Thoracic spine pain.

Despite the very low quality of included studies, there is evidence of thoracic spine pain in a sub-acute WAD population (n = 11,576) [11, 14, 17, 34, 39, 43, 52, 60], with prevalence ranging between 21%-66%,. Findings were inconsistent in chronic WAD, with prevalence ranging 0–94% [17, 50]. Study quality, differing time points post injury, differing measurement approaches and higher degrees of WAD severity could partly account for the inconsistency. For example, chronic WAD, studies with less severe presentations (minor or WADII) [32, 50] demonstrated lower prevalence rates (0–15.3%) compared to studies investigating WADII/III where prevalence was 54% [58]. Just one study reporting thoracic pain specifically associated with central sensitisation (allodynia) where pain prevalence was 71% in individuals with CWADI/II [33].

Chest pain.

Prevalence of chest pain in acute/sub-acute was reported to range 0.0–19% [11, 14, 17, 52], although when considered as part of a widespread pain presentation ranged 9–19% [11, 14]. In one study where they only considered individuals with numerical rating scale (NRS 0–10) 4+ chest pain prevalence was lower at 8% [52]. In CWAD prevalence rates for chest pain ranged 6–22% [17, 53] although this reflects a, broad timescale with one study reporting results 6 month post injury [17] to one exploring prevalence at any time point following injury [53]. Drawing definitive conclusions on prevalence of chest pain is difficult given variation in approaches used to record pain (pain drawings, VAS, etc.), time points post injury, sample heterogeneity and the overall methodological low quality of research. This may also be a related to the focus of this review, being to those with mild to moderate presentations of WAD where studies including WADIV or fractures were excluded.

Thoracic posture.

Evidence of thoracic postural dysfunction is inconclusive given conflicting findings from a small number of studies of low methodological quality evidence where postural assessment was not a primary focus [44, 61]. Future studies should consider the use of a gold standard measure for postural evaluation [63].

Thoracic mobility and chest mobility.

There is a notable gap in the evidence exploring thoracic and chest mobility in WAD, with just two studies (n = 54) of very low quality suggesting a trend for reduced chest mobility (p>0.05) and flexion hypomobility at the cervico-thoracic junction in women. In terms of thoracic mobility, evidence from one study (n = 7) [61] suggests a slight increase in thoracic flexion-extension, although with such a small sample and lack of inclusion of a valid approach to quantify thoracic mobility, meaningful conclusions cannot drawn.

Thoracic outlet syndrome in CWAD.

Five studies found, a prevalence of 31–74+% [31, 35, 36, 47, 51] of thoracic outlet syndrome in CWAD. Although this suggests a relatively high prevalence, the methodological quality of included studies was generally poor (<4/9), resulting in a very low rating of quality according to GRADE.

Brachial plexus.

Acute/sub-acute WAD

Notwithstanding that evidence is drawn principally from one research group, there is evidence of thoracic dysfunction in relation to the brachial plexus provocation test (BPPT) in WADI-III. From the research by Sterling et al [12, 57, 59], there is evidence of a negative association between self-report symptom severity (VAS) and range of elbow extension during the BPPT in chronic WAD. Moreover, the extent of this dysfunction is in turn related to the degree of pain and disability, with those participants presenting with higher levels of self-reported pain and disability (NDI) having greater levels of dysfunction during BPPT.

Chronic WAD

For participants with CWADII and/or III, evidence indicates dysfunction detected during the BPPT, with pain levels and restriction in elbow extension almost double those found in asymptomatic controls [38, 55]. Furthermore, those with higher levels of self-reported pain and disability (NDI>30) continued to have evidence of dysfunction 6 months after the injury which was not seen in the mild group who were no different to the recovered group at 2 months [57]. Although quality of individual studies varied (4-6/9), the overall body of evidence for dysfunction of the brachial plexus remains very low overall, primarily due to risk of bias of the included studies.

Muscle activation.

