Anosmia

Anosmia — the complete loss of the sense of smell — and its partial form, hyposmia, are among the most underappreciated and under-treated conditions in medicine. Until COVID-19 brought olfactory dysfunction to widespread public attention, loss of smell was frequently dismissed by patients and clinicians alike as a minor inconvenience. In fact, the consequences of anosmia can be profound: impaired ability to detect gas leaks, smoke, and spoiled food creates real safety risks; the loss of flavour perception (since approximately 80% of what we perceive as “taste” is in fact aroma perceived retronasally) significantly diminishes the pleasure of eating; and the emotional and quality-of-life burden of living without smell is substantially greater than most patients anticipate before they experience it.

All new-onset anosmia or hyposmia warrants assessment by an ENT specialist — not because the cause is always serious, but because some causes are treatable and the window for effective treatment may be time-limited.

The Olfactory System — How Smell Works

Smell detection begins when inhaled airborne molecules (odorants) reach the olfactory epithelium — a specialised patch of sensory tissue covering approximately 2–3 cm² of the roof of the nasal cavity at the level of the cribriform plate. The olfactory epithelium contains approximately 6–10 million olfactory receptor neurons, each of which expresses one of approximately 400 functional olfactory receptor proteins. These receptors are members of the G-protein coupled receptor superfamily and bind odorant molecules with varying selectivity, generating electrical signals that travel along the olfactory nerve (cranial nerve I) through the cribriform plate directly into the olfactory bulb of the brain — one of the shortest and most direct neural pathways in the nervous system.

The olfactory pathway is unique among sensory systems in that it projects directly to the limbic system (amygdala, hippocampus) and orbitofrontal cortex, without passing through the thalamic relay nucleus that mediates all other senses. This explains the powerful emotional and mnemonic associations of smell — why a specific aroma can instantly and involuntarily trigger a vivid memory or emotional state. It also explains why olfactory loss affects emotional wellbeing so profoundly in many patients.

Olfactory receptor neurons are one of the few types of neuron in the adult body that can regenerate. New receptor neurons are continuously generated from basal stem cells in the olfactory epithelium, replacing neurons that are damaged by viral infections, environmental toxins, or normal ageing. This regenerative capacity underlies the potential for recovery from olfactory loss — but it is not unlimited, and the ability to regenerate declines with age.

Classification of Olfactory Disorders

By Degree

• Anosmia: Complete absence of smell perception
• Hyposmia: Reduced smell perception — odorants can be detected but at higher than normal concentrations
• Parosmia: Distorted smell perception — a known odour is perceived as a different, usually unpleasant smell. A common feature of recovery from post-viral olfactory loss, where regenerating neurons initially make incorrect connections
• Phantosmia: Perception of a smell in the absence of any external odorant — an olfactory hallucination. May arise from irritation of the olfactory epithelium or central olfactory pathway disease
• Cacosmia: Perception of everything as having a foul or unpleasant smell

By Mechanism

Causes of Anosmia and Hyposmia

Nasal Polyps and Chronic Rhinosinusitis

The most common cause of conductive anosmia in adults. Nasal polyps arising from the ethmoid sinuses frequently extend into the olfactory cleft — the narrow space at the roof of the nasal cavity adjacent to the olfactory epithelium — and mechanically obstruct odorant access to the receptor neurons. Even without complete cleft obstruction, the chronic eosinophilic inflammatory milieu of CRS with nasal polyps directly damages the olfactory epithelium, contributing a sensorineural component. Anosmia is the cardinal symptom most closely correlated with polyp disease and is a primary driver of treatment-seeking in many CRS patients. Treatment of the underlying CRS — medically and surgically — can substantially restore olfaction, though the sensorineural component may recover more slowly and incompletely than the conductive component.

Post-Viral Olfactory Loss

Viral upper respiratory infections have long been recognised as a common cause of post-infectious anosmia — accounting for approximately 20–30% of all anosmia cases in most pre-COVID series. COVID-19 brought this mechanism to international attention by causing sudden, profound olfactory loss in a very high proportion of infected patients — estimated at 60–80% in the Alpha strain, somewhat lower with subsequent variants. The mechanism of COVID-19-related anosmia differs from other viral causes: rather than directly infecting olfactory receptor neurons (which do not express the ACE2 receptor to a significant degree), SARS-CoV-2 infects supporting cells of the olfactory epithelium, causing a secondary inflammatory response that disrupts receptor neuron function. This explains the rapid onset and, in most patients, eventual recovery.

The majority of patients with COVID-19-related anosmia recover within weeks to months. A minority — estimated at 5–10% — experience persistent olfactory dysfunction lasting more than a year. These patients may experience parosmia (distorted smell) as the first sign of recovering but incorrectly remapping olfactory neurons, which is a positive prognostic sign but can be profoundly unpleasant in itself. Olfactory training (structured daily exposure to four reference odorants) has the strongest evidence base for promoting recovery and should be commenced early.

Head Trauma

Traumatic anosmia follows head injury in approximately 5–15% of significant head injuries, depending on the mechanism. The olfactory nerve filaments passing through the perforations of the cribriform plate are vulnerable to shear injury even without direct orbital or facial trauma — a deceleration injury that accelerates the brain relative to the skull base can stretch and tear these delicate filaments. Post-traumatic anosmia has a less favourable prognosis for recovery than post-viral anosmia, because the structural injury to the nerve filaments is more severe and the regenerative response more limited. Patients with post-traumatic anosmia should nonetheless be offered olfactory training and appropriate follow-up.

