Whiplash-Associated Dysphagia: Considerations of Potential Incidence and Mechanisms

Abstract

Non-specific self-reports of dysphagia have been described in people with whiplash-associated disorders (WAD) following motor vehicle collision (MVC); however, incidence and mechanistic drivers remain poorly understood. Alterations in oropharyngeal dimensions on magnetic resonance imaging (MRI), along with heightened levels of stress, pain, and changes in stress-dependent microRNA expression (e.g., miR-320a) have been also associated with WAD, suggesting multi-factorial issues may underpin any potential swallowing changes. In this exploratory paper, we examine key biopsychosocial parameters in three patients with persistent WAD reporting swallowing change and three nominating full recovery after whiplash with no reported swallowing change. Parameters included (1) oropharyngeal volume with 3D MRI, (2) peritraumatic miR-320a expression, and (3) psychological distress. These factors were explored to highlight the complexity of patient presentation and propose future considerations in relation to a potential deglutition disorder following WAD. The three participants reporting changes in swallowing all had smaller oropharyngeal volumes at < 1 week and at 3 months post injury and lower levels of peritraumatic miR-320a. At 3 months post MVC, oropharyngeal volumes between groups indicated a large effect size (Hedge’s g = 0.96). Higher levels of distress were reported at both time points for those with persistent symptomatology, including self-reported dysphagia, however, this was not featured in those nominating recovery. This paper considers current evidence for dysphagia as a potentially under-recognized feature of WAD and highlights the need for future, larger-scaled, multidimensional investigation into the incidence and mechanisms of whiplash-associated dysphagia.

Introduction

The incidence of non-catastrophic injury associated with motor vehicle collision (MVC) in the United States has been documented to affect nearly 4 million per annum, comprising 77% of all motor vehicle-related injuries [1]. Collision mechanics commonly result in a rapid acceleration/deceleration of the head and neck, giving rise to the term whiplash [2, 3]. Injury is sustained from the maximum and rapid displacement of the head and neck during collision, resulting in abnormal extension and flexion of the cervical spine [4]. Whilst the majority are expected to recover within the first 2–3 months [5], ~ 25% will transit from acute to chronic whiplash-related disability, with widespread bodily pain and heightened levels of stress [6-10]. It is not uncommon for patients to present with a host of other complex signs and symptoms known as whiplash-associated disorders (WAD). These include, but are not limited to, neck muscle degeneration [8, 11, 12], sensory and motor disturbances [13-19], muscle weakness [20, 21] and psychological distress [13, 22, 23]. The economic burden of this complex condition is vast; estimated at $USD28 billion/annum and a total lifetime cost of $14 million per person injured [1]. Unfortunately, diagnostic options and effective population-based treatments remain limited [8, 11, 24-26].

Early observational studies indicate dysphagia is a presenting issue within the complex WAD presentation. A re-examination of over 7000 patients with chronic whiplash highlighted 10% reported non-specific swallowing difficulty, suggesting this to also be an important, but potentially under-recognized consequence [27]. Evidence from cross-sectional and case-based studies have revealed whiplash-related changes to swallow function, including (i) descriptions of functional dysphagia due to laryngeal muscle tensioning [28], (ii) difficulty managing solid-textured foods [29], (iii) swallow fatigue [30] and (iv) abnormal tongue tension, pain on swallowing and reduced mouth opening [31]. Sensory distortion involving trigeminal and hypoglossal neural pathways has also been described in WAD [31], however, to our knowledge, its impact on swallowing has not been investigated. Despite these interesting studies, there is disparity for reported outcomes and to our knowledge, no standardized measures of swallowing have been utilized or reported across the whiplash condition. Consequently, the incidence of a potential whiplash-associated dysphagia remains unknown.

Mechanistic drivers of a potential dysphagia in WAD are also unknown but could span a range of etiologies. Considering the proximity of the anterior neck muscles to the hyolaryngeal complex, a muscle tension dysphagia could be plausible. Certainly, the impact of tightness in the anterior cervical region on swallowing biomechanics has been reported in other populations [32, 33]. Furthermore, intervention targeting muscle unloading has reportedly improved dysphagia symptoms [28]. Damage to the superior laryngeal nerve [34] and hypoglossal nerve [35] due to traction injury has been described in case reports of post-whiplash injury. Articular dysfunctions have also been suspected as potential drivers of disturbed jaw function influencing eating (and potentially, swallowing) behaviors [30].

