Smell and taste
Smell and taste: olfactory pathway, taste buds, taste nerves and disorders
How olfactory neurons and taste buds work, which cranial nerves carry taste from each part of the tongue, and the central pathways, for FCPS Part 1. Covers anosmia after head injury, Kallmann syndrome, Bell palsy and drug-induced taste change.
Olfactory receptors
- The olfactory epithelium lies in the roof of the nasal cavity and upper septum. It contains olfactory receptor neurons (bipolar cells with cilia carrying odorant receptors), supporting cells, Bowman glands (mucus) and basal stem cells.
- Olfactory neurons are replaced throughout life (roughly every 1–2 months) from basal stem cells, which is unusual for neurons. Each neuron expresses one of about 400 receptor types.
- Odorants dissolve in mucus and bind G protein-coupled receptors coupled to G_olf, which raises cAMP and opens cyclic nucleotide-gated cation channels; Ca²⁺ then opens Cl⁻ channels and Cl⁻ efflux adds to depolarisation.
- Smell adapts rapidly, partly centrally.
Olfactory pathway
- Unmyelinated axons gather into about 20 olfactory filaments that pass through the cribriform plate of the ethmoid to the olfactory bulb, synapsing with mitral and tufted cells in glomeruli.
- The olfactory tract runs to the primary olfactory cortex (piriform cortex and uncus), amygdala and entorhinal cortex, then to the orbitofrontal cortex.
- Smell is the only sense that reaches the cortex without a thalamic relay, and its direct limbic connections explain why smells evoke strong emotions and memories.
Disorders of smell
- Head injury: a blow to the back of the head jolts the brain forward and back, shearing the olfactory filaments where they cross the cribriform plate (contrecoup injury); anterior cranial fossa fractures do the same and may leak CSF. Because flavour depends largely on smell, the patient often complains that food tastes bland.
- Kallmann syndrome: GnRH neurons fail to migrate from the olfactory placode to the hypothalamus with the olfactory axons, giving anosmia with hypogonadotrophic hypogonadism (delayed puberty, low LH, FSH and sex steroids); MRI shows absent or small olfactory bulbs and sulci.
- Others: viral upper respiratory infection, nasal polyps, ageing, early Parkinson and Alzheimer disease, olfactory groove meningioma (with Foster Kennedy syndrome).
- Uncinate fits: brief unpleasant olfactory hallucinations from temporal lobe (uncus) epilepsy.
Taste buds and taste qualities
- Taste buds sit on fungiform papillae (anterior tongue), foliate papillae (sides), circumvallate papillae (in front of the sulcus terminalis), and on the soft palate, epiglottis and pharynx. Filiform papillae are the most numerous but have no taste buds; they give the tongue its rough texture.
- Each bud has 50–100 taste receptor cells, replaced every 10–14 days.
| Quality | Stimulus | Mechanism |
|---|---|---|
| Salty | Na⁺ | Entry through epithelial Na⁺ channels (ENaC) |
| Sour | H⁺ | Proton channels; acid blocks K⁺ channels |
| Sweet | Sugars, sweeteners | GPCR (T1R2 + T1R3), gustducin |
| Umami | Glutamate | GPCR (T1R1 + T1R3) |
| Bitter | Quinine, many toxins | GPCRs (T2R family), gustducin |
- Every part of the tongue can detect every quality; the old "tongue map" is wrong. Bitter sensitivity is somewhat greater over the posterior tongue (circumvallate papillae), which protects against swallowing toxins and is why bitter quinine is felt most at the back.
- Salt appetite rises with adrenal insufficiency or after bilateral adrenalectomy without replacement (loss of aldosterone causes sodium wasting and salt craving).
Nerves carrying taste
| Region | Taste nerve | Route |
|---|---|---|
| Anterior two-thirds of tongue | Chorda tympani (facial, VII) | Travels with the lingual nerve, then through the middle ear to the geniculate ganglion |
| Posterior third, including circumvallate papillae | Glossopharyngeal (IX) | Through the jugular foramen; inferior ganglion |
| Epiglottis, root of tongue near it, pharynx | Vagus (X) | Inferior (nodose) ganglion |
| Soft palate | Greater petrosal nerve (VII) |
- General sensation of the anterior two-thirds is carried by the lingual nerve (V3); of the posterior third by IX. Motor supply of the tongue is hypoglossal (XII): a lesion makes the tongue deviate towards the side of the lesion on protrusion, with taste intact.
