Smarter Stretch Studio

Using Science To Overcome Chronic Whiplash

whiplash-consequencesWith our overly crowded roads, whiplash injuries are almost an epidemic and if you haven’t personally been affected, I am sure you know someone who has. In addition to pain, whiplash victims also have to deal with the stress of an insurance claim and the mounting cost of repeated therapy treatments.

The common held belief is that the ensuing pain from whiplash is caused by damage to various tissues in the neck. As the head moves backwards, then forward it puts strain on muscles, ligaments, bones and intervertebral discs causing them to become injured in some way. While this seems logical, tissue damage cannot be detected in the majority of whiplash-associated disorders (Curatolo, 2011 and Sterling, 2013).

Although whiplash has been studied extensively over the last 50 years and every attempt has been made to find the physical cause of the pain, the data does not suggest that a specific type of tissue damage is responsible. This is especially worrying considering the majority of treatment modalities available are biomechanically focused.

In this article I will outline the research showing that tissue damage is not responsible for the chronic pain. I will also discuss how application of new research focused on the nervous system can be used to effectively deal with chronic pain. 

Vertebrae and Intervertebral Disk

Numerous studies have attempted to find a correlation between injuries to the spine and chronic pain. Matsumot et al. (2013) looked at modic changes in whiplash victims over a 10 year period. They concluded that changes occurred at the same frequency as control subjects. And that changes were as a result of aging rather than a result of damage from the accident.

Other studies have shown a similar thing. In 2009 Ichihara et al. performed a 10-year follow-up study looking at spinal degeneration after whiplash injury. They also concluded “progression of degenerative changes of the cervical spine on MRI was not associated with clinical symptoms during the 10-year period after whiplash injury.”

Based in the available scientific evidence it isn’t reasonable to conclude that injury to the spine or intervertebral disks would be the cause of long-term pain. Especially when imaging techniques frequently come back negative.


Biomechanical studies show that the forces involved in whiplash can exceed those shown to cause muscle injury (Vasavada 2007). Based on this, it is plausible that muscular injuries could be a cause of long-term pain. However, this doesn’t match up with clinical evidence. We know from experience that the results of treatments like massage and IMS do not work in chronic cases. Treatments targeting muscle provide temporary relief, but clearly do not get to the root cause of pain.

Studies measuring chemical markers for muscle damage highlight this fact. Scott and Sanderson (2002) found that “whiplash injury produces no measurable biochemical evidence of muscle cell damage and that prolonged symptoms following whiplash injury cannot be attributable to muscle damage.”

Even if pain was initially created by muscle injury, it isn’t logical or reasonable for muscle related pain to last for longer that the physiologic healing time of muscles. Therefore, there must be other causes of pain in those victims who don’t respond to repeated treatments.

Ligaments and Joint Capsule

Computational studies indicate that the anterior longitudinal ligament could lengthen or be injured during whiplash (Stemper 2006 and Dang 2008). However, in the absence of observable findings via imaging, there is not enough evidence to say that damage to these structures is the cause of long term pain.

Research into facet joint capsules provides clues about potential causes of long-term pain. Tissue damage is not detectable by MRI or radiographic testing, but scientists were able to reduce pain by using nerve blocks and consequently used this method to diagnose and treat whiplash (Lord 1996 and Ketroser 2000).

Additionally, studies on cadavers have shown microscopic tears to capsular ligaments (Curatolo 2011). The question mark surrounds the fact that treatment only works for 50-70% of people and tends to wear off after a period of time.

Panjabi (2006) hypothesised that micro damage to ligaments altered mechano receptor feedback to the central nervous system, which in turn created a negative cycle leading to long-term dysfunction and pain.

Quinn et al. (2007) studied changes in capsular ligament structure after subfailure loading. They concluded, “these findings demonstrate that certain subfailure loading conditions are associated with altered joint mechanics and collagen fibre disorganization and imply ligament damage. Damage in the capsule has the potential to both directly modulate nerve fibre signalling and produce sustained physiologic modifications that may initiate persistent pain.”

The research into capsular ligament damage provides a compelling link to chronic pain. Although the mechanism seem to be more related to the interrupted feedback to the central nervous system than the ligament damage itself.

Spinal Chord

While research into potential damage to the spinal chord is far from conclusive preliminary findings are starting to suggest a possible link to chronic pain.

In 2007, Lo et al. Studied 20 patients with chronic whiplash injury. They found that while there was only a small incidence of visible spinal chord damage, neurological dysfunction of whiplash might occur at several possible spinal cord functional pathways.

Since then studies using small sample sizes have managed to correlate deep cervical muscle degeneration with chronic pain following whiplash (Elliott 2014 and Abbott 2015). Researchers think the muscle degeneration is a product of interrupted feedback via a damaged spinal chord. Smith et al. (2015) drew a similar conclusion after correlating chronic pain and weakness in lower extremity muscles.

