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Picture this scenario: a patient suffers what appears to be a relatively minor concussion. The initial symptoms—headache, dizziness, light sensitivity—seem predictable. But weeks later, instead of improving, they develop profound fatigue, cognitive dysfunction, joint pain, mood disturbances, and a constellation of seemingly unrelated symptoms that their healthcare providers struggle to explain.
What's happening here isn't just a prolonged concussion recovery. It's a fundamental principle of neuroimmune health that's often overlooked: The concussion is merely the match that ignites a puddle of gasoline that was already there.
This "gasoline" can take many forms—dormant Epstein-Barr virus from a bout of mononucleosis years ago, lingering effects from streptococcal infections that were never fully cleared, Borrelia burgdorferi from an undiagnosed tick bite, or mycotoxin exposure from a water-damaged building. The patient may have been living with these underlying factors for years without noticeable symptoms, their immune system keeping these challenges in check—until the concussion disrupted this delicate balance. As a patient, you might experience this as a sudden onset of symptoms that seem entirely disproportionate to your head injury. As a healthcare provider, understanding this connection is crucial for properly diagnosing and treating patients whose post-concussion symptoms defy conventional explanation.
This article explores the science behind how concussions can unmask and activate these pre-existing, often undiagnosed conditions that were lurking beneath the surface, waiting for a trigger.
Before diving into how concussions trigger these reactions, it's important to understand the "gasoline" that may already be present in many patients:
Many common infections can establish persistence in the body, remaining dormant until triggered:
The critical insight is that many patients are completely unaware of these underlying factors. They may have had perfect health before their concussion, with their immune system successfully compensating for these hidden challenges—until the head injury changed everything.
A concussion is far more than just a momentary disruption of brain function—it's a whole-body event that can fundamentally alter immune function and neurological regulation. Here's how the "match" ignites the pre-existing "gasoline":
The blood-brain barrier (BBB) serves as a highly selective protective shield between the bloodstream and brain tissue. Following a concussion, this critical barrier becomes compromised—essentially creating openings where there shouldn't be any.
The hidden vulnerability exposed:
Research by Shlosberg and colleagues (2010) confirms that BBB disruption after head injury creates a window of vulnerability where the brain becomes exposed to substances it was previously protected from—including pathogens and toxins that may have been quietly circulating in the body for years.
Microglia are the brain's resident immune cells—constantly monitoring for threats. Previous infections or toxin exposures can "prime" these cells, making them more reactive to future challenges, even when the person feels perfectly healthy.
How concussion fans the flames:
The result can be amplified brain fog, heightened pain sensitivity, sleep disturbances, and mood changes that seem disproportionate to the concussion itself.
Perry and colleagues (2007) demonstrated that when microglia have been previously sensitized by infections or toxins, they mount a significantly more aggressive response to a secondary challenge like a concussion—a phenomenon that explains why seemingly minor head injuries can produce devastating symptoms in some individuals.
Our immune system operates on a precisely calibrated balance of pro-inflammatory and anti-inflammatory signals. A concussion temporarily disrupts this balance throughout the entire body, not just the brain.
The pre-existing conditions unmasked:
For someone with undiagnosed Lyme disease, previous streptococcal infections, or chronic mycotoxin exposure, this immune dysregulation can be the tipping point that transforms subclinical issues into debilitating symptoms.
The hypothalamic-pituitary-adrenal (HPA) axis coordinates our stress response and influences nearly every body system. Concussions can significantly disrupt this master control system.
How this reveals hidden vulnerabilities:
Research shows that even mild head injuries can create lasting HPA axis alterations, potentially explaining why some patients develop profound fatigue, stress intolerance, and metabolic disturbances after concussion—especially when pre-existing infections or toxin exposures are present.