Previous work has highlighted profound structural changes in the size and shape of the oropharynx measured on magnetic resonance imaging (MRI) in 79 patients with chronic WAD compared to 34 healthy controls [36] and to participants nominating recovery over time [37]. Whether or not volumetric changes in the oropharynx contribute to a potential post-whiplash dysphagia is unknown, however, a previous study has highlighted the potential utility of measuring pharyngeal lumen size to investigate pharyngeal contractile forces [38]. Interestingly, those with small oropharyngeal volumes also report higher levels of bodily pain and heightened levels of stress [36], suggesting molecular models of stress-related muscular tensioning could be a potential driver behind a WAD-related dysphagia.

One peritraumatic type of molecular target with prognostic promise is microRNA, the small non-coding RNA molecules that regulate the expression of large sets of genes. Although more than 2000 miRNAs have been identified as potential blood-based biomarkers of disease, previous studies have found one particular miRNA, miR-320a, to be associated with higher levels of stress [39], poor recovery following trauma [9, 40] and other musculoskeletal conditions [41-46]. Whether or not altered levels of circulating miR-320a occur in post-whiplash complaints consistent with dysphagia is unknown. Considering the limited diagnostic options and effective treatments available for those with WAD, early biomarkers of adverse outcomes may prove significant towards a more informed diagnostic landscape and the development of more effective interdisciplinary management schemas for patients determined to be at high-risk for poor recovery.

While dysphagia may well be a component of the multisystem condition of WAD, assessment of swallowing has not been a typical practice. Dysphagia is, however, highly associated with reduced quality of life [47], mortality [48] and increased health costs [49, 50]. Therefore, the identification of a potential post-whiplash dysphagia is considered of utmost importance in enhancing the quality of care for those suffering from this enigmatic condition. To explore a potential whiplash-associated dysphagia and guide future research directions, the aim of this exploratory study is to describe the disparate clinical presentations of six people; three with persistent WAD and all with reported swallow change and three nominating recovery following whiplash injury with no reported change in their swallow.

Method

Participants

Participant Selection

Cases for this study were selected from a recently completed longitudinal cohort study (ClinicalTrials.gov Identifier: NCT02157038) investigating the neuromuscular mechanisms underlying poor recovery following whiplash injury and are detailed in Table 1. The parent longitudinal cohort study, which included 97 acutely injured participants, aimed to quantify that a mild incomplete spinal cord injury occurs in and is a critical contributor to chronic WAD for a discrete number of those exposed and injured. Consenting participants for the longitudinal cohort study were recruited at time of presentation to an urban emergency medicine department with Level 1 trauma designation following MVC. Participants in the parent study included all individuals presenting with whiplash injury from an MVC but without radiologic confirmation of cervical spine fracture, need for surgical referral and without traumatic brain injury. Data measuring (1) neck disability, (2) traumatic distress, (3) oropharyngeal volume, and (4) miRNA (described below) were collected by an experienced researcher at multiple time points (< 1 week to 3 months post injury). Only 43 of the 97 participants in the parent study consented to providing blood for miRNA within < 1 week post injury. Observations that some patients self-reported swallow difficulty following whiplash prompted the addition of a non-specific, yes/no question. All participants of the parent study were asked—Have you felt that swallowing fluids or solids has been more difficult since the collision? A response of ‘yes’ indicated swallow change. A response of ‘no’ indicated no swallow change.

Table 1.

Participant demographics

	Chronic whiplash			Recovered whiplash
Participant	1	2	3	4	5	6
NDI%	53;42	48;46	48;36	36;4	32;0	14;20
Age (gender) [Body Mass Index]	18.6 (F) [32.6]	45 (F) [23.17]	39 (F) [27.90]	22.4 (M) [22.46]	40 (M) [28.3]	59 (F) [24.8]
Timing of initial assessment (days post injury)	4	3	4	4	2	3
Timing of second assessment (days post injury)	113	94	90	116	97	102
Employment Status at 3 months post MVC	Unemployed	Employed	Unemployed	Unemployed	Self-employed	Retired
Filed third party claim and has hired an attorney	Yes to third party claim No to attorney	No to both	Yes to both	No to both	No to both	Yes to both

NB: NDI% < 1 week; 3 months score

Potential participants for the current exploratory case series were required to have complete sets of all data collected in the parent study (including miRNA, MRI and psychological distress measures). The final cases were then selected on the basis of two extreme recovery presentations: (a) recovered whiplash with no swallow changes versus (b) chronic whiplash and co-existing reported swallow changes following whiplash. These recovery presentations were determined based on the outcome measures from the parent study regarding (1) self-reported swallowing difficulty (yes/no) and (2) recovery status (recovered/not recovered) as determined by Neck Disability Index (NDI) [51] percent threshold scores.

