1. What is a smell disorder?
A smell disorder — medically summarised as dysosmia — describes any change in the normal perception of smell. This ranges from a slight reduction through distorted perception of individual scents to a complete loss of the sense of smell (anosmia). In Germany, about 5 per cent of the population are affected by a relevant smell disorder, from age 65 even up to 25 per cent — many of them without a medical assessment.
Smell disorders are often underestimated — by those affected and by those treating them. Yet they influence quality of life as strongly as hearing loss or loss of vision: eating loses its appeal, safety risks increase (burnt food, gas, smoke go unnoticed), emotional experience changes (scents are closely linked with memories), and social situations such as cooking, wine or cheese tasting lose their depth. Studies show increased rates of depression and reduced life satisfaction in people with anosmia.
With the COVID-19 pandemic, the smell disorder suddenly moved into public consciousness — it was one of the most characteristic symptoms of the illness and to this day affects millions of people worldwide in the post-Covid phase. At the same time, a smell disorder can be the early sign of serious neurological diseases — Parkinson's disease and Alzheimer's dementia often begin with a gradual, for years unrecognised reduction in smell.
2. How does the sense of smell work?
The sense of smell is neuroanatomically fascinating: in the upper area of the nasal cavity, at the so-called olfactory epithelium, sit about 350 different smell receptors — a far greater variety than with the sense of taste with its only 5 basic qualities. These receptors recognise different scent molecules and send the information via the olfactory nerve (the 1st cranial nerve) directly to the brain — without the 'detour' via other brain structures that most other senses take.
This direct connection to the limbic system explains why smells are so strongly linked with emotions and memories — the scent of a perfume or an old chalkboard can call up whole worlds of experience. At the same time, the anatomy makes the sense of smell vulnerable: the thin olfactory epithelium has direct contact with the outside world and is unprotectedly exposed to pollutants, viruses, bacteria and injuries.
Important to understand: we smell via two routes — orthonasally when actively breathing in through the nose and retronasally when eating, when scent substances rise from the mouth and throat space. The latter makes up about 80 per cent of what we perceive as 'taste' — hence the close connection to taste disorders. Anyone who can no longer smell properly automatically tastes less.
3. Forms of smell disorder
ENT medicine distinguishes clearly defined forms that are diagnostically and therapeutically relevant:
- Anosmia: a complete loss of the sense of smell — no longer being able to smell anything
- Hyposmia: reduced smell perception — the most common form, often setting in gradually
- Hyperosmia: increased smell sensitivity — rare, with pregnancy, migraine or certain neurological diseases
- Parosmia: distorted smell perception — known scents are perceived wrongly or unpleasantly (coffee smells of petrol)
- Phantosmia: smell perception without an external stimulus — usually unpleasant scents (burnt, foul, chemical) without a source
- Cacosmia: everything or almost everything smells unpleasant — a special form of parosmia
- Specific anosmia: loss of only individual scent qualities — e.g. the genetic inability to smell sweat odour (androstenone)
Clinically particularly distressing are parosmia and phantosmia — which have become considerably more common through SARS-CoV-2. Patients report in part for years of unbearable smell distortions that can make every meal a torment. These forms are often harder to treat than simple anosmia.
4. Post-Covid: the most common cause of recent years
SARS-CoV-2 infects the supporting cells of the olfactory mucosa and leads in a large part of those ill to an acute smell disorder. Depending on the virus variant, this affects 30 to 80 per cent of all COVID-19 patients — and thereby millions of people worldwide.
Acute course: the loss of smell typically occurs in the first days after the onset of symptoms, often as an isolated early symptom without further complaints. Most of those affected recover completely within 1 to 4 weeks. In a relevant proportion — about 5 to 10 per cent — the complaints persist, however, longer than 6 months.
Post-Covid phase: characteristic here are not rarely parosmias and phantosmias — coffee suddenly smells of petrol, meat of decay, onions of chemicals. These distortions can be agonising and ruin eating. They are a sign that the olfactory neurons are regenerating — but are at first still faultily 'wired'. Patience is decisive here: studies show that even after 1 to 2 years, marked improvements are still possible.