A critical insight for healthcare providers is that many patients won't present with obvious signs of infection reactivation. Instead, they develop symptoms that mirror Chronic Inflammatory Response Syndrome (CIRS)—a complex, multi-system condition characterized by:
These symptoms often develop or intensify 2-4 weeks after the concussion—a timeline that correlates with the body's evolving immune response to the injury.
The reason these symptoms emerge is that the concussion has triggered what immunologists call a "cytokine storm" or persistent inflammatory cascade. This inflammation isn't limited to one system but affects multiple body systems simultaneously. The source may be reactivated infections, unmasked toxin sensitivity, or autoimmune responses—but the presentation often looks remarkably similar regardless of the specific trigger.
Dr. Ritchie Shoemaker's research on CIRS provides a valuable framework for understanding how different triggers (mold, Lyme disease, viral infections) can create similar symptom patterns through shared inflammatory pathways. The concussion simply serves as the event that pushes a compensating system into decompensation.
Mycotoxins—toxic compounds produced by certain molds—deserve special mention in this context. Many patients have been exposed to water-damaged buildings without developing overt symptoms, their detoxification systems managing the toxin load adequately—until a concussion occurs.
Post-concussion, several factors converge to unmask previously tolerated mycotoxin exposures:
This explains why some patients suddenly develop building sensitivity, becoming unable to tolerate environments they previously inhabited without issue. Their symptoms may worsen dramatically in water-damaged buildings or improve when they change environments—a crucial diagnostic clue that the concussion has unmasked an underlying mycotoxin sensitivity.
Once triggered by the concussion, these mechanisms don't operate in isolation—they interact, creating feedback loops that can perpetuate and amplify symptoms long after the initial brain injury should have resolved:
| Mechanism | Primary Effect | How It Perpetuates the Cycle |
| BBB Disruption | Allows pathogens/toxins into the brain | Creates ongoing neuroinflammation |
| Microglial Activation | Amplifies brain inflammation | Causes neuronal dysfunction, further immune activation |
| Immune Dysregulation | Reduces pathogen control | Allows greater spread of infections, more inflammation |
| HPA Axis Dysfunction | Alters stress response | Impairs immune regulation, disrupts sleep, reduces recovery |
| Infection Reactivation | Increases pathogen burden | Triggers more immune activation, inflammatory cascades |
| Mycotoxin Sensitivity | Heightens reactions to environments | Creates ongoing toxin exposure, immune activation |
For patients caught in this cycle, standard concussion protocols often fail because they don't address the underlying immune, infectious, or toxin-related factors that the concussion has unmasked.
Note: These are composite cases based on typical presentations, not actual individuals.
Emma, a 27-year-old fitness instructor, had always been healthy and active. She had experienced a bout of mononucleosis in college but recovered completely. Unknown to her, the Epstein-Barr virus remained dormant in her system.
After a minor concussion from hitting her head during a workout class, Emma initially experienced typical symptoms—headache, dizziness, sensitivity to light. Her doctor advised rest, and light aerobic exercise as she expected to recover within days.
Two weeks later, instead of improving, she developed crushing fatigue, cognitive difficulties she described as "thinking through mud," muscle and joint pain, and anxiety that seemed to come out of nowhere. Her symptoms were far more severe than expected from her relatively minor concussion.
Multiple specialists attributed her condition to post-concussion syndrome or anxiety. That didn’t make sense to me. After reviewing her history and presentation, I referred her to a provider familiar with neuroimmune interactions who tested for viral reactivation that they discovered significantly elevated EBV antibody levels, indicating the concussion had reactivated her dormant EBV infection.
Her treatment included:
Emma's case illustrates how a concussion can unmask and activate a dormant viral infection that the patient had no idea was still present in her body. The concussion was merely the match that lit the pre-existing viral "gasoline."
Michael, a 42-year-old accountant from outside of Seattle, WA, had been working in the same office building for five years without health issues. Unknown to him, water damage behind a wall had created a reservoir of mold producing mycotoxins. His body had been compensating for this toxic exposure without obvious symptoms.