There are limited and very variable findings of thoracic muscle dysfunction (activation) in WAD with studies investigating a relatively small number of muscles: sternocleidomastoid [12, 49, 56]; serratus anterior [45]; middle and lower fibres of trapezius [45, 54]. Although it is difficult to derive meaningful conclusions with respect to serratus anterior and trapezius, there is evidence supporting changes in sternocleidomastoid muscle activation with heightened levels of activation during a task of cranio-cervical flexion; this increase in sternocleidomastoid activity however, was not seen during neck rotation [49]. There appears to be a positive relationship between sternocleidomastoid activation and higher levels of pain severity, with participants with CWADII/III and moderate to severe levels of disability demonstrating increased levels of sternocleidomastoid activation of between 27–47% [12, 56]. Individuals with mild, moderate/severe presentations all share comparative levels of sternocleidomastoid activation in the acute [56] and chronic phases [12].

Myofascial pain and trigger points.

Myofascial trigger points are highly prevalent in WAD with estimates ranging between 48–64% [16, 37, 40]. Muscles that have been investigated include the middle/lower trapezius [16], scaleneus medius [40, 41] and sternocleidomastoid [37, 40, 41], all with similar prevalence levels. Findings suggest that latent trigger points are more prevalent in sub-acute WADII [41] whereas in chronic WAD there is a higher prevalence of active trigger points [37]. It should however be noted that the sample of chronic WAD comprised both WADII and III, so perhaps severity could partly explain the differences seen. Likewise, age may account for some of the differences given the sub-acute sample was 28.7 years [41] compared 41.6 years in the chronic WAD group [37].

Pain.

Although there is a high prevalence of acute and chronic pain experienced in the thoracic spine region following injury, distinguishing the interplay of pain mechanisms is however challenging. Whilst we know peripheral and central sensitisation begin immediately following injury [64], it is plausible that damage to thoracic musculoskeletal tissues contributes to the relatively high prevalence of pain reported in the acute/sub-acute stages from peripheral nociceptor stimuli [11, 14, 17, 43, 52]. Relatively few studies in this review reported perceived pain levels e.g. VAS, making it difficult to consider an association between injury severity and tissue damage. Although reviewed in detail by Van Oosterwijck et al, [64] the current review found just one study reporting thoracic pain specifically associated with central sensitisation, with allodynia reported in 71% of individuals with CWADI/II [33], arguably contributing to the lack of consistency with findings for chronic WAD where differing pain mechanisms may co-exist. Likewise distinguishing local from referred pain is challenging where injury in the cervical spine may refer pain caudally to the upper and mid thoracic region [65]. Unlike the thoracic spine, reported chest pain prevalence was relatively low, perhaps more closely associated with severe injuries, including fractures, which were excluded from this review. Future studies should, in addition to using the QTF Classification, include self-reported pain severity for each anatomical region.

Thoracic posture and mobility.

With limited very low quality evidence and relative to the cervical spine, there is a paucity of research investigating thoracic posture and mobility in WAD [44, 45, 48, 61]. This may be explained with priority being given to areas with most severe pain, with the cervical spine and associated tissues being most vulnerable to stress and damage compared to the relatively stable and stiff thoracic spine [21], arguably enhanced with the mandatory use of seatbelts offering additional stability. However, considering the effect of a forceful injury on posterior structures, and neck stiffness being a hallmark of chronic WAD further research is required, specifically to investigate thoracic posture, mobility and muscle stiffness in WAD, all of which may offer new directions for research into management of WAD.

Thoracic outlet syndrome.

Although this review suggests a relatively high prevalence of thoracic outlet syndrome, the quality of evidence is very low and derived from relatively older studies, including two studies from the same group of authors [35, 36]. Whilst the mechanism of injury and resultant strain on the scalene triangle in WAD would, in theory, place the thoracic outlet at risk of injury, this does needs to be investigated further. Likewise as a ‘syndrome’, this does not provide primary evidence of a primary structural dysfunction; it merely provides evidence of a dysfunction which, in turn, could be neurogenic, myogenic, vasculogenic in nature. Perhaps, in the absence of evidence of thoracic outlet syndrome in acute WAD, this condition is secondary to the consequences of whiplash, altered posture, changes in muscle behaviour etc. [66]. Future studies should use robust observational study designs and include valid assessment techniques to diagnose thoracic outlet syndrome.

Brachial plexus.

