Mild traumatic brain injury is diagnosed by its characteristic symptoms and neurological effects, and visible damage to brain tissue is rare in these cases. That leaves a genuine mystery — significant symptoms, nothing observable. The name supplies an answer to that mystery before anyone has examined it.
What Do Sideline Concussion Tests Actually Measure?
When an athlete takes a hit and comes off the field, the stated purpose of the sideline exam is to check whether the brain has been injured.
What actually gets performed is a series of cranial nerve tests. Pupil response to light. Eye tracking. Facial sensation, speech, coordination, balance.
I learned that protocol in undergrad. My background before chiropractic was sports medicine, and athletic training covered injury prevention, rehabilitation, and fieldside triage, with concussion assessment as part of it. At the same time, we were taking anatomy courses.
The two started to conflict in a way I could not reconcile.
Where Do Cranial Nerves Actually Come From?
To see the conflict, you need one piece of anatomy.
Your cranial nerves are the twelve pairs of nerves that handle most of the sensation and movement in your head and face — your pupils, your eye movements, facial sensation, hearing, swallowing, speech. When someone shines a light in your eye or asks you to follow a finger, they are testing cranial nerve function.
Those nerves do not originate in the cortex. The cortex is the outer surface of the brain — the large, folded outer layer usually shown in illustrations, and the exact region the impact model says gets damaged when the brain supposedly strikes the skull.
Cranial nerves originate in the **brainstem**: a stalk sitting low and toward the back, underneath the main body of the brain, connecting it to the spinal cord. It handles the functions you never think about — heart rate, breathing, balance, arousal, and the routing of sensory information.
Its position matters here. The brainstem does not stay neatly inside the skull. The spinal trigeminal nucleus, which processes sensation from your entire head and face, extends downward through the base of the skull into the upper cervical spinal cord, where it receives input from the top segments of the neck — an overlap known as trigeminocervical convergence (Piovesan et al., 2003).
So put those two facts side by side. The explanation said the injury was at the surface of the brain. The examination measured the function of a structure that sits several inches away, low and behind, and partly inside the neck.
Every test we ran was a brainstem test. Every conclusion we drew was about the cortex.
I raised this with my professor. I asked why, if we believed the cortex was injured, we were exclusively testing structures that come from somewhere else. I never received an answer that resolved it — not in undergrad, and not for a long while afterward.
Why Did a Normal MRI Never Change Anyone's Mind?
The second thing I couldn't reconcile was simpler, and in some ways more troubling.
Athletes with concussion symptoms were sent for an MRI of the brain. In all my time doing that work, I cannot recall a single instance where a standard brain MRI came back positive for an actual brain injury. Not one.
That is not unusual, and it isn't a failure of the imaging. Conventional CT and MRI are well documented as insensitive to the changes involved in mild traumatic brain injury; a review and meta-analysis of neuroimaging after mTBI found that standard structural imaging is typically unremarkable, which is why the field has moved toward advanced sequences to detect anything at all (Eierud et al., 2014).
Now consider how that result was interpreted.
A negative scan is evidence. Specifically, it's evidence that the imaging did not find damage in the region it examined. That result could reasonably prompt a question: if the brain looks normal, is it possible the problem is somewhere the scan didn't cover?
That question was not asked. Instead the reasoning ran this way: the person clearly has neurological symptoms, and we know neurological symptoms come from the brain, so the brain must be injured in some way the scan can't detect. Rest them, wait, and return them to activity once they pass a few basic tests.
Look carefully at what happened there. A finding that could have challenged the assumption was absorbed as support for it. The scan didn't revise the premise. The premise reinterpreted the scan.
Once a starting assumption is strong enough to do that, it can no longer be disproven by evidence, because every possible result gets read as consistent with it.
What Does "Mild" Actually Mean in Mild Traumatic Brain Injury?
Here is where the language deserves a closer look, because it's easy to assume the name carries more information than it does.
Mild traumatic brain injury is **diagnosed by its characteristic symptoms and neurological effects** following an impact — headache, confusion, altered awareness, memory disruption, dizziness, changes in balance and cognition. Those findings are what establish the diagnosis. It is not diagnosed by pointing at something on a scan.
In a more severe **traumatic brain injury**, damage to brain tissue can be seen. There's a bleed, a lesion, visible disruption. It's observable and documentable, and nobody is confused about the location of that injury, because you can look at it.
In mild traumatic brain injury, visible damage to brain tissue is **rare**. The symptoms can be substantial and lasting while the imaging stays unremarkable.
That combination is the real mystery, and it deserves to be stated plainly: the symptoms are significant, and there is no observable damage to account for them. So where are they coming from?
That is an open question. And notice what the name does with it — it supplies an answer. Calling the condition a *brain* injury asserts a location before anyone has established one.
