I am traveling back to New York to teach the Cervical Spine II portion of the NAIOMT series. As chance would have it, JOSPT just published in July an issue dedicated to the cervical spine and whiplash specifically. This issue is Part II, (Part I was published in October 2016.) From cover to cover both issues offer a lot of information. I will address a few of the items I felt were important from this chock-a-block issue.
Anatomy Doesn’t Lie
From (Ita, Zhang, Holsgrove, Kartha, & Winkelstein, 2017)...
Ita et. al. present some interesting facts about motor vehicle collisions (MVCs) and the resulting changes in the cervical spine.
- The spine undergoes a characteristic “S” deformation and it is induced at 60 to 100 ms after impact due to the torso moving under the spine superior and anterior.
- This is quicker than the reflexive contraction of the muscles in the cervical spine (Siegmund, Timothy Inglis, & Sanderson, 2001) predisposing the inert tissue of the cervical spine to greater forces, specifically the capsule, cartilage and the synovium.
- The anatomy of the capsule of the zygapophyseal “Z” joints in the cervical spine demonstrate two anatomically different layers.
- The outer later is primarily collagen and oriented across the joint itself. Capsular damage can occur below its failure point of 35% to 65%. When it fails, it does not generate a pain response, but pain responses can be produced at deformations as low as 14%.
- The inner layer is primarily elastin and functionally it is designed to assist the joint to recover quickly to a neutral position after movement, particularly extension.
- Looking at the afferent pathways from the capsule of the “Z” joints, they have cell bodies in the dorsal root ganglion (DRG) and synapse with neurons in the spinal cord in the dorsal horn. This is an important feature because in “chronic” pain and central sensitization there is neuronal hyperexcitablility and altered neurotransmitter production and release” in this region. (Ita et al., 2017) This demonstrates a direct link between mechanical changes in the capsule and the altered sensory interpretation of this.
- Lastly, the authors conclude that there is a lot of anatomical variation in different cervical spines. Therefore, “relying on any single injury metric as the gold standard is challenging at best and inappropriate or inadequate at worst.”
The Body Heals in a Predictable Manner
Here are some facts about healing after an MVC…
- 40-45% of people who undergo a MVC recover and have symptoms related to a peripheral lesion. (Walton & Elliott, 2017)
- Due to the complex neurology of the “z” joint and its relationship to the DRG and dorsal horn, allodynia and hyperalgesia can develop if appropriate rehabilitation is not applied.
- After stress is placed on the joint capsule, spinal astrocytes are activated for at least 14 days after injury. As soon as one day, nerve growth factor (NGF) increases, and it has been found that inhibiting this factor can prevent the onset of the cascade of events for hyperexcitability. (Note: these studies were performed on rats and goats and the researchers do note the limitations in translating this to humans). But, we do have to realize that early intervention is of utmost importance.
In understanding the finding that there isn’t a “silver bullet” in rehabilitation after whiplash, but the tissues will heal predictably. Specifics of injury to the capsule, the neurophysiological changes and as we find out patient impression will have to be juggled to manage this challenging condition.
Pain is in the Brain
Taking the time to read the work by (Walton & Elliott, 2017) is well worth the investment. The article summarizes the work of the Quebec Task Force and prior attempts to create a model for addressing Whiplash-Associated Disorder (WAD). Of note is a proposed change to the Fear Avoidance Model, which has been actively pursued for the past decade. The bottom line is that “those who rate their experience as more terrible in the acute posttraumatic phase are more likely to continue to rate the experience as terrible” at follow-up.
The model created in this article merges models and finds that there are interchangeable times when a condition may go from progressing quickly to regressing.
Looking at a “Diathesis-Stress Model” is helpful. All people who undergo a traumatic event have a “personal and contextual” background which will influence their response/reaction to the event. This model looks at different vulnerabilities and protections including:
- Tissue itself
I like how the NOI group terms this particular area, they will call these “DIMs” dangers inside of me and “SIMs” safety in me.
I will just ask one question: when you look at a patient, do you look at them holistically, and have the understanding that different people can experience the exact same trauma and have a different outcome based on the above factors?
We Are Prone to Logical Errors
For years I have learned all the specifics about a MVC including the angle of the impact, if the person was anticipating the impact or not, and their head position. There are some suggestions that these factors may not be as important. There is emerging evidence that “speed, direction of impact and airbag deployment” have little or no effect on post injury recovery. (Walton & Elliott, 2017) It is import to understand this as we talk to patients about their accident and the resulting injury. How often have you heard a patient relate the magnitude of the damage to their car to the damage that they experienced internally? Let’s make sure we are using our words correctly and not jumping to unhealthy conclusions.
Treat the Person and You Win Every Time
“The science of implementation is evolving, but we have enough knowledge to move forward toward improving care. The imperative of enhancing the health and well-being of patients with WAD ought to prompt us all to action.” (Fritz, 2017)
Video of the Week
We have been looking at non-tissue related models to assess and treat WAD. That being said, I would like to share a useful video that looks at the assessment and treatment of the upper cervical joints.
Have a great week!
Fritz, J. (2017). Toward Improving Outcomes in Whiplash: Implementing New Directions of Care. Journal of Orthopaedic & Sports Physical Therapy, 47(7), 447–448. https://doi.org/10.2519/jospt.2017.0107
Ita, M. E., Zhang, S., Holsgrove, T. P., Kartha, S., & Winkelstein, B. A. (2017). The Physiological Basis of Cervical Facet-Mediated Persistent Pain: Basic Science and Clinical Challenges. Journal of Orthopaedic & Sports Physical Therapy, 47(7), 450–461. https://doi.org/10.2519/jospt.2017.7255
Siegmund, G. P., Timothy Inglis, J., & Sanderson, D. J. (2001). Startle response of human neck muscles sculpted by readiness to perform ballistic head movements. Journal of Physiology, 535(1), 289–300. https://doi.org/10.1111/j.1469-7793.2001.00289.x
Walton, D. M., & Elliott, J. M. (2017). An Integrated Model of Chronic Whiplash-Associated Disorder. Journal of Orthopaedic & Sports Physical Therapy, 47(7), 462–471. https://doi.org/10.2519/jospt.2017.7455