All applicable institutional regulations concerning the ethical use of human volunteers were followed during this investigation.

Outcome Measures

The following outcome measures were observed in each participant at 1 week and 3 months post injury by an experienced researcher. MiR-320a expression levels were measured at the peritraumatic (i.e., < 1 week) time point only.

RNA Collection and miR-320a Quantification

Sample Collection

Total RNA (including miRNA) was isolated using PAXgene blood miRNA kits (QIAGEN) and stored at – 80 °C until use. RNA concentration and purity (RNA Integrity Number > 7.0) were measured using a NanoDrop ONE (Nanodrop Technologies, Wilmington, DE) and a Bioanalyzer 2100 (Agilent) [27, 52, 53].

MiR-320a expression levels were quantified using real-time reverse transcription quantitative polymerase chain reaction (RT-qPCR), a sensitive and specific method of miRNA profiling [54]. Stem-loop RT primers and TaqMan probes were obtained from Life Technologies (Carlsbad, CA). Relative miR-320a expression levels were calculated as described previously [55]. Briefly, miR-320a cycle threshold (C_t) values were normalized to U6 C_t values for each sample (to generate a ΔC_t value). ΔC_t values were then compared to the reference sample ΔC_t to generate ΔΔC_t values. Fold difference in expression relative to a randomly selected sample was then calculated using 2^^−ΔΔC_t. This value was then averaged across all three samples among the three individuals with chronic symptoms versus the samples among the three individuals who recovered following MVC and standard deviation was calculated.

Measure of Neck-Related Interference

The Neck Disability Index: Recovery status at 3 months was determined by NDI [51] percentage (%) scores, collected as part of the parent study. Based on previous work [56-58], those participants with NDI% scores ≥ 30% at 3 months post injury were selected to represent the chronic whiplash group indicating poor recovery and persistent symptomatology. Those cases scoring 0 to < 30% were selected to represent the recovered group.

Measure of psychological distress: The Traumatic Injuries Distress Scale (TIDS) [52] was completed by all consenting participants at < 1 week and 3 months post injury. The TIDS is a 12-item self-report tool with three subscales (uncontrolled pain, negative affect, intrusion/hyperarousal). Each item represents the extent to which the reporter has experienced each symptom since injury, with 0 = never, 1 = occasionally, 2 = often or always. It has demonstrated adequate internal and longitudinal properties, holding promise as a prognostic screening tool and offers estimates of both magnitude and nature of risk of chronic problems following acute musculoskeletal injury [52]. Higher scores (maximum 24) indicate higher levels of distress.

Magnetic Resonance Imaging

MRI was performed for all participants as part of routine assessment and follow-up, within < 1 week and then again at 3 months post MVC. Oropharyngeal volume (mm³) was calculated for each participant at both intake and 3 months, detailed below.

Imaging Protocol

Imaging was performed on a Siemens 3.0 Tesla Prisma Syngo MR D13D magnetic resonance scanner, equipped with a 64-channel head/neck coil (Erlangen, Germany). A localizer scan was acquired followed by 3D T2-weighted sagittal isotropic imaging, representing all regions of the oropharyngeal anatomy (OP). Imaging parameters for the Sagittal T2 included Repetition Time (TR) = 1500 ms, Echo Time (TE) = 135.0 ms, flip angle = 140°, bandwidth = 625 Hz/Px and an imaging matrix of 320 × 320. The field of view = 250 × 250 mm, the number of slices per slab = 64 with a slice thickness of 0.80 mm. The slice oversampling = 12.5%, turbo factor = 88, voxel size = 0.4 × 0.4 × 0.8 mm. The acquisition time = 4:08 min. Anatomical landmarks were identified using a cross-sectional 3D gradient echo with the 2-point Dixon [59]. Landmarks were the superior portions of the C1 condyles to the most inferior portion of the C7 vertebral endplate (Fig. 1a).

Fig. 1.

