Ross Hauser, MD

Medical update: Chronic traumatic encephalopathy (CTE) still cannot be definitively diagnosed during life. Its diagnosis requires postmortem examination of brain tissue. Researchers use the term traumatic encephalopathy syndrome (TES) for a clinical syndrome associated with substantial exposure to repetitive head impacts, but TES is not the same as pathologically confirmed CTE. No study has shown that treating cervical instability prevents CTE.

When I first published this open letter in August 2017, my purpose was to ask a question that I believed deserved more attention: when an impact is powerful enough to injure the brain, what happens to the neck—and could an unresolved cervical injury contribute to the symptoms that persist after concussion?

That remains an important clinical question. However, the scientific language surrounding CTE, tau imaging, cerebrospinal fluid (CSF), and cervical instability has evolved. This update separates what is established, what is emerging, and what remains a hypothesis.

The clearest evidence-based message is this: reducing exposure to repetitive head impacts is presently the most defensible strategy for reducing CTE risk. At the same time, the cervical spine should not be forgotten. A concussion-producing mechanism can also strain the neck, and cervical dysfunction may contribute to headache, dizziness, visual difficulty, imbalance, neck pain, and other prolonged post-concussion symptoms.

That is why I believe the brain and cervical spine should be evaluated together—without claiming that a neck treatment has been proven to prevent a neurodegenerative disease.

What CTE is—and what it is not

CTE is a neuropathologic disease associated with exposure to repetitive head impacts, including both concussive and nonconcussive blows. Its defining lesion is an abnormal accumulation of hyperphosphorylated tau around small blood vessels at the depths of cortical sulci. A 2023 consensus paper reported that more than 97% of published CTE cases occurred in people with known repetitive-head-impact exposure. (1)

CTE should not be diagnosed from symptoms alone. Memory problems, depression, impulsivity, headache, sleep disturbance, and balance problems can occur in many treatable conditions. In a living patient, clinicians should investigate neurologic, vestibular, cervical, sleep, psychiatric, medication-related, cardiovascular, and metabolic contributors rather than assume that CTE is present.

The 2021 National Institute of Neurological Disorders and Stroke consensus criteria introduced TES as a research diagnosis for living people with substantial repetitive-head-impact exposure, characteristic cognitive or behavioral features, progressive symptoms, and no better explanation. These criteria do not provide an antemortem confirmation of CTE. (2)

This distinction matters. Telling a symptomatic former athlete that he or she “has CTE” can create fear and therapeutic nihilism. A careful evaluation may instead identify treatable contributors—including a cervical injury.

What happened to the reported “living diagnosis” of CTE?

In 2017, Omalu and colleagues reported a former professional football player whose experimental FDDNP-PET scan showed a pattern interpreted as consistent with CTE; after his death, the brain was examined and CTE pathology was reported. This was an important case, but it did not establish FDDNP-PET—or any other scan—as a validated way to diagnose CTE in living people. (3)

Tau PET and other biomarkers remain active areas of investigation. At present, an abnormal scan cannot replace neuropathologic examination, and CTE remains a postmortem diagnosis.

Prevention starts with repetitive head impacts

The strongest known association with CTE is cumulative exposure to repetitive head impacts. This includes impacts that do not cause a recognized concussion. Therefore, prevention cannot focus only on counting diagnosed concussions.

Practical risk-reduction measures include:

• reducing unnecessary head-impact exposure in practices and competition;
• enforcing rules against dangerous contact;
• teaching sport-specific techniques that reduce head contact;
• recognizing concussion promptly and removing the athlete from play;
• following a medically supervised, graduated return-to-sport process; and
• avoiding a return while symptoms or clinical deficits remain.

Helmets and other protective equipment are essential for reducing skull and facial injuries, but no helmet can eliminate the movement of the brain inside the skull or guarantee prevention of concussion or CTE.

A concussion mechanism can also injure the neck

The force that accelerates and rotates the head also loads the cervical muscles, joints, discs, and ligaments. The neck may be flexed, extended, compressed, or rotated within milliseconds. This overlap helps explain why concussion and whiplash can produce similar symptoms.

Research supports looking for cervical dysfunction after concussion. A 2024 (4)  study found persistent cervical sensorimotor deficits in people after concussion and noted that concussion mechanisms stress the cervical spine in a manner similar to whiplash. These findings do not mean that every prolonged symptom comes from the neck, but they strengthen the case for a cervical examination when symptoms persist.