Correlation is not the same as causation, but the findings of these studies suggest alterations in spinal chord function play a role in chronic pain. Again in the absence of visible damage it more likely that the interruption is of a functional nature rather than a pathological. As imaging technology improves, future studies may be able to clarify this.

Looking At Pain In A Different Way

After reviewing the literature, it is clear that tissue damage is not to blame for chronic whiplash associated disorder. But if tissue damage isn’t to blame, what is? In order to answer this you need and understanding of what pain is.

In 1999 Melzack proposed the neuromatrix of pain theory, which says that “pain is a multidimensional experience produced by characteristic “neurosignature” patterns of nerve impulses generated by a widely distributed neural network.” This theory paved the way for much research into the mechanisms of pain and it is now understood that pain is more than just the relaying of nociceptive stimuli from damaged tissue. Pain is a protective mechanism created to prevent further harm to the body (Baliki 2015).

In order to help people recover from chronic pain after whiplash we need stop looking at pain as a direct result of injury. While pain often occurs with injury, one is not the direct cause of the other. There are many examples of when people can become severely injured and feel no pain, like a soldier wounded on a battlefield that doesn’t feel pain until days after the injury. Likewise, there are many examples when people have no apparent physical injury, yet experience debilitating pain, like those suffering from fibromyalgia.

In fact it has been shown that people in chronic pain following whiplash exhibit spinal chord hypersensitivity similarly to those with fibromyalgia. In 2004 Bancic et al. compared the nociceptive withdrawal reflex of chronic whiplash and fibromyalgia sufferers to a control group. They found that the chronic whiplash and fibromyalgia group both had lower reflex thresholds compared to the control group. That is to say that they felt more pain in response to low-level nociceptive or innocuous stimuli.

Using A Brain Based Approach To Help People Recover From Chronic Whiplash

Chronic pain is a response to the combination of neural threats a person is subject to. Nociceptive input is important, but so too are emotions, fear of expectations, and sensory deficits. The only way to help someone out of chronic pain is to look at all the different inputs and improve their quality to reduce the level of threat. This involves a combination of training and education.

From the studies on capsular ligaments we can see that alterations in proprioception play a pivotal role in the development chronic pain. So improving proprioception is an important first step to becoming pain free. While it seems like this is the aim of traditional therapy when you look closer you can see that this does not happen.

The brain creates movement. Before any body part can move there is a firing in the pre-motor cortex of the brain. This is followed by firing in the motor cortex, which sends a message down the brain stem to the spinal chord and then to the muscles that create movement. At the same time information is sent to the cerebellum, which compares the intended movement to what is happening. The cerebellum also communicates with the visual and vestibular system to fine-tune the movements.

Therapy normally involves a therapist manually adjusting or passively moving a patient’s body. While this does stimulate some mechano reception, there is no involvement by the brain and central nervous system. Also, the majority of time treatments are done lying down, so the communication with the vestibular system doesn’t get trained in a meaningful way. To improve proprioception, it is necessary to synchronize joint, visual and vestibular feedback with programming that occurs in the motor cortex of the brain.

Additionally after whiplash, people are often unable to take part in their normal activities. This results in reduced mechano-receptive feedback from all areas of the body, not just the effected area. Traditional therapy only tends to focus on the part of the body in pain, which does not address the system as whole. In order to reduce neural threat it is necessary to improve whole body proprioceptive mapping.

At Smarter Stretch Studio we do not act as therapists and we don’t diagnose or treat any conditions. What we do is teach people how move better. A big part of this is showing people how to mobilize all of their joints to improve proprioception. By moving joints on a daily basis, the brain starts to re-learn correct proprioception and starts to rely on mechano-receptors for feedback rather than noci-receptors.

The self-mobilizations are performed in seated and standing positions to help synchronize feedback with the vestibular apparatus. The extra benefit of learning self-mobilizations is that people are able to do them frequently enough to make a difference. Frequency is absolutely essential for creating neural plastic change. Which is precisely what improving proprioception is.

Another important part of the process is client education. It is well established that fear and anxiety are strongly related to disability (Meeus et al 2010). One of the biggest problems we see with people is that they become very fearful of normal movements. People think the pain they experience is creating more damage, which will lead to more pain. This faulty thinking creates a negative spiral, which can make recovery difficult.

Once a client someone understands about pain they begin to start interpreting their own body sensations differently. This makes them more likely to engage in activities that will help them to become pain free. We have found that by using this combined approach people are able to quickly reduce their pain levels.

Each month we hold a FREE workshop about back and neck pain. To find out when our next workshop is and to register please follow the link below

Free Workshop – Why Do I Still Have Back Pain?


Curatolo, M., Bogduk, M,. Ivancic, P.C., McLean, S.A., Siegmund, G.P, Winkelstein, B., (2011), The Role of Tissue Damage in Whiplash Associated Disorders, Spine Journal, v. 36,

Scott, s., Sanderson, P.L., (2002) Whiplash: a biochemical study of muscle injury, European Spine Journal, v. 11: p. 389–392.

