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Sports Concussion: Beyond the Sideline Evaluation

A normal CT scan does not mean a normal brain. Most sports concussions produce diffuse axonal injury, metabolic crisis, and neuroinflammation that standard emergency imaging was never designed to detect. If your athlete is still symptomatic weeks later, the injury is real—it just hasn’t been properly measured.

The Concussion Your Emergency Room Missed

Here is what happens after most sports concussions. The athlete gets hit. A sideline evaluation is performed—symptom checklist, balance test, maybe a SCAT5. If symptoms persist, the athlete goes to an emergency department. A CT scan comes back normal. The patient is sent home with instructions to rest and follow up with their primary care physician if symptoms don’t improve.

This protocol is designed to rule out neurosurgical emergencies—bleeds, skull fractures, midline shift. It accomplishes that goal. What it does not do is evaluate the actual concussion injury: the diffuse axonal shearing that disrupts white matter tracts, the acute metabolic crisis that starves neurons of energy, and the inflammatory cascade that prolongs recovery for weeks or months. CT imaging is not sensitive to any of these. McCrory et al., in the 2017 Consensus Statement on Concussion in Sport, acknowledged that “conventional structural neuroimaging is typically normal in concussion.”

The result is a population of athletes—youth, collegiate, professional, and recreational—who are told their brain is fine when it is not. They are cleared to return to play based on symptom resolution rather than neurological recovery. They accumulate additional impacts on a brain that has not yet healed. And when symptoms become chronic, they are often dismissed or attributed to psychological factors rather than the structural and metabolic injury that is actually driving them.

Cumulative Damage: Why Every Hit Counts

The conversation about sports concussion has shifted substantially over the past fifteen years, driven in large part by the neuropathological work of McKee et al. (2009, Journal of Neuropathology & Experimental Neurology). Their examination of brains from athletes with histories of repetitive head trauma revealed chronic traumatic encephalopathy (CTE)—a progressive tauopathy characterized by perivascular accumulation of hyperphosphorylated tau protein in patterns distinct from Alzheimer’s disease.

What made this finding particularly significant was the discovery that CTE pathology was present not only in professional athletes with documented concussion histories but also in younger athletes whose exposure consisted primarily of subconcussive impacts—the routine hits that occur in practice and competition and never trigger clinical evaluation. Bailes et al. (2013, Neurosurgery) estimated that a high school football lineman sustains between 600 and 1,000 subconcussive head impacts per season.

Each impact, whether it meets the clinical threshold for concussion or not, produces some degree of axonal strain, blood-brain barrier disruption, and microglial activation. When these insults accumulate faster than the brain can repair them, the neurological burden compounds. The metabolic reserve narrows. The threshold for the next symptomatic concussion drops. Recovery from each successive injury takes longer.

This is why parents, coaches, and athletes need to understand that concussion management extends beyond the single-event model. The relevant question is not just “did they get a concussion?” but “what is the cumulative state of this brain?” Answering that question requires diagnostic tools that go far beyond a sideline screening.

How We Actually Evaluate a Concussion

At The Neurogenesis Project, Dr. Orr evaluates sports concussion the way a neurologist should—by measuring the injury rather than simply cataloging symptoms. Our evaluation begins with a comprehensive neurological examination and proceeds through three diagnostic pillars.

Advanced Neuroimaging. We use MRI sequences specifically sensitive to concussion pathology—diffusion tensor imaging to evaluate white matter tract integrity, susceptibility-weighted imaging to detect microhemorrhages, and volumetric analysis to identify regional atrophy. These sequences detect injuries that are invisible on the standard CT and routine MRI protocols used in emergency departments and most outpatient settings.

Cognitive Testing with Normative Comparison. We perform validated neuropsychological assessments that measure processing speed, reaction time, working memory, executive function, and attention. Results are compared against age- and education-matched normative data to identify deficits that fall outside expected performance ranges—deficits that an athlete may not recognize because they have no baseline awareness of their own decline.

