Could Neck Injury Be the Culprit in Post-Concussion Symptoms and the Development of Chronic Traumatic Encephalopathy?
In this article and open letter to the medical community, we will discuss prevention of Chronic Traumatic Encephalopathy by way of cervical instability.
Since I first wrote this open letter in August 2017, the following has occurred:
- November 2017: Dr. Bennet Omalu, who first pioneered research on Chronic Traumatic Encephalopathy (CTE), announced that his team of researchers confirmed a diagnosis of Chronic Traumatic Encephalopathy in a living person. Previously, Chronic Traumatic Encephalopathy could only be detected in autopsy. Dr. Omalu used a revolutionary brain scan device in 2012 on former NFL player Fred McNeill to measure tau proteins. When Mr. McNeill died in 2015, autopsy confirmed what the brain scan showed, traces of the signature tau proteins unique to CTE. The study on this case was published in the November 10, 2017 issue of the journal Neurosurgery.1
In the most simplest terms, tau proteins help stabilize the neurological system When tau proteins are damaged or defective, Alzheimer’s can result, as well as Chronic Traumatic Encephalopathy.
In September of 2017, University medical researchers in Greece publishing in the Journal of Alzheimer’s disease, made a link between oxygen deprivation and defective tau proteins.2
Understanding cervical instability as a possible cause of Chronic Traumatic Encephalopathy is understanding the difference between cellular damage in the brain caused by repeated blows to the head and cellular damage’s cause by cervical instability pinching and compromising oxygen flow and interrupting message signaling between the brain and the body.
If you can make a connection to cervical instability, healing and prevention can begin.
1 Omalu B, Small GW, Bailes J, Ercoli LM, Merrill DA, Wong KP, Huang SC, Satyamurthy N, Hammers JL, Lee J, Fitzsimmons RP. Postmortem Autopsy-Confirmation of Antemortem [F-18] FDDNP-PET Scans in a Football Player With Chronic Traumatic Encephalopathy. Neurosurgery. 2017 Nov 10.
2 Mavroeidi P, Mavrofrydi O, Pappa E, Panopoulou M, Papazafiri P, Haralambous S, Efthimiopoulos S. Oxygen and Glucose Deprivation Alter Synaptic Distribution of Tau Protein: The Role of Phosphorylation. Journal of Alzheimer’s Disease.
My open letter appears below as it appeared in August of 2017.
An open letter to the medical community
An estimated 1.6-3.8 million sports and recreation-related concussions occur in the United States per year. Football accounts for 60% of the concussions sustained in organized high school sports.1
The effects of concussions are cumulative in athletes, meaning it is harder and harder to recover with each successive concussion. Concussion and the traumatic brain injury that occurs with it, induces a barrage of ionic, metabolic and physiological events, and manifests in a composite of symptoms affecting a patient’s physical, cognitive, and emotional states, and his or her sleep cycle, any of which can be fleeting or long-term in duration.
Symptoms can range the gamut from headache, dizziness, vertigo, ringing in the ears, speech difficulty, vision changes, concentration difficulties and neck pain. While many symptoms subside, others persist, and even worsen, over time. Those who have suffered concussions are at risk for chronic traumatic encephalopathy (CTE), also called dementia pugilistica, a progressive degenerative disease, where the person actually loses brain tissue over time and is at risk for significant memory loss, even suicidal ideation.
While much of the focus on concussion prevention and treatment has been targeted towards the brain tissue proper, what has largely been forgotten are the injuries sustained in the neck
While much of the focus on concussion prevention and treatment has been targeted towards the brain tissue proper, what has largely been forgotten are the injuries sustained in the neck at the same time as the initial and subsequent impacts (person with multiple concussions). When a person’s cranium sustains enough force to cause a loss of consciousness (concussion), the neck also undergoes a traumatic event. The initial collision of the skull causes a tremendous force on the neck structures, but even more importantly, the upper neck twists or rotates quickly to try and get the head away from the force.2 This sudden rotational force (twist) right after impact injures the upper cervical ligaments at the atlas (C1) and axis (C2). Both animal and human research demonstrate cranial frontal impacts cause significant cervical spine ligament injuries.3 These ligament injuries cause conditions known as post-traumatic cervical or upper cervical instability.
What has not been appreciated until recent years is the impact excessive upper cervical vertebral motion can have on cerebral spinal fluid flow throughout the brain. (See figure 1 above.)
The technology now exists to document the cervical instability (excessive motion compared to normal) through motion imaging such as Digital motion X-ray as well as visualize and measure cerebral spinal fluid flow dynamics in patients with upright, flexion extension (motion) Cine cervical MRI.4
What is even more exciting is that treatments such as specific adjustments to correct the vertebral subluxations, Prolotherapy to tighten the ligament laxities and surgical fusions cannot just resolve the post-concussion or whiplash-associated symptoms, but also restore cerebrospinal fluid flow.5
It may just be that unresolved cervical instability and resultant obstruction of cerebrospinal fluid flow, is what causes toxic substances to accumulate in brain tissue not only causing unremittent headaches, poor concentration and the rest of the “mysterious” symptoms that occur after a concussion, but also may be the cause of CTE. If this is so, it brings hope as there are effective treatments that can unclog the brain circulatory system and restore proper hemodynamics in the brain so brain tissue functions optimally. It is my hope that more research on concussions and its aftermath, will focus on these neck injuries and the treatments that resolve them. By doing this, we may just stop CTE from developing.
1 Faul M, XuL, Wald MM, Coronado V. Traumatic Brain Injury in the United States. Emergency Department visits, Hospitalizations and Deaths 2002-2006. Atlanta (GA): Center for Disease Control and Prevention, National Center for Injury Prevention and Control; 2010.
2 Kaale B, Krakenes J, Albriektsen G, Wester K. Head position and impact direction in whiplash Injuries: associations with MRI-verified lesions of ligaments and membranes in the upper cervical spine. Journal of Neurotrauma. 2005;22:1294-1302.
3 Pearson AM, Panjabi MM, Ivancic PC, et al. Frontal impact causes ligamentous cervical spine injury. Spine (Phila Pa 1976). 2005;30(16):1852-8.
4 Battal B, Kocaoglu M, Bulakbasi N, Husmen G, Tuba Sanal H, Tayfun C. Cerebrospinal fluid flow imaging by using phase-contrast MR technique. The British journal of radiology. 2011 Aug;84(1004):758-65.
5 Smith FW, Dworkin JS (eds): The Craniocervical Syndrome and MRI. Bael, Karger, 2015, pp 48-66. DOI: 10.1159/000365470