pain conditions, and may also be related to genetic factors [7, 8, 20]. Patients with initial moderate or severe headache or neck pain without previous pain had a fourfold higher risk of work
disablement after 1 year, and patients with more than 14 days of minor headache/neck pain during the last year had a 2.5-fold higher risk [23]. An altered general response to cold pain 5 days after trauma may relate to genetic or pretrauma susceptibility of ascending and/or descending pathways for nociceptive sensitization, but for the time being this is only speculative.

Several clinical and epidemiological studies support pretrauma nonspecific stress, depression, catastrophizing, expectation, future despair, and perceived injustice, and other psychological factors play a role for nonrecovery [3, 5, 14, 27, 32, 36, 37]. Psychological factors such as fear of movement, kinesophobia, catastrophizing, and coping strategies play a role in reduced neck mobility and nonrecovery, persistence, or worsening of pain [2, 31]. In similarity to the CROM test being a psychophysical test, many nonpainful symptoms may reflect both the severity of a physical injury and also the presence of bodily distress [10]. The role of the examiner, the therapist, as a fear-inducer has been debated [6, 37].

The initial evaluation of easily obtainable clinical parameters, including visual analogue scale (VAS) for neck pain and headache, and the number of nonpainful neurological symptoms and active neck mobility (cervical range of motion [CROM] [24]) is easily done at the first visit after WL trauma. From a clinical point of view, it is reasonable to stratify WL-exposed patients into different risk categories soon after exposure based on early clinical findings. We conducted two clinical prospective studies using clinical assessment and patient-reported symptoms with 12-year follow-up (Flowchart in Fig. 9-1) [18, 23].

First, we performed a 1-year observational study of 141 acute WL patients (WAD grade I-III) exposed to rear-end motor vehicle accident (MVA), and 40 sex-matched and age-matched controls exposed to acute nonsport ankle sprain. The two patient groups reported similar disability and global pain within the first week after trauma, but at 1 year posttrauma, only the WL patient group reported nonrecovery [18], whereas all ankle sprain patients recovered. Neurological examination was performed at the first visit. Semistructured interviews were conducted after 1 week, 1 month, and 3, 6, and 12 months following trauma. In addition, patients completed a set of self-reports, namely, The McGill Pain Questionnaire [9], the Danish version, The Millon Behavioral Health
Inventory [11], the symptom check list (SCL-90R), The Copenhagen Neck Functional Disability Scale [16]. We were particularly interested in the role of sensitization of the nociceptive system as a possible mechanism for development of long-term pain and disability. Therefore, we examined the development of the functioning of the diffuse noxious inhibitory control system in a cold pressor test [20] prospectively. We observed the development of remote and regional pain with pressure algometry detection and tolerance thresholds, and applied the methodical palpation technique in the neck and jaw muscles of the WL patients and
controls [29]. We measured active neck mobility (CROM test [24]), and maximal voluntary contraction and duration for neck flexion and neck extension. In a second study, we performed a multicenter interventional randomized trial of 740 acute WL patients divided into high- and low-risk strata based on risk factors derived from the former observational study [18, 23]. The derived risk factors from the former study were: (1) intense initial neck pain or headache, (2) multiple nonpainful neurological symptoms, and (3) reduced active neck mobility from early aftertrauma (median 4.5 days after trauma). These factors were used for an algorithm to classify patients in the treatment study into either a low-risk or a high-risk group. (For details on the intervention study results refer to [23, 28].) High-risk patients had a 10-fold raised risk of 1-year work disability. However, these factors do not reveal the mechanisms responsible for chronic disability after WL trauma, but merely allude to the multifaceted nature of disability in WAD.