Smell Disorders and Anosmia
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Direct answer
Smell disorders split into conductive (transport) loss — odour molecules never reach the olfactory epithelium because polyps, rhinitis, tumours or septal deviation block the nasal airway — and sensorineural loss, where the olfactory neuroepithelium or its central connections are destroyed by viral injury, head trauma, toxins, tumours or congenital aplasia. History alone separates most cases: gradual loss with nasal obstruction suggests conductive disease, treatable by clearing the airway, while sudden loss after influenza-like illness (notoriously including COVID-19) or after head injury suggests sensorineural damage with guarded recovery. Quantitative testing uses validated smell identification kits, and every unexplained anosmia deserves nasal endoscopy plus — where central lesions are suspected — imaging of the anterior skull base.
What you must remember
- Vocabulary: anosmia (no smell), hyposmia (reduced), parosmia (distorted smell of present odours), phantosmia (smell without a stimulus), cacosmia (foul odour perception) and congenital versus acquired loss — definition questions appear in short-answer papers.
- Three commonest acquired causes: upper respiratory infection (post-viral anosmia), head trauma tearing olfactory filaments at the cribriform plate, and sinonasal disease — sinonasal disease being the only fully reversible group.
- Conductive mechanisms: nasal polyposis, chronic rhinosinusitis, marked septal deviation, turbinate hypertrophy and nasal tumours — endoscopy and computed tomography paranasal sinuses settle these, and treatment restores smell.
- Sensorineural mechanisms: post-viral (including SARS-CoV-2 anosmia, usually recovering within weeks), traumatic shearing of olfactory axons (anosmia proportionate to injury severity, often permanent), congenital absence — Kallmann syndrome pairs anosmia with hypogonadotropic hypogonadism and is a standing multiple-choice answer.
- Foster Kennedy syndrome: frontal lobe tumour causing ipsilateral optic atrophy from direct pressure, contralateral papilloedema from raised intracranial pressure and ipsilateral anosmia — the classical triory of signs examiners ask you to complete.
- Testing tools: University of Pennsylvania Smell Identification Test (UPSIT), Sniffin' Sticks, and simpler alcohol-sniff thresholds; smell is the one special sense testable with a strip at the bedside and should be part of any cranial-nerve examination where relevant.
- Management reality: treat the conductive causes surgically or medically; sensorineural loss has no proven pharmacological rescue — smell training (repeated deliberate exposure to defined odours) has supportive evidence and is the standard recommendation; safety counselling about gas, smoke and spoiled food matters practically.
Working through two contrasting consultations
A 34-year-old man reports two years of fading smell with heavy nasal blockage and snoring. Endoscopy shows polyps filling both middle meati; computed tomography confirms pansinusitis with an obliterated olfactory cleft. This is transport anosmia: a course of oral corticosteroids followed by continued intranasal steroid and endoscopic sinus surgery to open the olfactory cleft gives him a genuine chance of restored smell — the cleft must be specifically cleared, or smell recovery is incomplete even when breathing improves.
Contrast a 26-year-old woman whose smell vanished with a febrile illness eight months ago and never returned; her nasal airway and endoscopy are normal, and magnetic resonance imaging shows no mass. This is post-viral sensorineural anosmia. There is no blockage to relieve, so the plan shifts to structured smell training — twice-daily supervised exposure to rose, lemon, clove and eucalyptus odours over months — with honest counselling that recovery is partial and slow when present at all, and safety advice about smoke and gas. The pair of cases carries the entire logic of the topic: same symptom, entirely different disease, opposite prognoses.
Where examiners dig
The viva favourite is localisation: anosmia with visual field loss or endocrine dysfunction moves the problem from nose to skull base — craniopharyngioma, olfactory groove meningioma or esthesioneuroblastoma — and imaging changes accordingly. The second probe is Kallmann syndrome: anosmia plus absent puberty from gonadotropin-releasing hormone neuron migration failure, tested with the smell bottles at the bedside of a delayed-puberty clinic patient. Third, the trauma question: why does occipital head injury cause anosmia? Contre-coup shearing of the delicate olfactory filaments as they cross the cribriform plate — anosmia after head injury is commoner than the textbook-thin coverage suggests, and it is frequently missed because nobody asks.
Frequently asked questions
How are conductive and sensorineural anosmia differentiated?
Conductive loss blocks odour delivery — polyps, rhinitis, tumours — with nasal symptoms and endoscopic findings; sensorineural loss destroys the neuroepithelium or central pathways, with a history of viral illness, toxin or head injury and a normal nasal airway.
What is Kallmann syndrome?
Congenital hypogonadotropic hypogonadism with anosmia, from failed migration of gonadotropin-releasing hormone neurons and olfactory axons — a classic link between smell and endocrinology.
What is Foster Kennedy syndrome?
Ipsilateral anosmia and optic atrophy with contralateral papilloedema, produced by a frontal-lobe tumour compressing the olfactory tract and optic nerve while raising intracranial pressure.
How is smell tested objectively?
Validated identification tests such as UPSIT or Sniffin' Sticks, or bedside alcohol-sniff threshold testing — comparing side to side and against age norms.
What treatment exists for post-viral sensorineural anosmia?
Structured smell training with repeated exposure to a fixed set of odours over months has the best supportive evidence; pharmacological rescue is unproven, and counselling includes smell-related safety precautions.