Findings on imaging for whiplash? It’s a miracle! What does it actually mean?

Whiplash is one of those conditions that often strikes fear into the hearts of clinicians, mainly because chronic whiplash is very hard to treat. This not helped by the fact that there is scepticism regarding the condition itself due to its lack of objective findings. Whiplash associated disorders (WAD) are largely diagnosed based on mechanism of injury (eg, most often a motor vehicle accident) and reports of persistent symptoms of pain and/or sensory hyperalgesia. Radiological findings often demonstrate no structural changes that would explain the symptoms and thus raise questions as to whether there is anything wrong at all.

Recently, however, a group from the University of Queensland have found evidence of structural muscle changes in people with chronic WAD – specifically muscle fatty infiltrates (MFI) were found in the neck extensor muscles.[1] From this, they hypothesised that it was plausible that these muscular changes may be related to who develops chronic pain following whiplash. Their most recent study[2] (see here…available for free!) has evaluated just that – how soon following injury do these muscle changes occur and do they occur only in people who report persistent symptoms of WAD? They were also interested in testing the relationship between known prognostic factors for whiplash (pain intensity, neck range of motion, and symptoms of post-traumatic stress disorder) and MFI. To answer these questions, they recruited 55 participants with acute whiplash, and imaged them (MRI) at 4 weeks, 3 months and 6 months. They also grouped people based on their neck disability index (NDI) scores at 6 months: recovered (NDI<10%), mild symptoms (NDI 10-28%), and moderate/severe symptoms (NDI ≥30%).

Their results were intriguing. Most staggering was the finding that MFI, whilst not different between the groups at 4 weeks post-injury (ie, baseline), was significantly greater in the moderate/severe group as compared to the others at both follow-up points. Importantly, the moderate/severe group was the only group to display an increase in MFI over time. Also of interest was their finding that whilst all the predictors (pain intensity, cervical ROM, and PTSD symptoms) related to MFI, symptoms of PTSD partially mediated the relationship between pain intensity and MFI. In other words, when they controlled for PTSD levels, the relationship between pain intensity and MFI was no longer significant.

What does this mean?? First, based on the results of this study we cannot say that the presence of MFI causes poor recovery from whiplash. However, the authors speculate that it is possible that the presence of MFI is the result of an initial and persistent inflammatory response to injured tissues. This could be plausible; people with moderate/severe NDI scores had the highest levels of MFI and were the only group who had increases in MFI over time, raising the possibility of a more severe injury in those with poor functional recovery. On the other hand, it may be that disuse of the neck muscles could relate to accumulations of intermuscular fat. Indeed, cervical ROM was significantly related to MFI levels. However, the ability of ROM to act as a correlate for actual disuse is a bit questionable as you can have reduced ROM but still use your neck muscles.

Second, that PTSD mediated the relationship between pain intensity and MFI raises the possibility of a neuro-psycho-biological link with poor outcomes. For example, in other PTSD populations, stress can increase the release of cortisol, which has been found to impact overall health and degeneration of skeletal muscle.[3] Also, prolonged increased sympathetic nervous system activation that may occur with PTSD may cause vasoconstriction, which can lead to metabolic and muscular changes.[4]

It is important to note that the present study did not actually measure any of the immune, nervous, or endocrine/metabolic function, so it is merely speculation to discuss these systems as reasons why MFI might be higher in patients with higher NDI scores. This is necessary to study in future research, which by the sounds of it, is currently underway. At the end of the day, we don’t know what the presence of MFI actually means, although that its’ presence is related to outcome certainly provides impetus for further investigation.

About Tasha

Tasha Stanton post doc bodyinmindTasha Stanton is a postdoctoral research fellow working with the Body in Mind Research Group both in Adelaide (at University of South Australia) and in Sydney (at Neuroscience Research Australia). Tash has done a bit of hopping around in her career, from studying physio in her undergrad, to spinal biomechanics in her Master’s, to clinical epidemiology in her PhD, and now to clinical neuroscience in her postdoc. Amazingly, there has been a common thread through all this hopping and that common thread is pain. What is pain? Why do we have it? And why doesn’t it go away?  Tasha got herself one of the very competitive Canadian IHR post-doctoral fellowships and is establishing her own line of very interesting investigations.  Her research interests lie in understanding the neuroscience behind pain and its clinical implications. She also really likes nifty experiments that may have no clinical value yet, but whose coolness factor tops the charts. Last, Tash is a bit mad about running, enjoying a good red with friends and organizing theme parties. Tasha, aka Stanton Deliver, was the all round best performer at the Inaugural BiM Table Tennis Comp.

Here is Tasha talking more about what she does and a link to her published research.
We have put BiM author’s downloadable PDFs here.


[1] Elliott J, Jull G, Noteboom JT, Darnell R, Galloway G, & Gibbon WW (2006). Fatty infiltration in the cervical extensor muscles in persistent whiplash-associated disorders: a magnetic resonance imaging analysis. Spine, 31 (22) PMID: 17047533

[2] Elliot J, Pedler, A, Kenardy J, et al. The temporal development of fatty infiltrates in the neck muscles following whiplash injury: An association with pain and posttraumatic stress. PLoS One 2011;6:e21194.

