For many families, a diagnosis of PANS, PANDAS, or autoimmune encephalitis finally provides an explanation for symptoms that seemed to come out of nowhere.
A previously healthy child suddenly develops obsessive-compulsive behaviors, anxiety, tics, rage episodes, restrictive eating, cognitive decline, depression, insomnia, or other dramatic neuropsychiatric symptoms. The change can be abrupt and frightening, often leaving parents searching desperately for answers.
These diagnoses have helped us understand an important reality: the immune system can profoundly influence brain function.
But after caring for these patients for many years, I found myself asking a different question.
Not simply, "What triggered this?"
But rather, "Why did this happen to this child in the first place?"
What Are PANS and PANDAS?
PANDAS, or Pediatric Autoimmune Neuropsychiatric Disorders Associated with Streptococcal Infections, was originally described in children who developed sudden-onset obsessive-compulsive symptoms or tics following a streptococcal infection.
The proposed mechanism involves an abnormal immune response in which antibodies produced against strep mistakenly interact with structures within the brain, particularly the basal ganglia. This neuroinflammatory response is believed to contribute to the abrupt onset of psychiatric and neurological symptoms.
As research evolved, clinicians recognized that many children developed an almost identical clinical picture without evidence of strep infection. This led to the broader diagnosis of PANS, or Pediatric Acute-onset Neuropsychiatric Syndrome.
Today, potential triggers may include streptococcal infections, Mycoplasma, Epstein-Barr virus, influenza, COVID-19, and a variety of other infectious or inflammatory exposures.
The concept has expanded even further into the broader category of autoimmune encephalitis and autoimmune encephalopathy, reflecting growing recognition that immune dysfunction can significantly alter brain function.
I believe this model is largely correct.
I simply do not believe it is complete.
Why I Started Looking Beyond the Trigger
One observation continued to stand out.
Most children are exposed to strep.
Most children contract viral infections.
Most children encounter Mycoplasma and other common pathogens.
Yet only a small percentage develop PANS, PANDAS, or autoimmune encephalitis.
If the trigger alone explained the illness, we would expect these conditions to be far more common.
The same question applies to recovery.
Why do some children experience a single episode and recover completely, while others develop chronic symptoms, repeated flares, or require years of treatment?
Over time, it became increasingly clear to me that the trigger was only part of the story.
The more important question was why the immune system responded so differently in the first place.
What I Consistently Find Upstream
This question eventually led me to develop what I now refer to as the IACIRS model—Infection-Associated Chronic Inflammatory Response Syndrome.
From this perspective, PANS, PANDAS, and many cases of autoimmune encephalitis are not isolated disease processes. They are downstream manifestations of a chronically dysregulated immune system.
When I evaluate these patients, I repeatedly find the same three categories of upstream stressors, what I call the Root Cause Triad:
Stealth Microbes
Many patients demonstrate evidence of chronic infectious burden long before the onset of neuropsychiatric symptoms. The organisms I encounter most commonly include Borrelia, Babesia, Bartonella, Candida, and Aspergillus. In some cases, I suspect these microbes may have been present since birth through congenital transmission.
Toxins and Biotoxins
Environmental mold exposure and mycotoxins are among the most common contributors I see. These exposures can alter immune signaling, increase inflammatory burden, and impair the body's ability to maintain immune balance.
Stress Response Dysregulation
The stress response system serves as one of the body's master regulators. Physical illness, chronic inflammation, trauma, poor sleep, environmental stressors, and psychological stress can all contribute to a nervous system that becomes stuck in survival mode. When this occurs, immune regulation often suffers as well.
These three factors rarely exist in isolation.
They interact continuously, amplifying one another and gradually pushing the immune system further from healthy regulation.
By the time neuropsychiatric symptoms emerge, the immune system has often been under strain for years.
The Role of Antigenic Triggers
Once this vulnerable terrain exists, an additional trigger may be enough to push the system beyond its capacity to compensate.
I refer to these events as antigenic triggers.
These may include strep, Mycoplasma, Epstein-Barr virus, influenza, COVID-19, or other acute infections. In some susceptible individuals, vaccines may also function as an antigenic trigger.
Importantly, I do not view these events as the root cause of the illness.
Rather, they often represent the final event that exposes an already dysregulated immune system.
Parents frequently describe symptom onset as though a switch flipped overnight.
From my perspective, the groundwork for that switch may have been developing for years.
The antigenic trigger may pull the trigger.
The Root Cause Triad is what loaded the gun.
Why This Changes How I Approach Treatment
This perspective naturally leads to a different treatment philosophy.
Conventional treatment often focuses on reducing inflammation, preventing recurrent infections, and modulating the immune system through therapies such as IVIg, corticosteroids, Rituximab, plasmapheresis, and other immune-directed interventions.
These therapies can be tremendously valuable.
In some situations, they are absolutely necessary.
I have seen IVIg produce remarkable improvements, and there are certainly patients who experience dramatic and lasting recovery after one or two treatments.
However, that has not been the most common pattern I have observed.
Far more often, IVIg becomes a recurring therapy.
Patients improve, symptoms begin to return, another infusion is administered, and the cycle repeats.
Months become years.
At that point, I believe an important question deserves consideration:
If the immune system has been reset, why does it continue to require resetting?
From an IACIRS perspective, the answer is often that the underlying drivers remain active.
The stealth microbes remain.
The mold exposure remains.
The toxin burden remains.
The stress response system remains dysregulated.
Immune modulation can temporarily quiet the fire, but it does not necessarily remove the fuel.
This is why my primary focus is not simply suppressing the autoimmune response.
It is identifying and addressing the factors that created the immune dysfunction in the first place.
A Different Goal
The goal is not merely symptom control.
The goal is restoring immune balance.
That requires addressing the upstream factors driving illness while using immune-modulating therapies strategically when necessary.
This stepwise approach forms the foundation of our IACIRS treatment model, which you can read about in greater detail here:
**IACIRS: A Stepwise Path to Recovery: **https://www.restorativemedcenter.com/blogs/iacirs-a-stepwise-path-to-recovery
When the Root Cause Triad is addressed, immune-modulating therapies may still have a role. But they are no longer carrying the entire burden of recovery.
Final Thoughts
PANS/PANDAS/Autoimmune Encephalitis are real and potentially devastating conditions.
The autoimmune response is real.
The neuroinflammation is real.
But in many cases, they are not the beginning of the story.
They are the consequence of an immune system that has been struggling for much longer than anyone realized.
If we want lasting recovery, we must look beyond the trigger, beyond the antibodies, and beyond the diagnosis itself.
We must understand what pushed the immune system off balance in the first place.