A symptom, not a diagnosis.
Loss of smell is not a single disease — it's a symptom that can come from any point along the olfactory pathway. Odor molecules reach the olfactory epithelium high in the nasal cavity, are detected by olfactory sensory neurons that project through the cribriform plate, synapse in the olfactory bulb, and travel to the primary olfactory cortex. Damage at any of these levels produces some form of olfactory dysfunction.
Categorically, smell loss falls into four buckets — sometimes overlapping:
- Conductive — odorants can't physically reach the olfactory epithelium, usually because of nasal polyps, severe inflammation, or anatomic obstruction
- Sensorineural — the olfactory epithelium or olfactory neurons are damaged, typically by viral injury, head trauma, or chemical exposure
- Central — the problem is in the olfactory bulb or central pathways, as in Parkinson's, Alzheimer's, or after stroke
- Idiopathic — no clear cause despite a thorough workup
About a quarter of adults have some degree of olfactory dysfunction; the rate rises sharply after age sixty and rose dramatically during the COVID-19 pandemic. Loss of smell is consistently underdiagnosed because it doesn't hurt and because most patients only realize it's gone when food stops tasting right (about 80 percent of what we experience as flavor is actually olfactory).
Where it came from drives what to do.
Post-viral (including post-COVID)
The single most common cause of smell loss in adults — and the dominant cause since 2020. Viral injury to the olfactory epithelium and supporting sustentacular cells produces sudden anosmia, often associated with parosmia ("things smell wrong") during recovery. Most patients recover spontaneously within several weeks to a few months. The subset whose smell loss persists beyond six months has lower spontaneous recovery rates and benefits from active treatment.
Sinonasal / inflammatory
Nasal polyps, chronic rhinosinusitis with eosinophilic inflammation, and severe allergic inflammation all reduce smell by blocking odorant access to the olfactory cleft. This category is the most treatable because the underlying mechanism is mechanical — once the airway to the olfactory epithelium is restored (with topical steroids, surgery, or biologics), smell recovers. Chronic rhinosinusitis with polyposis is the most common surgically reversible cause.
Post-traumatic
Head trauma can shear the olfactory nerve filaments where they pass through the cribriform plate. The injury is often invisible on routine imaging. Recovery, when it occurs, is gradual — measured in months to a few years. Olfactory training is the mainstay of treatment.
Neurodegenerative
Anosmia can precede the motor symptoms of Parkinson's disease by years, and can precede the cognitive symptoms of Alzheimer's disease similarly. Unilateral, progressive smell loss in older adults — particularly when paired with other subtle neurologic findings — warrants neurologic referral. This is not common, but it's important not to miss.
Structural / mass lesions
Tumors of the anterior skull base — particularly esthesioneuroblastomas and meningiomas — can present with unilateral, progressive smell loss. MRI of the brain with attention to the anterior cranial fossa identifies these. Imaging is part of the workup for any persistent unilateral anosmia.
Other
Medications (some antihypertensives, antibiotics, and chemotherapy agents), chemical exposure (chronic occupational), congenital anosmia (Kallmann syndrome and isolated congenital anosmia), and idiopathic anosmia round out the differential. The history alone usually distinguishes among these.
Measure first, then treat.
Patients often arrive with a vague sense that their smell is "not quite right" — sometimes from years ago. The first job of the workup is to quantify the loss objectively, then to identify a treatable cause.
Validated smell testing
The UPSIT (University of Pennsylvania Smell Identification Test) and Sniffin' Sticks are validated, standardized instruments that take ten to fifteen minutes in the office. They distinguish anosmia from hyposmia from normal smell, and they establish a baseline against which to measure treatment response. Without an objective baseline, "did my smell get better" becomes a vibes-based question.
Focused history and endoscopy
Onset (sudden vs. gradual), preceding illness, head trauma history, prior sinus disease, medications, occupational exposure, and any neurologic symptoms anchor the differential. Nasal endoscopy at the visit visualizes the olfactory cleft, identifies polyps or inflammation, and rules out a structural cause within the nose.
Imaging — when warranted
MRI of the brain with attention to the olfactory bulbs and anterior cranial fossa is ordered for unilateral or progressive smell loss, when the history is unclear, or when a central or structural cause is on the differential. CT of the sinuses is added when sinonasal disease is the suspected driver.
Selective additional workup
For patients with concerning neurologic features, referral to neurology for evaluation of an early neurodegenerative prodrome. For patients with eosinophilic features, allergy testing and peripheral eosinophil count to evaluate for biologic candidacy.
Olfactory training, plus what fits the cause.