Potential cervical contributors include:

• cervicogenic headache;
• painful or restricted neck motion;
• impaired cervical proprioception and head-neck control;
• dizziness or disequilibrium associated with neck movement;
• irritation of upper cervical joints, ligaments, muscles, or occipital nerves; and
• autonomic-type symptoms that require a broader differential diagnosis.

For more detail, see Caring Medical’s discussions of post-concussion syndrome, whiplash injury, and post-traumatic cervical instability.

Tau, oxygen deprivation, and what laboratory studies can tell us

Tau normally helps stabilize structures inside nerve cells. In CTE and several other neurodegenerative diseases, abnormal tau becomes phosphorylated, misfolds, and accumulates in characteristic patterns.

A 2017 laboratory study (5) showed that oxygen and glucose deprivation changed the synaptic distribution and phosphorylation of tau. This supports the biologic principle that metabolic stress can affect tau. It does not show that cervical instability causes oxygen deprivation in the human brain, that this mechanism causes CTE, or that correcting cervical instability prevents tau pathology.

Mechanistic research is valuable because it generates testable questions. It must not be presented as clinical proof.

CSF, the glymphatic system, and traumatic brain injury

The brain has pathways that help exchange CSF with interstitial fluid and clear metabolic waste. This network is commonly described as the glymphatic system. Animal research has shown that traumatic brain injury can impair glymphatic transport and promote abnormal protein accumulation. In a mouse model, glymphatic dysfunction after traumatic brain injury was associated with tau pathology. (6)

A 2023 review (7) concluded that the literature connecting traumatic brain injury, glymphatic disruption, and neurodegeneration is promising but still based largely on animal models. Human imaging and biomarkers require further validation.

This research makes CSF and venous outflow scientifically interesting in post-traumatic illness. It does not yet demonstrate that a mechanical obstruction in the cervical spine causes CTE. Nor does it establish that restoring a particular imaging measurement will prevent neurodegeneration.

The Caring Medical cervical-instability hypothesis

In our clinical work, we see selected patients with chronic headache, brain fog, dizziness, concentration problems, visual symptoms, and neck pain whose symptoms began or worsened after head or neck trauma. Our working hypothesis is that, in some patients, cervical ligament injury and abnormal vertebral motion may coexist with altered cervical sensorimotor signaling and, potentially, compromise of venous or CSF dynamics.

In 2024, we published a retrospective chart review of 227 consecutive patients (8) selected because they had chronic brain or mental-health symptoms without an obvious cause. The paper reported cervical structural findings and measurements involving the internal jugular veins, vagus nerves, and optic nerve sheaths, and proposed a relationship among cervical dysstructure, impaired cranial fluid outflow, and symptoms.

The limitations of our study are:

• it was a retrospective observational study of a selected clinic population;
• it did not study athletes with neuropathologically confirmed CTE;
• it did not test whether cervical treatment prevents CTE;
• associations on imaging do not by themselves establish that one finding caused another; and
• controlled, independent, prospective studies are needed.

Our 2014 research (9) described the proposed relationship between cervical capsular ligament laxity, excessive vertebral motion, and chronic neck pain. That paper provides a biomechanical rationale for evaluating instability in appropriately selected patients, but it also does not establish a CTE-prevention effect.

Our research therefore supports a research agenda and a clinical hypothesis, not a declaration that cervical instability is the cause of CTE.

Can treating cervical instability prevent CTE?

At present, the scientifically responsible answer is we do not know, and prevention has not been demonstrated.

Treating a coexisting cervical disorder may help an appropriately diagnosed patient’s neck pain, headache, function, or other cervical-mediated symptoms. That clinical goal is distinct from preventing or reversing CTE.

At Caring Medical, Prolotherapy may be considered for selected patients when history, examination, and imaging support painful ligament injury or instability. Prolotherapy is not an established treatment for CTE. Likewise, chiropractic manipulation, cervical fusion, or any other intervention should not be offered as a CTE-prevention treatment without evidence. High-velocity neck manipulation can be inappropriate in some patients, while surgery carries material risks and should be reserved for accepted indications after specialist evaluation.

