There is a sentence I hear from older patients that bothers me more than it used to.
“I guess I’m just getting old.”
They say it almost apologetically. They came to see me because they can’t breathe through their nose, they wake up exhausted, or have lived with sinus pressure and congestion for years. But somewhere near the end of the visit, another symptom slips out.
“I can’t concentrate like I used to.” “I lose words.” “I walk into a room and forget why I’m there.” “My kids think I’m getting forgetful.”
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Then comes the explanation they have already given themselves: “I guess I’m just getting old.”
Maybe. But age is a risk factor. It is not a diagnosis. And before we decide that an older patient’s brain is failing, perhaps we should ask what the rest of the body has been asking that brain to endure.
I started thinking about this because of a problem with the questionnaire in my office. It asks about congestion, drainage, facial pressure, loss of smell, and sleep. It does not ask whether the patient can think clearly or concentrate without any difficulty.
It is a small omission. But I have come to believe medicine is full of omissions like it, questions we never think to ask because we are already sure we know the answer.
The symptom hiding outside the sinuses
Patients with chronic rhinosinusitis (CRS) have been describing “brain fog” for years. The phrase sounds imprecise, almost nonmedical. Patients use it because they do not have a better word for what is happening.
They are not necessarily forgetting who the president is or getting lost driving home. They describe something more subtle. They reread emails before sending them. They lose their train of thought halfway through a conversation. Tasks that once required one pass now require three.
One patient described it to me better than any questionnaire could: “I feel like I’m operating at about seventy percent.”
For a long time, medicine had several convenient places to put symptoms like that: stress, anxiety, depression, poor sleep. And, in an older patient, aging.
But what happens when we actually measure cognition? That is where this story becomes more interesting.
A 2025 systematic review and meta-analysis examined 10 studies involving more than 107,000 patients and found poorer global cognitive function in people with chronic rhinosinusitis. Other investigators have demonstrated differences in reaction time, processing speed, attention, memory, and executive function.
Researchers have even looked at the brain itself. A functional MRI study found altered connectivity in people with sinonasal inflammation, particularly involving the frontoparietal network, the circuitry involved in attention, working memory, and cognitive control.
Brain fog suddenly becomes a less satisfying phrase. Something measurable appears to be happening.
Now make the patient 72
This is where I think the problem becomes clinically important. A 35-year-old software engineer who tells us she cannot concentrate gets a differential diagnosis. A 72-year-old who says the same thing risks getting an explanation. “You’re getting older.” That should make us uncomfortable.
I am not suggesting that chronic sinus disease is secretly dementia. It isn’t. Nor am I suggesting that evaluating and treating chronic rhinosinusitis substitutes for evaluating cognitive decline. Progressive memory loss, personality change, impaired judgment, difficulty managing finances, getting lost in familiar places, or other concerning neurologic changes require appropriate evaluation.
The mistake would be replacing “it’s dementia” with “it’s the sinuses.” But there is an equally important mistake on the other side: assuming that every cognitive complaint in an older adult originates from neurodegeneration.
The aging brain does not exist in isolation. It sleeps inside an aging body. It receives signals from that body’s immune system. It experiences its medications, pain, oxygenation, sensory loss, mood, metabolic disease, and sleep fragmentation. And sometimes that body has been inflamed and sleeping poorly for years.
The nose is close to the brain. Chronic rhinosinusitis is not simply a plumbing problem. It is an inflammatory disease. Patients with CRS commonly experience fatigue, sleep dysfunction, loss of smell, reduced productivity, mood symptoms, and cognitive complaints alongside the symptoms we traditionally call “sinus symptoms.”
Exactly how those pieces produce cognitive dysfunction remains unsettled. Sleep is an obvious suspect. Chronic sinus disease is strongly associated with disturbed sleep, and chronic sleep disruption can impair attention, memory, processing speed, and executive function.
Inflammation is another possibility. Persistent inflammatory signaling does not respect the departmental boundaries we have created in medicine.
Then there is the anatomy. The olfactory nerves pass from the nasal cavity through the cribriform plate directly toward the brain. The region around them is increasingly understood as a complicated neuroimmune interface rather than simply the wiring that allows us to smell.