There is considerable evidence of brachial plexus dysfunction in both acute/sub-acute and chronic WAD from research investigating the brachial plexus provocation test. Although coming from a relatively small group of researchers, the evidence supports further investigation. Future research could usefully consider the relationship of brachial plexus dysfunction to other musculoskeletal changes in the cervical and thoracic spine following a whiplash injury, but also approaches to managing this; a notable gap within the whiplash management evidence [9, 10, 66]. Although inclusion of the brachial plexus in this review may at first appear tenuous, with contributions from the level of T1 and its relationship to the thoracic outlet, its inclusion provides good evidence to further explore this anatomically and functionally challenging cervico-thoracic-supraclavicular region; a transitional zone between the stable/stiff thoracic spine and relatively mobile cervical spine.

Muscle activation.

There is unequivocal evidence of altered function of muscles following whiplash injury [66], however this evidence is largely limited to cervical muscles, with this review identifying just three muscles with insertions to the thoracic region, sternocleidomastoid [12, 49, 56]; serratus anterior [45]; middle and lower fibres of trapezius [45, 54]. Although it is difficult to derive meaningful conclusions with so few muscles investigated and the quality of the evidence, the observed positive relationship between sternocleidomastoid activation and pain severity, and evidence across all stages post injury [12, 49, 56] supports the need for further research into altered activation of cervico-thoracic and thoracic muscles, ideally involving functional spinal movements; something that is now feasible with advances in technology, including high density EMG.

Myofascial pain and trigger points.

This review has identified that myofascial trigger points are highly prevalent in WAD [16, 37, 40], although again from very low quality evidence and limited to a small number of muscles; middle/lower trapezius [16], scaleneus medius [40, 41] and sternocleidomastoid [37, 40, 41]. Nonetheless all muscles have similar prevalence levels of trigger points, with a higher prevalence of latent trigger points in sub-acute WAD [41] and active trigger points in chronic WAD [37]. With evidence of trigger points across all muscles and across the stages and severity of presentations, research is now required to explore other muscles in the thoracic region and better understand the development of pain, and persistent pain seen in chronic WAD, perhaps with longitudinal studies. Notwithstanding the quality, evidence was found of myofascial-entheseal dysfunction [16], a relatively new clinical entity and arguably similar to insertional tendinopathies. With rapid advances in our understanding of injury induced tendinopathies in the lower limb, this does offer new insights to possible muscle pathologies which may contribute to persistent pain and disability seen in WAD.

This review provides unequivocal evidence of thoracic dysfunction in WAD, albeit from evidence of low/very low quality. The findings do support a more extensive clinical evaluation of patients following a whiplash injury and the need for more methodologically robust observational studies to further characterise thoracic dysfunction in WAD across stages of the condition and levels of severity. Knowledge and understanding of thoracic dysfunction, where anatomical and biomechanical relationships with the cervical spine exist, offers novel directions for research into management of this disabling condition.

Research into WAD management has been, and continues to be primarily focused on managing cervical spine dysfunction, with interventions such as manual therapy, exercise etc. targeting the cervical spine [66], and targeting the psychological impact of a whiplash injury [66]. With inconclusive evidence of the therapeutic value of the above [67] it is perhaps time to consider new directions for research.

Whilst exercise as part of multimodal packages of care is recommended in the management of acute and chronic WAD [66, 68], the range of approaches available are considerable e.g. graded functional exercise, postural exercises, and strengthening and motor control exercises etc.[66]. The authors are not however aware of any recommendations or research specifically supporting the inclusion of thoracic spine exercises, although these could reasonably be incorporated within functional exercise programmes. With at best short term modest improvements in current exercise interventions [9, 10] and some evidence of some therapeutic value of thoracic spine manipulation in WAD [69] further research to investigate interventions targeting the thoracic spine and related dysfunction is justified.

It has not until recent years that the thoracic spine, coined the ‘Cinderella’ of the spine [21], has started to receive more research interest. This has been attributed partly to the relatively lower prevalence of symptoms than the cervical and lumbar spine more generally, but also due to the lack of affordable, non-invasive and valid measurement tools to evaluate motion in this anatomically complex and relatively stiff spinal region [21]. With the development of new measurement approaches for thoracic posture and mobility [63, 70, 71] we now have tools to support research of thoracic posture and mobility in the thoracic spine region in painful neck disorders.