Age-Related (Presbyosmia)

Olfactory sensitivity declines progressively with age — this is one of the most reproducible and universal findings in olfactory research. More than 50% of people over 65 years of age have measurable olfactory impairment on objective testing, though many are unaware of it. This decline reflects both peripheral changes (reduced density of receptor neurons from cumulative damage, reduced mucosal perfusion) and central changes (reduced olfactory bulb volume, central processing changes). Age-related olfactory loss is rarely complete (anosmia) but the progressive reduction in sensitivity and ability to discriminate odours is clinically significant. It contributes to food-related malnutrition in elderly patients (reduced appetite and food enjoyment) and increased risk of gas leak accidents.

Medications

A substantial number of medications can impair olfactory function, including ACE inhibitors, calcium channel blockers, some antihypertensives, antihistamines, antibiotics (particularly aminoglycosides), anti-thyroid medications, nasal decongestant sprays (with prolonged use), and chemotherapy agents. Medication review by the prescribing GP or specialist is appropriate when drug-induced anosmia is suspected.

Neurological Causes

Anosmia is an early and sometimes presenting symptom of Parkinson’s disease and Alzheimer’s dementia — olfactory dysfunction precedes motor symptoms in Parkinson’s by up to a decade in some patients, reflecting early alpha-synuclein deposition in the olfactory bulb. Olfactory testing is therefore not only an ENT concern — it is a potential early biomarker for neurodegenerative disease. Olfactory groove meningioma and other anterior cranial fossa tumours compressing the olfactory tracts are rare but important to exclude in patients with unexplained unilateral anosmia.

Assessment

History

The assessment begins with a focused history: onset (sudden vs gradual), laterality (unilateral vs bilateral), any preceding infection or head injury, whether taste is affected, whether parosmia or phantosmia are present, any previous nasal surgery, relevant medications, and family history of anosmia. Sudden complete anosmia following an identifiable viral illness has a different significance from slowly progressive bilateral hyposmia developing over years without precipitant.

Nasal Endoscopy

Direct visualisation of the olfactory cleft — the most important single examination step. Polyps, mucosal oedema, crusting, or structural obstruction in the olfactory cleft can be directly identified. A normal-appearing olfactory cleft in a patient with anosmia suggests a sensorineural rather than conductive mechanism.

Objective Smell Testing

The University of Pennsylvania Smell Identification Test (UPSIT) — a standardised 40-item scratch-and-sniff smell identification test — provides an objective, validated score that documents the degree of olfactory loss and allows monitoring of recovery over time. It is available in Dr Roth’s consulting rooms. The Sniffin’ Sticks battery is an alternative test with threshold, discrimination, and identification components that provides a TDI score. Objective documentation of olfactory function is important both clinically and for medicolegal purposes following head injury.

CT and MRI

CT sinuses identifies polyps, mucosal thickening, and structural sinus disease. MRI of the olfactory apparatus (olfactory bulb and tract, anterior cranial fossa) is indicated in patients with unexplained anosmia without identified nasal cause, post-traumatic anosmia, or where a central cause is suspected. MRI can demonstrate olfactory bulb atrophy or aplasia, anterior cranial fossa lesions, and changes in the olfactory cortex.

Treatment

Conductive Anosmia — Treat the Obstruction

For patients with anosmia from nasal polyps or chronic rhinosinusitis, treatment of the underlying condition — medically and surgically — is the most effective intervention for restoring smell. Oral corticosteroids produce rapid (days) but temporary improvement in olfactory function in CRS with nasal polyps by reducing polyp bulk and olfactory cleft inflammation. Surgical removal of polyps and opening of the olfactory cleft at FESS provides more durable improvement. Post-operative topical corticosteroid therapy is essential to delay polyp recurrence and maintain olfactory function long-term. The new biological agents (dupilumab) produce substantial and sustained improvement in olfactory function in severe CRS with nasal polyps — anosmia improvement is one of the most dramatic and consistent benefits documented in the dupilumab clinical trials.

Olfactory Training

Olfactory training — also called smell training — is the most evidence-based intervention for sensorineural olfactory loss, including post-viral anosmia, post-COVID anosmia, and post-traumatic hyposmia. The protocol involves twice-daily structured sniffing of four reference odorants (rose, eucalyptus, lemon, and cloves — the original Hummel protocol) for at least twelve weeks. Each odorant is sniffed for approximately 20 seconds with focused attention on the experience. The repetitive, attentive exposure promotes neural plasticity and regeneration in the olfactory epithelium and central olfactory pathway. Multiple randomised controlled trials demonstrate benefit over observation alone. The effect is modest in absolute terms but meaningful for patients with no other treatment options, and the intervention is low cost, safe, and free of side effects.

An extended protocol using eight odorants (four high-familiarity and four less-familiar) appears more effective than the original four-odorant protocol and is now preferred by many centres.

Systemic and Topical Corticosteroids

For post-viral anosmia with a significant inflammatory component, systemic corticosteroids and topical nasal steroid drops (betamethasone drops delivered to the olfactory cleft in the head-down-forward position) may provide benefit. The evidence is less robust than for olfactory training but remains the most commonly used pharmacological adjunct.

Emerging Treatments

Platelet-rich plasma (PRP) injected into the olfactory cleft is under investigation as a potential treatment for refractory post-COVID anosmia, based on the hypothesis that growth factors in PRP may support olfactory neuron regeneration. Early data is promising but the evidence base remains preliminary. Omega-3 supplementation has also been proposed based on its role in neural membrane integrity. Both should be regarded as experimental pending further evidence.

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