After suffering a concussion in a car accident, Michael initially recovered as expected from the head injury itself. However, one month later, he began experiencing severe cognitive problems, dizziness, fatigue, and a new and puzzling development: whenever he entered his office building, his symptoms would dramatically worsen within an hour.
His chiropractic physician attributed these symptoms to post-concussion syndrome and anxiety about returning to work. After multiple failed treatments, Michael was referred to my consultation. His symptom profile did not fit the typical persisting concussion profile, so I referred him to my colleague who is a functional medicine practitioner. He connected his building-related symptom flares to possible mold exposure.
Testing revealed elevated mycotoxin levels in both his blood and in samples from his workplace. Further investigation discovered the hidden water damage and mold growth.
His treatment included:
Michael's case demonstrates how a concussion can suddenly unmask environmental sensitivities that were previously subclinical. The concussion didn't create the mycotoxin problem—it simply reduced his body's ability to compensate for an exposure that was already there.
If you've experienced a concussion, be alert for these patterns that suggest your injury has triggered pre-existing vulnerabilities:
Important validation: If you're experiencing these patterns, understand that you're not imagining things, being dramatic, or "just anxious." These symptoms have a physiological basis—your concussion has uncovered an underlying vulnerability that was already present.
When evaluating patients with unusual or persistent post-concussion symptoms, consider these key assessment strategies:
Effective management requires a dual focus on both neurological recovery and immune modulation:
It's important to note that treatment should be individualized and developed in partnership between patients and knowledgeable healthcare providers. The complexity of these interconnected systems means that standard one-size-fits-all approaches often fall short.
James, a 13-year-old student, had experienced multiple strep throat infections as a child but hadn't had one in over 5 years. His parents had no idea that these infections had left an immunological imprint that his body was quietly managing.
After sustaining a concussion while playing recreational basketball, James initially seemed to recover normally. But approximately one month later, he began experiencing severe anxiety, intrusive thoughts, irritability, fidgetiness, and emotional lability that seemed completely out of character. He also developed tics and obsessive behaviors that he had never exhibited before.
Several mental health professionals diagnosed him with anxiety disorder and post-concussion syndrome. When traditional treatments failed to help, James sought out my care. We treated him from a functional neurology perspective and stabilized the majority of his symptoms, except the tics. At that point, I believed his symptoms were probably consistent with PANDAS/PANS—autoimmune conditions triggered by streptococcal antibodies cross-reacting with brain tissue.
Testing revealed elevated anti-streptococcal antibodies and anti-neural antibodies, suggesting an autoimmune brain reaction that had been triggered by the immune dysregulation following his concussion. I referred him to a PANDAS literate medical doctor for continued care.
His treatment protocol included:
James's case illustrates how a concussion can unmask autoimmune vulnerabilities created by infections years earlier. The concussion didn't create the autoimmune tendency—it simply disrupted the regulatory mechanisms that had been keeping it in check.
The connection between concussions and infection reactivation represents an important intersection of neurology, immunology, and infectious disease—areas that have traditionally operated separately in conventional medicine. Bridging this knowledge gap requires:
If you're experiencing a resurgence of Lyme or strep-related symptoms following a concussion, your experience is valid and has a biological basis. The complex interplay between brain injury and immune function can reawaken dormant infections or trigger immune responses that manifest as familiar symptoms.
For healthcare providers, recognizing this connection opens new avenues for effectively treating patients with persistent or unusual post-concussion symptoms. By addressing both the neurological and immunological aspects of recovery, we can provide more comprehensive care.
The brain and immune system are not separate entities but deeply interconnected partners in health and disease. A concussion is never "just" a brain injury—it's a whole-body event with far-reaching effects. By understanding these connections, we gain powerful insights that can transform our approach to healing and recovery.
This article is for informational purposes only and does not constitute medical advice. Always consult with qualified healthcare providers for diagnosis and treatment of medical conditions.
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