Parosmia

Qualitative distortion of smell perception in the presence of an odorant, in which a familiar smell is perceived as different and, almost always, unpleasant. It is distinguished from phantosmia, which is the perception of a smell with no odorant present, and from cacosmia, which is the perception of a genuinely present foul smell.

Mechanism

Two complementary explanations are supported.

• Peripheral: after injury, olfactory receptor neurons regenerate from basal stem cells, but the regenerating axons make disordered connections to the glomeruli of the olfactory bulb. The odorant map is therefore miswired, and a given molecule activates the wrong combination of glomeruli, producing a coherent but incorrect percept. Partial regeneration means only some receptor subtypes are restored, so the brain receives an incomplete pattern that it interprets as a different, usually aversive, smell.
• Central: altered processing and reduced top down modulation in the piriform and orbitofrontal cortex, with reduced olfactory bulb volume and altered functional connectivity.

The strong bias toward unpleasant distortions probably reflects the fact that incomplete or unfamiliar odour patterns default to an aversive interpretation, which is protective in evolutionary terms.

Prognostic significance

Parosmia is a marker of regeneration, not of deterioration. Its appearance during recovery from post viral or post traumatic olfactory loss predicts better eventual recovery. This is a genuinely reassuring point for patients who experience it as a worsening of their condition.

Causes

• Post viral, which is the commonest, and which became far more prevalent after SARS-CoV-2. Onset is typically 2 to 6 months after the initial loss, in the recovery phase.
• Head trauma, appearing during recovery.
• Chronic rhinosinusitis and nasal polyps.
• Neurodegenerative disease, particularly Parkinson disease.
• Temporal lobe epilepsy, which more often produces phantosmia in the form of an olfactory aura, and which requires exclusion when the episodes are stereotyped and brief.
• Toxin and drug exposure.
• Migraine.
• Psychiatric disorders, in which olfactory hallucination occurs in psychotic illness and severe depression, and which requires a different approach.
• Iatrogenic after sinus and skull base surgery.

Trigger foods

Certain substances are near universal triggers: coffee, roasted or fried meat, onion, garlic, chocolate, eggs, toothpaste, mint, citrus, and cooking odours. Coffee and meat are the most frequently reported and are the most disabling because they are unavoidable in shared living and working environments.

• Distorted perception of familiar smells, described as rotten, sewage, chemical, burning, metallic, or a smell the patient cannot name but finds intensely aversive.
• Almost always unpleasant. Pleasant distortion, or euosmia, is rare.
• Onset typically during recovery from a period of reduced or absent smell, which is a key historical point.
• Severe impact on eating, since retronasal olfaction distorts flavour. Patients avoid entire food groups, and weight loss is common and can be marked.
• Nausea and retching provoked by trigger foods, which makes food preparation and family meals difficult.
• Avoidance of restaurants, cooking, supermarkets, and social eating, with substantial social withdrawal.
• Anxiety and depression, which are common and severe in this group, and which are frequently dismissed by clinicians who underestimate the impact of a symptom that sounds minor.
• Concern about personal hygiene and about the smell of a partner, which strains relationships.
• Occupational impact for those working with food, in healthcare, or in any environment with strong odours.

History that localises the cause

• Preceding viral illness or head injury and the interval to onset.
• Whether it is triggered by odorants, which indicates parosmia, or occurs spontaneously without an odorant, which indicates phantosmia.
• Stereotyped, brief, spontaneous episodes with altered awareness, automatisms, déjà vu or a rising epigastric sensation, which indicate temporal lobe epilepsy and require neurological assessment.
• Nasal symptoms suggesting sinonasal disease.
• Neurological and cognitive symptoms.
• Psychiatric history and features of psychosis or severe depression.
• Weight change and dietary restriction, which must be quantified.

• Objective olfactory testing with threshold, discrimination and identification, which typically shows reduced quantitative function alongside the qualitative distortion. Standard tests do not measure parosmia directly, and validated parosmia specific questionnaires or structured symptom instruments should be used alongside.
• Nasal endoscopy in every patient, examining the olfactory cleft.
• Computed tomography of the sinuses where sinonasal disease is suspected.
• Magnetic resonance imaging of the brain and olfactory apparatus where there is no clear post viral or post traumatic explanation, where the symptom is unilateral, where there are neurological signs, or where epilepsy is suspected. Reduced olfactory bulb volume is a common finding and correlates with severity.
• Electroencephalography where the pattern suggests temporal lobe seizures.
• Blood tests as for anosmia: glucose, thyroid function, vitamin B12, zinc, renal and liver function.
• Neurology referral for suspected epilepsy or neurodegenerative disease, and psychiatric referral where olfactory hallucination occurs in the context of psychosis or severe depression.
• Nutritional assessment with documented weight, since weight loss in this condition is frequently substantial and unmeasured.