3D T2-weighted sagittal isotropic imaging method. Left to right: a landmarks were the superior portions of the C1 condyles to the most inferior portion of the C7 vertebral endplate, b T2-weighted midsagittal image was used to identify anatomical markers of the oropharynx and c the slice immediately inferior to C1–2 was designated as the superior portion of the volumetric stack and the slice immediately superior to the C7/T1 intervertebral disc space was used to designate the inferior portion of the volumetric stack

MRI Analysis

Analysis was performed by an experienced assessor, blinded to the clinical presentation of each participant. OsiriX image processing software (Pixmeo, Geneva, Switzerland) was used to manually contour the volume (mm³) in each axial slice of a structural T1-weighted image series containing the pharynx. The T2-weighted midsagittal image was used to identify anatomical markers of the oropharynx (Fig. 1b). The slice immediately inferior to C1-2 was designated as the superior portion of the volumetric stack and the slice immediately superior to the C7/T1 intervertebral disc space was used to designate the inferior portion of the volumetric stack (Fig. 1c). Cross-sectional areas (mm²) from the relevant slices were then “stacked” and summed to calculate total oropharyngeal volume (mm³) for each participant at both time points (Fig. 2). Mean oropharyngeal volumes at both time points for the recovered and chronic groups were also calculated. A percent difference score was calculated for each participant to determine the difference between volumes < 1 week compared to 3 months post injury. A percent difference score was also calculated for both groups to determine increase or reduction in volume between the two time points.

Fig. 2.

Total oropharyngeal volume method. NB: C1–C7 slices stacked to obtain total volume

Analysis

Due to the small case series, inferential statistics were not calculated. However, to explore the difference in mean oropharyngeal volume and miRNA expression levels between the recovered vs non-recovered groups, a measure of effect size was calculated from mean scores and standard deviations. Due to the small sample size, Hedge’s g was used to correct for bias, with categories of g ≤ 0.2 considered a small effect, 0.3 to 0.5 a medium effect, and ≥ 0.8 a large effect [60, 61].

Case Studies

Demographics and Recovery Status

From the 97 participants of the parent study, 43 had complete data sets. Of these 43, five participants followed a poor recovery trajectory based on NDI% scores and three of those reported changes to their swallow. The remaining 38 participants nominated full recovery or mild pain-related disability with no swallow deficits. Three recovered patients were selected to highlight the opposing extreme recovery presentation. After selecting three participants in each group, a blinded analysis of traumatic distress, oropharyngeal volumes and miRNA data was performed, utilizing outcomes taken from the parent study.

Table 1 details the demographics of the selected cases including age, gender, body mass index, time since MVC, employment status at 3 months post MVC and whether they filed a third party claim or retained legal services. Although not specifically controlled or matched for demographics, other than a higher proportion of females, the demographics were largely comparable across the six participants. All cases fell into the WAD Grade II grouping, meaning limited cervical spine mobility, tenderness to palpation but no neurological signs [62]. Three selected participants with low NDI scores and a ‘no’ response on the swallow question were classified as ‘recovered’ while three selected participants with higher NDI scores and a ‘yes’ swallow response were classified as having persistent symptoms of WAD.

Table 2 details the observed outcomes for the six cases, divided between two groups representing recovery status.

Table 2.

Case study observations

	Chronic whiplash						Recovered whiplash
Participant	1		2		3		4		5		6
Change in swallow (yes/no)	-	Yes	-	Yes	-	Yes	-	No	-	No	-	No
Traumatic Distress Index % (/24 High indicates worse score	20	18	17	15	15	14	5	0	3	0	6	4
Oropharyngeal volume (mm3)	7515	6972	6942	4478	5264	5173	5881	6521	6328	7981	4922	6173
[% change]	− 7.9%		− 55.0%		− 1.8%		+ 9.8%		+ 20.7%		+ 20.3%
Oropharyngeal volume (mm3) group mean (SD)	< 1 week 6573.7 (1169.8) 3 months 5541.0 (1287.1)						< 1 week 5710.3 (718.4) 3 months 6891 (959.5)
Oropharyngeal volume % change	− 18.6%						+17.1%
Acute miRNA-320a levelsb	0.26		0.19		0.34		1.91		0.50		1.52
miRNA-320a Group mean (SD)	0.26 (0.08)						1.31 (0.73)

^aMonths

^bmiRNA was measured using RT-qPCR and cycle threshold values were normalized to U6 RNA then expressed relative to a randomly chosen sample

Bold text highlights an increase of decrease in oropharyngeal volume between time points for each participant

Chronic WAD

Traumatic distress scores for the three chronic participants were higher than 12/24 at baseline and they remained above this score at the 3-month follow-up, demonstrating higher levels of acute and persistent distress over time. Oropharyngeal volumes (mm³) of each participant and the mean volume of each group are detailed in Table 2. While comparable volumes can be seen in all participants at the < 1 week time point, all three chronic participants demonstrated an overall 18.6% reduction in volume at the 3-month follow-up (Fig. 3). Finally, lower levels of miRNA-320a expression were observed in the three participants who nominated poor recovery and perceived swallow deficit.