Vasavada, A.N.,  Brault, J.R., Siegmund, G.P., (2007), Musculotendon and fascicle strains in anterior and posterior neck muscles during whiplash injury. Spine, Apr 1;32(7):756-65.

Davis, C.G., (2013) Mechanisms of chronic pain from whiplash injury. Journal For Forensic and Legal Medicine, v. 20: p. 74-85.

Banic, B., Petersen-Felix, S., Andersen, O.K., Radanov, B.P., Villiger P.M., Arendt-Nielsen, L., Curatolo, M., (2004), Evidence for spinal cord hypersensitivity in chronic pain after whiplash injury and in fibromyalgia. Journal of Pain, Jan;107(1-2):7-15.

Sterling. M, Elliott. J.M., Cabot P.J., (2013), The Course of Serum Inflammatory Biomarkers Following Whiplash Injury and Their Relationship to Sensory and Muscle Measures: a Longitudinal Cohort Study. PLoS ONE 8(10): e77903. doi:10.1371/journal.pone.0077903

Ketroser, D.B., (2000) Whiplash, chronic neck pain, and zygapophyseal joint disorders. A selective review. Minnisota Medical Journal, Feb;83(2):51-4.

Quinn, K.P., Lee, K.E., Ahaghotu, C.C., Winkelstein, B.A., (2007), Structural changes in the cervical facet capsular ligament: potential contributions to pain following subfailure loading, Stapp Car Crash Journal, Oct;51:169-87.

Panjabi, M.M, (2006)A hypothesis of chronic back pain: ligament subfailure injuries lead to muscle control dysfunction, European Spine Journal, v. 15: p. 668–676

Ichihara, D., Okada, E., Chiba, K., Toyama, Y., Fujiwara, H., Momoshima, S., Nishiwaki, Y., Hashimoto, T., Ogawa, J., Watanabe, M., Takahata, T., Matsumoto, M., (2009), Longitudinal magnetic resonance imaging study on whiplash injury patients: minimum 10-year follow-up. Journal of Orthopedic Science, Sep;14(5): p. 602-10.

Matsumoto, M., Ichihara, D., Okada, E., Toyama, Y., Fujiwara, H., Momoshima, S., Nishiwaki, Y., Takahata, T., (2013), Modic changes of the cervical spine in patients with whiplash injury: a prospective 11-year follow-up study. Injury Journal, Jun;44(6):819-24

Dang, A.B., Hu, S.S., Tay B.K., (2008), Biomechanics of the anterior longitudinal ligament during 8 g whiplash simulation following single- and contiguous two-level fusion: a finite element study. Spine Journal, Mar 15;33(6):607-11.

Stemper, B.D., Yoganandan, N., Pintar, F.A., Rao, R.D., (2006), Anterior longitudinal ligament injuries in whiplash may lead to cervical instability. Medical Enginerring and physics Journal, Jul;28(6):515-2

Lord, S.M.,., Barnsley, L., Wallis, B.J., McDonald, G.J., Bogduk, N., (1996 ), Percutaneous radio-frequency neurotomy for chronic cervical zygapophyseal-joint pain. New England Journal of Medicine, Dec 5;335(23):1721-6.

Smith, A.C., Parrish, T.B., Hoggarth, M.A., McPherson, J.G., Tysseling, V.M., Wasielewski, M., Kim, H.E., Hornby, T.G., Elliott, J.M., (2015), Potential associations between chronic whiplash and incomplete spinal cord injury, Spinal Chord Series and Cases, Oct 8th, v.1

Elliott, J.M., Dewald, J,P., Hornby, T.G., Walton, D.M., Parrish, T.B., (2014), Mechanisms underlying chronic whiplash: contributions from an incomplete spinal cord injury? Pain Medicine, v. 11, p. 1938-44.

Abbott, R., Pedler, A., Sterling, M., Hides, J., Murphey, T., Hoggarth, M., Elliott. J., (2015), The geography of fatty infiltrates within the cervical multifidus and semispinalis cervicis in individuals with chronic whiplash-associated disorders. Journal of Orthopedic Sports Physical Therapy Apr;45(4), p. 281-8

Lo, Y.L., Tan, Y.E., Fook-Chong, S., Boolsambatra, P., Yue, W.M., Chan, L.L., Tan, S.B., (2007), Role of spinal inhibitory mechanisms in whiplash injuries. Journal of Neurotruma, Jun;24(6): p. 1055-67.

Meeus, M., Nijs J., Van Oosterwijck, J., Van Alsenoy, V., Truijen, S., (2010), Pain physiology education improves pain beliefs in patients with chronic fatigue syndrome compared with pacing and self-management education: a double-blind randomized controlled trial. Archives of Physical Medicine and Rehabilitation,  Aug; 91(8):1153-9.

Melzack, R., (1999), Pain–an overview. Acta Anasthesiology Scandanavia, Oct;43(9):880-4.

Baliki, M.N., Apkarian, A.V., (2015), Nociception, Pain, Negative Moods, and Behavior Selection. Neuron, Aug 5;87(3):474-91

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