[3] Paddon-Jones D, Sheffield-Moore M, Cree MG, Hewlings SJ, Aarsland A, Wolfe RR, & Ferrando AA (2006). Atrophy and impaired muscle protein synthesis during prolonged inactivity and stress. J Clin Endocrinol Metab, 91 (12), 4836-41 PMID: 16984982

[4] Passatore M, & Roatta S (2006). Influence of sympathetic nervous system on sensorimotor function: whiplash associated disorders (WAD) as a model. Eur J Appl Physiol, 98 (5), 423-49 PMID: 17036216


  1. Very interesting read, I myself sufferes whiplash. From my experience I can tell you there is something not right with my cortisol levels ever since I was rear ended in 2008. I have episodes of inflammation turned on in part to what I believe is an over active SNS. I have always had super fast reflexes so it may in fact be something that I am indeed predisposed to.
    There is a mental aspect to it as well; but the only post traumatic stress I experience is when I`m in a vehicle. Its not something that has traumatized me mentally otherwise; so I do not believe it to be soley a post traumatic stress disorder.
    Physically for me the pain has become chronic, 1st set of Mris were normal 2 years later a 2nd set showed facet arthropathy with bone spurring in my thorasic. Im am certain there is more going on involving my SNS but it is most likely physical with the mental aspects being secoundary.
    .From the pain I have experienced, even when the mri was normal, I can attest that there is definately something structurally damaged. It makes sense it is within the muscle as cortisol also effects those tissues and may not show up on an mri/xray.
    I was stopped at a redlight when I was struck from behind by an Suv going between 40-50 mph. Totalled my car and did 12,000 damage to his suv it would be nearly impossible for my body to withstand frame bending impact and not be damaged. The evidence of the damage and subsequent pain may be an enigma but its definately there. Maybe one day you will find i, I believe your looking in the right places.
    Remember they labeled the Hiv virus an Auto Immune Disorder when it was hiding in white blood cells the whole time.

  2. Hi Jordan

    Given your last point, they must all share some biological underpinnings/mechanisms. Any thoughts?

  3. Theodore Jordan, DO says

    Robert Scaer, MD – a neurologist who specializes in PTSD, considers ‘whiplash syndrome’ as undiagnosed PTSD based on clinical findings. Typically, all whiplash victims will improve over a month, or so, then 4-8 weeks out, a small percentage (10-20% if my memory serves) will then experience an increase of pain, and proceed to a life of chronic pain, increased pain/tempreature sensitivity throughout their body (studied by Jull), increased cognitive dyfunction, increased alertness/insomnia, etc. All suggesting central sensitization. Dr. Scaer makes an interesting observation that of approx 2000 whiplash syndrome patients that he had seen, none of them were drunk at the time of accident. Because alcohol blocks the development of PTSD (as does benzodiazepines & beta adrenergic blockers), this is a strong, but anectdotal, indication that whiplash syndrome is PTSD. The link between trauma and chronic pain and musculoskeletal dysfunction is essential to the understanding of all three (IMHO).

  4. Frédéric Wellens,pht says

    Thanks Michele and Tasha,

    I’m no specialist in PTSD so it felt quite intuitive to think of a relation between the gravity of the crash and the PTSD symptoms. Judging by your answers, once again, it’s not necessarily the reality that is important but rather what the brain perceives of this reality. Looking forward for the next twist eagerly!

  5. Tasha Stanton says

    Thanks Michele – great to have your feedback on this!

  6. Tasha Stanton says

    Thanks for the comments Danny and Frederic (sorry I can’t put the accent aigu on your name!).

    Danny that’s a really interesting theory. I’m not sure that neuropathic injury can be ruled out based on the study’s results (importantly, we weren’t given much info about other signs/symptoms commonly occuring with neuroapthic injury), but I’d also argue we can’t just rule in neuropathic injury. MFI has also been reported due to disuse, which could be due to many factors, including pain.

    Frederic – great question and I think one that makes good common sense. I certainly am not very well versed in PTSD, but it does seem based on what I’ve read it seems that the relationship between development of PTSD and the severity of a situation isn’t that straightforward (ie, there are other factors that affect this development). For example, some people that witness a horrible accident or event do not go on to develop PTSD. Also, it seems that PTSD can sometimes develop over time (ie, a seemingly innocuous incident can later become something that is perceived as very traumatic to the person). So I’m not sure if the relationship is that cut and dried.

    Michele Sterling Reply:

    Dear Tasha

    You are correct. The injuries suffered by the participants in this study were all relatively ‘minor’ eg rear end, front end. It is generally felt that the person perceived a threat to their life/safety regardless of the accident severity to develop PTSD. Our research is showing that WAD has a very similar incidence of PTSD to more severe road traffic crashes that are admitted to ICU. Something for physios to consider.
    Also we shouldn’t forget that posttraumatic stress symptoms are not the same thing as a PTSD diagnosis. In this study of MFI development, it was the symptom level not the diagnosis that predicted MFI.


  7. Frédéric Wellens,pht says

    Interesting. About the link between PTSD and MFI. Could it be that people with more serious injuries had, on average, more important car accident thus increasing the risk of suffering both PTSD and MFI?

  8. Fatty infiltrates are commonly found in denervated muscle. Isn’t this study potentially examining a direct consequence of potential neuropathic injury? In which case the finding that those people with (likely?) neuropathic injury have more pain?

    Michele Sterling Reply:

    Hi Danny
    Thanks for your comments. We have considered the neuropathic (nerve injury) scenario for WAD for a while now. But despite spending lots of effort looking, we really can’t find conclusive evidence of a neuropathic injury. People with WAD have decreased pain thresholds (lots of papers on this) and increased detection thresholds (see papers by Chien and Sterling) – but in a very generalised way with no side to side differences etc. Also the MFI changes are very general – many muscles, extensors, flexors which begs the question as to which nerve/s are injured?
    The plot thickens. The relationship between psych symptoms ie posttraumatic stress symptoms and physical muscle chnages is intriguing and one we are following up on.