Olfactory training (smell rehabilitation)
The best-supported therapy for post-viral and post-traumatic anosmia. Structured exposure to a small set of distinct odorants — classically rose, eucalyptus, lemon, and clove — twice daily for at least three to six months. Each session is brief (about fifteen seconds per odorant) with intentional focus and recall. Multiple randomized trials show meaningful improvement compared to no treatment. The mechanism is thought to be neural recovery driven by repeated stimulation of olfactory pathways — neuroplasticity in the olfactory epithelium itself. Olfactory training is safe, low-cost, and the universal first-line therapy in our practice.
Topical intranasal corticosteroids
For inflammatory or sinonasal causes, topical steroids — particularly delivered via saline irrigation rather than metered-dose spray — reach the olfactory cleft far more effectively than aerosol formulations. Combined with olfactory training, this is the foundation for post-viral patients with any inflammatory component.
Endoscopic sinus surgery — for obstructive causes
When the cause is mechanical obstruction (large polyps, severe sinonasal disease, anatomic narrowing of the olfactory cleft), endoscopic surgery directly opens the pathway to the olfactory epithelium. For appropriately selected patients, smell recovery after surgery for polypoid disease is often dramatic and rapid. Patients with eosinophilic polypoid disease may benefit from concurrent biologic therapy to prevent recurrence.
Research-stage therapies
Platelet-rich plasma (PRP) injections into the olfactory cleft, theophylline supplementation, and novel topical agents are all under active investigation for post-viral and idiopathic anosmia. Some have promising early data; none are yet standard of care. We discuss research options during consultation and can connect interested patients with active trials at Mount Sinai.
What we generally don't recommend
Over-the-counter zinc supplementation — and especially zinc-containing intranasal sprays — should be avoided, as some formulations have been associated with worsening of smell loss. Heroic doses of vitamins and "smell cure" supplements lack supporting evidence. Olfactory training is more effective than any of these, costs nothing, and has no downside.
Earlier is better.
Smell loss is most treatable when addressed early. Specialist evaluation is appropriate when:
- Smell loss persists beyond three to four months after a viral illness
- Onset is gradual or progressive without an obvious viral or traumatic trigger
- Loss is unilateral (only one nostril)
- Smell loss is accompanied by other neurologic symptoms, headaches, or vision changes
- You've been told it's "just sinuses" but symptom relief from typical sinus treatments hasn't restored smell
- You've started noticing distorted smell (parosmia) — particularly when familiar foods or scents smell unpleasant
Anosmia is not benign just because it doesn't hurt. Loss of smell is associated with lower quality of life, depression, food safety risks (missed smoke, gas leaks, spoiled food), and — in older adults — increased all-cause mortality. It's worth taking seriously.
Common questions, direct answers.
I lost my sense of smell after COVID-19 — will it come back?
Most patients with post-COVID anosmia recover spontaneously within several weeks to a few months. For the subset whose smell loss persists beyond six months, recovery becomes less likely without active treatment. Olfactory training — structured, twice-daily exposure to a defined set of odorants — is the best-supported therapy and is most effective when started within the first year.
What's the difference between anosmia, hyposmia, parosmia, and phantosmia?
Anosmia is the complete absence of smell. Hyposmia is reduced sense of smell. Parosmia is distorted smell perception — familiar odors smell wrong, often unpleasant (a common phase of post-COVID recovery). Phantosmia is the perception of smells that aren't actually there. All four are forms of olfactory dysfunction and warrant evaluation when persistent.
Is loss of smell ever a sign of something serious?
Yes, occasionally. Anosmia can be an early sign of Parkinson's disease or Alzheimer's disease — often appearing years before motor or cognitive symptoms. It can also indicate a tumor at the anterior skull base, particularly when it is unilateral and progressive. Specialist evaluation distinguishes benign causes (sinus inflammation, post-viral injury) from those that warrant neurologic or imaging workup.
What is olfactory training, and does it actually work?
Olfactory training is structured exposure to a small set of distinct odorants (classically rose, eucalyptus, lemon, and clove) twice daily for at least three to six months. Each session is brief — about fifteen seconds per odorant, with intentional focus and recall. Multiple randomized trials show meaningful recovery rates compared to no treatment, particularly for post-viral and post-traumatic anosmia. It's safe, low-cost, and the first-line therapy in most evaluations.
Can surgery restore my sense of smell?
Yes, when the cause is obstructive — most commonly large nasal polyps blocking odorants from reaching the olfactory cleft. Endoscopic sinus surgery, often paired with biologic therapy in eosinophilic disease, restores smell in a meaningful fraction of these patients. Surgery does not restore smell when the cause is neural injury (post-viral, post-traumatic, or neurodegenerative) — though research on neural recovery is active.
I heard about PRP injections for anosmia — is that real?
Platelet-rich plasma (PRP) injections into the olfactory cleft are an active area of research for post-viral anosmia. Early-phase studies show promising results, but the therapy is still investigational and not yet standard of care. Patients interested in research-stage options can ask about active clinical trials at Mount Sinai.