How we evaluate the cervical component after concussion

A thoughtful evaluation begins with the mechanism of injury and symptom behavior. We ask whether symptoms are provoked by head position, neck motion, sustained posture, exercise, or visual and vestibular tasks. We examine cervical motion, tenderness, strength, neurologic function, proprioception, and signs that require urgent referral.

Imaging should answer a clinical question. Standard radiographs, CT, or MRI may be appropriate depending on the history. In selected cases, motion imaging may provide additional information, but an imaging finding should never be interpreted in isolation. We discuss the role and limitations of digital motion X-ray in suspected cervical instability.

Patients with progressive weakness, gait deterioration, bowel or bladder change, a sudden severe headache, new speech or vision loss, fainting, seizure, or other acute neurologic signs require urgent conventional medical assessment. Persistent mood change or suicidal thoughts require immediate mental-health support; these symptoms must never be assumed to be caused solely by the neck.

An updated open letter to the medical community

My request to colleagues is both simple and specific: when evaluating a patient after concussion, examine the neck as well as the brain.

Do not mistake that request for a claim that the cervical spine has been proven to cause CTE. The established prevention priority is reducing repetitive head impacts. The cervical question is whether concurrent injury contributes to persistent, potentially treatable symptoms and whether altered cervical biomechanics or cranial fluid dynamics influence recovery. Those questions deserve rigorous study.

Future research should include prospective cohorts with well-defined head-impact exposure; blinded, standardized cervical examinations; validated measurements of venous, CSF, and glymphatic function; appropriate control groups; and clinically meaningful outcomes. It should distinguish symptom improvement from disease modification and should never use a surrogate imaging change as proof of CTE prevention.

We can hold two ideas at once: the evidence does not support calling cervical treatment a CTE-prevention therapy, and the neck remains an important, sometimes overlooked part of post-concussion care.

For patients, that distinction offers a more honest form of hope. We cannot diagnose CTE during life or promise that a neck procedure will prevent it. We can reduce future impacts, evaluate all reasonable causes of ongoing symptoms, treat identified problems responsibly, and continue the research needed to determine how the cervical spine, cerebral circulation, CSF dynamics, and brain recovery interact.

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.

References

1  McKee AC, Stein TD, Huber BR, et al. Chronic traumatic encephalopathy (CTE): criteria for neuropathological diagnosis and relationship to repetitive head impacts. Acta Neuropathologica. 2023. [Google Scholar]
2  Katz DI, Bernick C, Dodick DW, et al. National Institute of Neurological Disorders and Stroke consensus diagnostic criteria for traumatic encephalopathy syndrome. Neurology. 2021;96(18):848–863. [Google Scholar]
3  Omalu B, Small GW, Bailes J, et al. Postmortem autopsy-confirmation of antemortem F-18 FDDNP-PET scans in a football player with chronic traumatic encephalopathy. Neurosurgery. 2018;82(2):237–246. [Google Scholar]
4 Kinney AET, et al. Cervical spine sensorimotor deficits persist in people post-concussion compared with people with non-concussion-related neck pain. 2024. [Google Scholar]
5 Mavroeidi P, Mavrofrydi O, Pappa E, et al. Oxygen and glucose deprivation alter synaptic distribution of tau protein: the role of phosphorylation. Journal of Alzheimer’s Disease. 2017. [Google Scholar]
6 Iliff JJ, Chen MJ, Plog BA, et al. Impairment of glymphatic pathway function promotes tau pathology after traumatic brain injury. Journal of Neuroscience. 2014;34(49):16180–16193. [Google Scholar]
7 Peters ME, Lyketsos CG. The glymphatic system’s role in traumatic brain injury-related neurodegeneration. Molecular Psychiatry. 2023;28(7):2707–2715. [Google Scholar]
8 Hauser RA, Matias D, Rawlings B. The ligamentous cervical instability etiology of human disease from the forward head-facedown lifestyle: emphasis on obstruction of fluid flow into and out of the brain. Frontiers in Neurology. 2024;15:1430390. [Google Scholar]
9 Steilen D, Hauser R, Woldin B, Sawyer S. Chronic neck pain: making the connection between capsular ligament laxity and cervical instability. The Open Orthopaedics Journal. 2014;8:326–345. [Google Scholar]

2017 references

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

803