Metabolic and Inflammatory Biomarkers. Concussion triggers a neuroinflammatory cascade. We measure inflammatory cytokines, oxidative stress markers, and metabolic indicators that reflect the current state of the brain’s recovery. These labs tell us whether the metabolic crisis is resolving or persisting, regardless of what the symptom checklist says.

Together, these three pillars produce an objective picture of brain health—one that supports informed decisions about treatment, recovery timelines, and return to play.

How We Treat This

Treatment is built from diagnostic findings, not applied as a generic concussion protocol. Each intervention targets a specific dimension of the injury.

Frequently Asked Questions

Why do I still have symptoms weeks after my concussion if the ER said my CT was normal?+
Emergency departments use CT imaging to rule out bleeds, fractures, and surgical emergencies. CT is not sensitive to the diffuse axonal injury, metabolic disruption, and microstructural white matter damage that concussions produce. A normal CT does not mean a normal brain. Advanced MRI sequences and metabolic testing reveal the injuries that standard emergency imaging was never designed to detect. Persistent symptoms after a concussion with a normal CT are not imaginary — they reflect real neurological damage that requires proper evaluation.
How is your concussion evaluation different from what my team doctor does?+
Sideline concussion evaluations — SCAT5, balance testing, symptom checklists — are screening tools designed for rapid field-side decisions. They are not diagnostic workups. Our evaluation includes advanced neuroimaging with sequences sensitive to axonal injury and metabolic disruption, comprehensive blood panels measuring inflammatory biomarkers and metabolic markers, and validated cognitive testing with age- and sport-matched normative comparisons. We are measuring the injury, not just documenting symptoms.
My child has had multiple concussions playing soccer. Should I be concerned about long-term effects?+
Yes, and the concern is supported by clinical evidence. McKee et al. demonstrated in 2009 that repetitive head trauma — including impacts below the concussion threshold — produces cumulative neuropathological changes. Each concussion compounds the metabolic vulnerability of brain tissue already compromised by prior injury. The recovery window after each successive concussion tends to lengthen, and the threshold for the next injury tends to lower. A thorough neurological evaluation after multiple concussions can quantify the current state of brain health and guide decisions about continued participation.
What does NAD+ therapy do for concussion recovery?+
Concussion triggers an acute metabolic crisis in the brain. Neurons that have been mechanically stressed shift into a state of increased glucose demand while simultaneously losing the mitochondrial efficiency needed to meet it. NAD+ is the central coenzyme in mitochondrial energy production. Intravenous NAD+ restores the depleted cellular fuel supply, supporting ATP generation, reducing oxidative stress, and enabling the metabolic machinery of recovery to function at capacity. This directly addresses the energy crisis that underlies persistent post-concussion symptoms.
When is it safe to return to play after a concussion?+
The honest answer is: when the brain has recovered, not when symptoms have resolved. Symptom resolution does not equal neurological recovery. Research consistently shows that metabolic normalization lags behind symptom improvement by days to weeks. Our return-to-play evaluations use objective measures — repeat cognitive testing, inflammatory biomarker trends, and when indicated, follow-up imaging — to determine whether the brain has actually healed, not just whether the athlete feels better. Premature return to play is the single largest modifiable risk factor for second-impact syndrome and prolonged recovery.
Does insurance cover sports concussion evaluation and treatment?+
The Neurogenesis Project operates outside of insurance networks. Our diagnostic and treatment protocols use advanced imaging sequences and metabolic therapies that are not typically covered by commercial insurance plans. We provide detailed superbills and medical documentation that patients can submit to their carriers for potential out-of-network reimbursement. Our patient coordinator can discuss costs, payment options, and documentation before you schedule.

Your Athlete Deserves a Real Evaluation

A normal CT does not mean a normal brain. If your athlete is still struggling after a concussion—or has a history of multiple head impacts—the injury needs to be measured, not guessed at. Dr. Orr at The Neurogenesis Project provides the advanced diagnostic workup that sideline evaluations and emergency departments are not designed to deliver.