Distinguishing parosmia from its mimics

• Phantosmia: no odorant present, often constant or episodic, more likely to be neurological or psychiatric in origin.
• Cacosmia: a genuine foul smell exists, from chronic rhinosinusitis, a foreign body, a rhinolith, dental infection, atrophic rhinitis or a tumour. Endoscopy identifies it, and treating the source resolves it.
• Olfactory hallucination in psychosis, usually with other psychotic features and often with a delusional interpretation.
• Olfactory aura in epilepsy, which is brief, stereotyped and paroxysmal.

There is no specific pharmacological cure, and management combines olfactory training, dietary strategy, nutritional support and psychological care. Acknowledging the severity of the impact is itself a therapeutic act, since many patients have been told it is trivial.

Explanation and reassurance

• Explain the mechanism plainly: nerves are regrowing and are temporarily connected to the wrong places, and the brain is receiving a scrambled signal.
• Explain that parosmia usually indicates recovery in progress and predicts better eventual outcome. This reframing changes the experience for most patients.
• Give a realistic timeline: most post viral parosmia improves over 6 to 24 months, though a minority persists longer.

Olfactory training

• The same protocol as for anosmia and hyposmia, and the intervention with the best evidence in parosmia specifically.
• Four odorants twice daily for 20 to 30 seconds each, for at least 12 weeks and preferably 6 to 12 months, with the set changed every 12 weeks.
• Where an odorant is a severe trigger, substitute a tolerable one rather than abandoning training.
• Training appears to accelerate the correction of the disordered mapping.

Dietary and practical strategies, which produce the most immediate relief

• Identify and temporarily avoid trigger foods, most often coffee, roasted meat, onion, garlic, eggs and chocolate, while maintaining nutritional intake.
• Eat cold or room temperature food, which releases fewer volatile molecules than hot food.
• Use bland foods with intact texture and basic taste: plain rice, pasta, potato, yoghurt, cheese, bread, and unflavoured protein sources.
• Use a nose clip while eating, which eliminates retronasal olfaction and allows the patient to eat.
• Avoid cooking where the odours are triggering, and use extraction and ventilation.
• Change toothpaste to an unflavoured or children's variety where mint is a trigger, and change soaps and detergents to unscented products.
• Reintroduce trigger foods gradually over months as tolerance returns, since permanent avoidance is neither necessary nor desirable.

Nutritional support

• Weigh at every visit and refer to a dietitian where there is weight loss, restricted intake or a narrow food range.
• Nutritional supplements where intake is inadequate, chosen for palatability.
• Attend specifically to protein and micronutrient intake in patients with prolonged restriction.

Psychological support

• Screen for depression and anxiety in every patient. The prevalence is high and the symptom is genuinely distressing.
• Refer for cognitive behavioural therapy where distress is significant, which helps with the avoidance behaviour and the anticipatory anxiety around eating.
• Patient support groups are valuable in this condition, both practically and in reducing the isolation that comes from a symptom that others cannot perceive.
• Involve the family, since parosmia affects meals, cooking and intimacy, and partners frequently do not understand it.

Pharmacological and interventional options

• Treat any underlying sinonasal disease with topical and, where indicated, oral corticosteroid.
• Oral corticosteroid trial where an inflammatory component is suspected, with limited evidence for benefit in isolated parosmia.
• Sodium citrate nasal spray, gabapentin and other agents have been trialled with weak evidence and should not be presented as established treatment.
• Platelet rich plasma injection into the olfactory cleft and intranasal insulin are under investigation with early positive data.
• Surgical excision of olfactory epithelium or bulbectomy has been described for intractable phantosmia, and is a last resort with permanent anosmia as the certain outcome. It has essentially no role in parosmia.
• Treat epilepsy or psychiatric disease specifically where these are the cause.

Follow up

Review at 3 to 6 month intervals with repeat objective testing and structured symptom assessment, together with weight. Reinforce olfactory training adherence, which declines over time and which is the intervention most likely to help. Reassess for an alternative diagnosis where the pattern changes or where symptoms progress rather than improve.