Animal studies suggest nasal inflammation can produce inflammatory changes within the olfactory system. That is fascinating. It is also where I stop.
We do not have evidence that inflammation travels from a patient’s sinuses into the brain and causes their cognitive symptoms. Rodent neuroinflammation is not human dementia, and an elegant mechanism remains a hypothesis until it is demonstrated in patients.
But we do not need to prove that mechanism to acknowledge the clinical observation in front of us. These patients are telling us they cannot think as well. Objective studies are beginning to tell us they may be right.
Here is the part I find most provocative. What happens to cognition when the sinus disease gets better?
Several studies have reported improvement in cognitive symptoms or selected measures of cognitive performance after CRS treatment. The 2025 meta-analysis found improvement in processing speed and working memory following treatment.
I want to be precise about what that means. These are not trials proving that sinus treatment reverses cognitive decline. Patients who feel better may sleep better. Their fatigue and pain improve. Mood changes. Expectation matters. Before-and-after studies cannot neatly separate those effects.
But consider the alternative hypothesis. If every bit of this cognitive slowing were simply inevitable aging, why should any of it improve when an inflammatory disease is treated?
That is a question worth studying. Especially because older adults are so often taught to accommodate decline rather than investigate it. We may be measuring the wrong outcome.
This has changed something small in my practice. I still ask whether patients can breathe. I still ask about drainage, facial pressure, smell, and sleep. But I have added another question: How has your concentration been?
It is not part of the formal diagnostic criteria for chronic rhinosinusitis. It does not determine whether someone needs surgery. It does something else. It tells me about the part of the disease that may matter most to the person sitting in front of me.
Medicine loves measurable endpoints. CT scores. Endoscopy scores. Polyp grades. Symptom questionnaires. A patient cares whether she can finish the book sitting on her nightstand. Those are not always the same outcomes.
And that may be the larger lesson here. I keep coming back to how much of medicine runs on the convenient explanation. The older patient’s fog is aging. The sinus infection is bacterial. The prescription is warranted. Each is the easy answer, offered before anyone has actually looked.
I have spent the last few years writing about the second one, the reflex to reach for an antibiotic without ever confirming there is a bacterium to treat. We prescribe for sinusitis at more than eight of ten visits and culture at almost none of them. And the two habits are the same habit. Many of the patients describing the fog are here because that reflex was applied to them for years: course after course for a disease no one stopped to investigate, an inflammation left to smolder while the prescriptions piled up.
Explaining away the aging brain and reaching for the reflexive antibiotic are one instinct wearing two faces: the willingness to answer a question we never actually asked. We should absolutely investigate cognitive decline in older adults. We should diagnose dementia when dementia is present. But we should be equally reluctant to diagnose age.
When an older patient tells us that something has changed, our job is not to explain the change away. Our job is to ask why. Because sometimes “I’m just getting older” really means:
“Something is different, and nobody has asked me about it yet.”
Franklyn R. Gergits is a board-certified otolaryngologist and fellowship-trained otolaryngic allergist with a clinical focus in rhinology and airway disorders and more than 30 years of clinical experience. He is affiliated with HonorHealth Scottsdale Shea Medical Center and is the founder of Sinus & Allergy Wellness Center of North Scottsdale.
Dr. Gergits performs in-office balloon sinuplasty, turbinate reduction, NEUROMARK posterior nasal nerve ablation, and Eustachian tube dilation under local anesthesia. He performed the first balloon sinuplasty in Pennsylvania and holds dual Entellus Centers of Excellence certifications.
His recent scholarly work includes “Posterior Sinonasal Syndrome: A Pepsin-Mediated Hypothesis for Chronic Rhinosinusitis” and “The Continuous Mucosal Liquid Layer: A Unified Hypothesis for Airway-Digestive Immune Surveillance, Mucociliary Transport, and Disease Susceptibility.” His ORCID profile is available at ORCID. He also publishes patient education and clinical commentary through the Airway & Sinus Wellness Review and shares updates through Facebook, Instagram, LinkedIn, X, YouTube, and TikTok.