That doesn't make the assumption false. Some of these injuries genuinely do involve brain tissue in ways current imaging isn't sensitive enough to show. It makes the assumption **untested** — which is a very different thing from wrong, and a very different thing from established.
Why Is a Wrong Starting Assumption So Hard to Notice?
First premises are hard to catch because they don't feel like assumptions while you're using them. They feel like the ground you're standing on.
Here is a familiar version of the same problem. Suppose you decide that a particular person doesn't like you. From that moment forward, everything they do gets filtered through that belief. A short reply becomes coldness. An unanswered message becomes avoidance. A neutral expression across a room becomes disapproval.
You're not reasoning poorly in that situation. You're reasoning carefully and consistently — from a starting point that may simply be untrue. And here's the important part: reasoning *more* carefully will not fix it. Every additional observation gets processed through the same faulty starting point, so more effort produces more confidence rather than more accuracy. The only thing that helps is going back and examining the assumption itself.
For years I approached mild traumatic brain injury the wrong way. I argued about treatments — whether this therapy worked better than that one, whether this protocol should replace that protocol. That was never the real disagreement, and I couldn't win it, because both sides of a treatment argument accept the same underlying premise about where the injury is.
The argument that actually matters is **premise versus premise.**
Where Does the Assumption Lead if Nobody Checks It?
Here is the full chain, one link at a time, because the last link is where the damage really gets done.
**One.** The premise is that a mild traumatic brain injury is an injury to the brain.
**Two.** Because of that premise, the brain is what gets evaluated and imaged. Nothing else is examined, because nothing else is suspected.
**Three.** In the majority of mild cases, the brain imaging comes back normal — which is the expected result, since visible damage is rare in these injuries.
**Four.** With no findings, there's nothing structural to treat. The only remaining option is managing symptoms as they appear.
**Five.** Because symptom management doesn't address whatever is producing the symptoms, the person doesn't recover. The symptoms persist, or worsen, and management escalates.
**Six.** The ongoing lack of results now needs an explanation. And since the entire process has been operating on the premise that this is a brain injury, the failure gets attributed to the brain rather than to the search.
The sentence at the end of that chain is one I've had repeated back to me by one veteran after another, delivered to them across a desk at an appointment:
*The brain doesn't heal. You need to learn to live with it.*
That statement is not a research finding. It's the final link in a chain of reasoning that began with an assumption nobody thought to examine — and it gets delivered to people as though it were settled fact about their future.
What Changes if the Injury Isn't Always in the Brain?
I want to be careful about the size of the claim, because it's smaller than it might sound.
Some mild traumatic brain injuries do involve direct injury to brain tissue. Shearing is real. Rotational forces produce real damage. In more severe impacts we see pressure-related injury that appears plainly on imaging and requires direct care. I'm not asking anyone to set that aside.
The question is narrower: what if it isn't *always* a brain injury?
If that's true even part of the time, then nothing needs to be discarded. What needs to change is the scope of the search. Instead of evaluating and imaging the brain alone, you evaluate and image the brain **and** the craniocervical junction — the area where the skull meets the top two vertebrae of the neck.
There's a straightforward reason to include that area specifically. It is the structure every force reaching your head has to travel through, it's the least mechanically stable segment in the spine, and it houses or surrounds the brainstem, the vertebral arteries, and the drainage pathway for fluid leaving your head. It sits directly beneath where standard brain imaging stops. The [force numbers make the same argument](post-how-much-force-injures-your-neck-versus-your-brain.html): it takes far less energy to injure that junction than to injure brain tissue.
When disruption turns up there, the work becomes correcting that structural problem so the brain has an environment in which it can recover. The brain does heal. It requires the right conditions to do it. But you have to identify what's driving the decline before you can remove it.
None of that becomes available while the search area is fixed in place by an assumption nobody ever checked.
Told Your Scan Was Clean, but Nothing Has Improved?
If your recovery stalled after normal imaging, the more useful question may not be why your brain is healing slowly. It may be whether the search was aimed at the right place to begin with.
Widening that search — to the brain **and** the [craniocervical junction](condition-concussion-and-mtbi.html) — is the work we do at Cerebral. If you'd like a real evaluation, we're here.
References
- Piovesan EJ, Kowacs PA, Oshinsky ML. Convergence of cervical and trigeminal sensory afferents. *Current Pain and Headache Reports*. 2003;7(5):377–383. https://pubmed.ncbi.nlm.nih.gov/12946291/
- Eierud C, Craddock RC, Fletcher S, et al. Neuroimaging after mild traumatic brain injury: review and meta-analysis. *NeuroImage: Clinical*. 2014;4:283–294. https://pubmed.ncbi.nlm.nih.gov/25061565/
- Sessle BJ, et al. Neuroanatomy, Spinal Trigeminal Nucleus. *StatPearls*. NCBI Bookshelf. https://www.ncbi.nlm.nih.gov/books/NBK539729/