Fig. 3.

Oropharyngeal Volume at < 1 week (left) and 3 months (right) post injury for one chronic participant. C2, 5, 7—Cross-sectional areas of cervical spine

Recovered Post-whiplash

Total scores on the TIDS for the three recovered/without swallow deficit cases exhibited scores no higher than 7 at both time points and demonstrated reductions in distress levels between 1 week and 3 months post injury, with two individuals reporting a score of zero. Oropharyngeal volumes of the three participants nominating recovery and no perceived swallow change following whiplash had an overall 17.1% increase in volume between < 1 week and 3 months following initial presentation (Table 2 and Fig. 4). Higher levels of peritraumatic miRNA-320a expression were observed in all three recovered individuals at < 1 week post injury.

Fig. 4.

Oropharyngeal volume at < 1 week (left) and 3 months (right) post injury for one recovered participant. C2, 5, 7 —Cross-sectional areas of cervical spine

Analysis

Effect size was moderate (Hedge’s g=0.71) immediately following injury, indicating a difference between groups. Three months following injury the effect size for the group difference in oropharyngeal volumes was large (Hedge’s g = 0.95), indicating an even greater difference. For miRNA expression, the effect size for the group difference in peritraumatic miRNA-320a levels measured within 1 week of the MVC, indicated a large effect size (Hedge’s g = 2.02), with those with chronic symptomatology demonstrating lower expression levels.

Discussion

The impact of dysphagia is significant and has far-reaching individual and epidemiological impacts [63]. Whiplash-associated dysphagia has been suggested [27, 29-31, 35, 64, 65], however, due to methodological limitations, the incidence and underlying mechanisms are largely unknown. This exploratory study aimed to highlight two potential, extreme post-recovery profiles, including self-reported dysphagia symptoms. Although exploratory, the purpose was to highlight the possibility of a post-whiplash dysphagia and to provide direction for future research. The results highlight some interesting observations.

Firstly, smaller and greater % change in oropharyngeal volumes were observed in the three cases of chronic whiplash and reported swallow changes, both at < 1 week and at 3 months following injury. Unlike the three cases nominating recovery and no swallow change, oropharyngeal volumes continued to reduce over time in the three nominating poor recovery. Previous studies have demonstrated smaller oropharyngeal volumes in 79 participants with chronic whiplash compared with 34 healthy controls [36] and in those with no or mild symptoms following injury [37]. Although speculative, such reductions in volume likely represent narrowing of the oropharyngeal space, resulting from early lymphoedema or tissue thickening/fibrosis of the pharyngeal wall [66, 67]. It may also potentially reflect tongue base retraction due to muscle tensioning [37]. Patients with acute and chronic neck pain have consistently demonstrated higher levels of electromyographic (EMG) activity in their neck flexor (anterior scalenes, sternocleidomastoid) and shoulder girdle (upper trapezius) muscles with functional tasks [68, 69]. While we did not measure EMG activity of the neck muscles, it is conceivable that the findings of smaller oropharyngeal volumes could be the consequence of cervical muscular tensioning which in turn could be related to the non-specific patient reports of swallow change. Considering previous studies describing muscle tension dysphagia [28, 70], an association between oropharyngeal volumes and muscle tension of key swallow musculature is plausible and future focused enquiry is warranted.

Secondly, the selected patients with persistent symptoms and self-reported swallow change exhibited high levels of trauma-related distress. These findings were not present to the same extent in those participants who indicated full recovery and no swallow change. Psychological disturbance as a primary feature of WAD is well accepted [8, 71-75]. It is noteworthy that stress-induced [76-78] and psychogenic dysphagia have been reported and dysphagia in mental health conditions in the absence of organic pathology, is well documented [79-81]. The possibility of high distress levels contributing towards cervical muscle tension is possible; however, this, in addition to its potential impact on swallowing, is worthy of more detailed investigation in larger-scaled, prospective studies.

Thirdly, the expression of miR-320a was chosen due to its demonstrated association with both the physiologic response to stress and trauma [82-85] and to similar musculoskeletal conditions [86-93]. Consistent with the direction of effect observed for individuals reporting poor recovery following MVC [9, 40], the three selected participants with WAD and reported swallow change also demonstrated lower expression levels of miR-320a compared to the three participants nominating recovery without swallow change. Due to sample size constraints, we were unable to perform analyses to determine statistical significance. However, the direction of effect was consistent with previous studies and future enquiry is warranted.