Therapy of post-Covid anosmia: what is effectively proven is above all olfactory training (see separate chapter further below). With a proven zinc deficiency, substitution can be sensible. Steroids (oral or as a nasal spray) have shown a limited effect in studies — only recommended with a clear sinusitis component. A specialised smell consultation can offer individual therapy options, e.g. plasma injections or local pentoxifylline applications — both off-label.
5. Chronic sinusitis and nasal polyps
The second most common cause after post-viral smell disorders — above all chronic rhinosinusitis with nasal polyps (CRSwNP). Polyps are benign, grape-like mucosal growths in the nasal cavity that mechanically block the access of scent substances to the olfactory epithelium. About 4 per cent of the population are affected — men twice as often as women. Common associations: bronchial asthma, ASA intolerance (Samter's triad), eosinophilic inflammations.
Symptoms: a gradual or fluctuating loss of smell, obstructed nasal breathing, a feeling of pressure in the face, postnasal drip, a compulsion to clear the throat, frequent bouts of sinusitis. The diagnosis is made by ENT nasal endoscopy and a CT of the sinuses.
Therapy: highly effective corticosteroid sprays as first-line therapy, nasal rinses with isotonic or hypertonic saline solution, with pronounced polyps operative removal (FESS — functional endoscopic sinus surgery). With severe eosinophilic CRSwNP, for some years there have been biologics (dupilumab, mepolizumab, omalizumab) — they show a very good effect on the sense of smell and polyp size.
6. Traumatic brain injury as a cause
Traffic accidents, falls, sports injuries — wherever a traumatic brain injury occurs, the fine smell fibres that run through the cribriform plate from the olfactory epithelium to the olfactory bulb can tear off. Even minor traumas with mild loss of consciousness can lead to anosmia — sometimes noticed directly, sometimes only days to weeks later.
Prognosis: post-traumatic smell disorders recover more slowly than post-viral ones — within 1 to 2 years a partial recovery is possible, but about half of those affected retain a relevant residual anosmia. Olfactory training can be helpful here too.
Forensic significance: a traumatically caused anosmia is a significant impairment for professions requiring a sense of smell (cooks, sommeliers, perfumers, firefighters, food chemists) and can be relevant in insurance law. An objective smell test by an ENT doctor is important here.
7. Smell disorder as an early sign of Parkinson's
About 90 per cent of all people with Parkinson's disease have a relevant smell disorder — often years, sometimes decades before the first motor symptoms (resting tremor, bradykinesia, rigidity). The smell disorder is among the earliest neuropathological changes — even in the olfactory bulb and in neighbouring brain regions, Lewy bodies are found, the typical protein deposits of Parkinson's disease.
Clinical significance: an isolated anosmia without sinusitis, without preceding trauma and without other explanation — above all in middle or older adulthood — should direct suspicion towards a prodromal Parkinson's disease. Further early signs are: REM sleep behaviour disorder with markedly active dreaming, constipation, mood swings and depression, mild cognitive changes, increased sweating.
What to do: an isolated anosmia alone does not justify a Parkinson's diagnosis — it is too unspecific. With accumulated prodromal signs, a neurological consultation with targeted examination (a motor test, DAT-SPECT if needed) can be sensible. Currently there is no established preventive therapy, but lifestyle factors (exercise, a healthy diet, social activity) are considered protective. More under tremor.
8. Alzheimer's dementia and other neurodegenerative diseases
With Alzheimer's dementia too, a smell disorder often precedes the clinical symptoms by years. The damage begins near the olfactory cortex, which is among the earliest affected brain regions. Studies show that a pronounced anosmia markedly increases the risk of a later dementia — it is, however, too unspecific to serve as the sole screening tool.
Further neurological causes: multiple sclerosis (in relapses), strokes in certain regions, brain tumours (above all meningiomas in the front skull area), epilepsy (in rare cases with an olfactory aura). An MRI examination is sensible with an unclear one-sided or neurologically suspicious smell disorder.
When to see a doctor: smell disorder over 4 weeks, one-sided, with neurological symptoms, accompanying symptoms or a considerable loss of quality of life