While interesting, such preliminary findings from these six reported cases cannot confirm a likely mechanistic driver of a whiplash-associated dysphagia. These cases highlight that self-reported swallow symptoms following whiplash may be co-associated with (1) recovery status, (2) changes to oropharyngeal volume, (3) levels of psychological distress and (4) peritraumatic microRNA expression levels. Given these preliminary findings, this paper encourages the speech pathology profession to consider the possibility of dysphagia following whiplash and highlights the need for future systematic investigations, utilizing larger cohorts and standardized and instrumental measures of swallowing, to more fully understand the nature and presentation of this condition. Our observations highlight what we already know; WAD is complex and not homogenous. However, it also generates new questions around what may be causing the perceived changes in swallow. Is it related to muscular tension causing a narrow oropharyngeal lumen? Is muscular tightness or narrow oropharyngeal volume contributing to reduced hyolaryngeal displacement or an altered pharyngeal constriction ratio? Are smaller oropharyngeal volumes following whiplash associated with functional changes in swallowing? Is it related to the pathomechanics of the whiplash event whereby damage involving white-matter pathways of the cord (or other vulnerable anatomical structures about the cervical spine) could be realized through quantitative imaging measures [94-96]? How does pain or psychological distress impact or in fact, cause self-reported dysphagia? Would such perceived changes in swallow also present in those with higher levels of everyday stress with or without a history of any non-catastrophic trauma? Answers to such questions would considerably add to the WAD profile; enhancing identification of symptomatology and as such, improve patient care.

The current case series results cannot yet endorse a new diagnostic/prognostic landscape for whiplash-related swallowing deficits. However, early indicators from existing data suggest that (1) swallow change is an under-recognized symptom in those with persistent WAD and (2) further investigation of swallowing physiology, molecular changes, psychological factors and quantitative myelin imaging measures of the spinal cord and brainstem pathways are needed to fully understand the underlying mechanisms behind whiplash-associated dysphagia. These are all underway.

Limitations

As this was an exploratory study, there are obvious limitations. Firstly, the addition of the yes/no swallow question was added due to observations of patient-reported swallow change during data collection as part of the parent study, resulting in the use of a crude outcome measure of swallowing. While acknowledging the lack of a standard swallow questionnaire, the authors considered these observations important to capture prior to the completion of data collection, particularly given the interesting profiles incorporating MRI, miRNA and traumatic distress data. Secondly, due to the small sample size and lack of statistical analysis, we cannot say the differences observed are statistically significant, though the large effect sizes provide some confidence the differences may be replicated in larger powered studies. It should also be clear that the magnitude of apparent differences and hence the calculated effect sizes, are likely inflated due to these very disparate groups. Thirdly, participant selection was based on known self-reported swallow change and recovery status. However, potential for selection bias was minimized through blinded analysis of oropharyngeal volume, traumatic distress and miRNA expression. Additionally, participants were not age-, or gender-matched and this could influence our findings.

Finally, the outcome measures used were selected for the purposes of the larger parent study and hence, there was no physiologic metric to describe the nature of presenting swallowing deficit. As such, this weakens any attempt to confidently determine the incidence of dysphagia and swallow physiology. Future studies should aim to utilize instrumental measures of swallow, with consideration of laryngeal and hyoid displacement and pharyngeal constriction ratio measures. The use of valid and standardized self-reported swallow questionnaires and qualitative analysis to identify potentially WAD-specific swallow complaints should also be the focus of future work. While interesting and relevant to the investigation of oropharyngeal volume, the authors acknowledge that the use of MRI to assess dysphagia is outside the realm of many clinical practices. As such, future work aims to evaluate the association between MRI findings and those of standard instrumental assessments such as videofluros-copy and endoscopic evaluation, with particularly in relation to displacement measures and pharyngeal constriction ratios.

Summary

The incidence and mechanisms of a potential post-whiplash dysphagia are unknown; however, this exploratory study suggests it may be multidimensional in nature, with both physiological and psychological drivers at play. Given the rates of poor recovery and current lack of effective treatment for some individuals post whiplash injury, insights into this trauma-related swallow change may improve the outlook for those suffering from this complex condition. This discussion supports larger-scaled prospective studies using instrumental measures of swallow impairment and the need to examine WAD and swallowing from a biopsychosocial perspective. Such information is critical if we are to develop appropriate interventions to understand and address the swallowing changes presenting in this population.