- Glossopharyngeal, vagus and accessory nerves all leave through the jugular foramen, so a lesion there causes loss of taste on the posterior third with weakness of shoulder elevation (trapezius) and sternocleidomastoid.
Central taste pathway
All taste fibres end in the rostral nucleus of the tractus solitarius (gustatory nucleus) in the medulla. Second-order fibres ascend ipsilaterally to the ventral posteromedial (VPM) nucleus of the thalamus, then to the primary gustatory cortex in the insula and frontal operculum (around Brodmann area 43). The NTS also feeds reflex salivation and gastric secretion.
| Feature | Smell | Taste |
|---|---|---|
| Receptor cell | True neuron, regenerates | Modified epithelial cell, regenerates |
| First central relay | Olfactory bulb | Nucleus of tractus solitarius |
| Thalamic relay | None before primary cortex | VPM nucleus |
| Primary cortex | Piriform cortex, uncus | Insula, frontal operculum |
| Main second messenger | cAMP (G_olf) | Varies: ion channels (salt, sour), GPCRs (sweet, bitter, umami) |
Disorders of taste
- Bell palsy (lesion of VII in the facial canal above the chorda tympani branch): loss of taste on the anterior two-thirds, with weakness of the whole half face, including the forehead, and often hyperacusis.
- Lingual nerve injury (third molar extraction, tongue surgery) damages chorda tympani fibres travelling with it: loss of taste and touch on the anterior two-thirds.
- Middle ear disease or surgery can damage the chorda tympani.
- Drugs: captopril and penicillamine contain a sulfhydryl (thiol) group that causes metallic or salty taste disturbance and taste loss; lisinopril, which lacks it, usually does not. Metronidazole gives a metallic taste; lithium and some chemotherapy drugs also alter taste.
- Zinc deficiency reduces taste; radiotherapy, smoking and ageing also blunt it.
- Frey syndrome (gustatory sweating after parotidectomy) is misdirected regrowth of parasympathetic fibres, not a taste disorder.
Remember Smell skips the thalamus; taste goes to the NTS and then VPM. Anterior tongue VII, posterior IX, epiglottis X.
Exam trap Loss of smell often presents as "loss of taste" because flavour depends on smell.
Exam trap The chorda tympani carries taste, but general sensation of the anterior tongue comes from the lingual nerve (V3).
How FCPS asks about this
- Loss of smell after a fall on the back of the head: shearing of olfactory filaments at the cribriform plate.
- Unusual feature of olfactory neurons: continuous replacement from basal stem cells.
- Anosmia with hypogonadism: Kallmann syndrome; small or absent olfactory bulbs.
- Taste from the anterior two-thirds: chorda tympani (VII); from the posterior third: glossopharyngeal (IX).
- First relay of all taste fibres: nucleus of the tractus solitarius, then VPM thalamus.
- Papillae without taste buds: filiform.
- Captopril taste disturbance: its sulfhydryl group.
Test yourself on this topic
5 of the 17 questions in our bank on this topic. Choose an answer to see why every option is right or wrong.
A 55-year-old man started on captopril for hypertension complains that food now tastes salty and metallic. Changing to lisinopril relieves it. Which feature of captopril is blamed for this effect?
Answer: Its sulfhydryl (thiol) group
Captopril has a sulfhydryl group, unlike most later ACE inhibitors such as lisinopril and enalapril. This group is linked to taste disturbance and rash, side effects shared with another thiol drug, penicillamine, possibly through binding of zinc and effects on taste receptor cells. Bradykinin build-up causes cough and angioedema in all ACE inhibitors. Captopril is an active drug, not a prodrug.
Captopril side effects
- Sulfhydryl group
- Taste disturbance, rash
- Bradykinin: cough, angioedema
- Switch to a non-thiol ACE inhibitor
Remember Thiol drugs spoil taste.
Exam trap Penicillamine causes taste loss by the same thiol mechanism.
Why the other options are wrong
- Its build-up of bradykinin Explains cough and angioedema, shared by all ACE inhibitors.
- Its prodrug ester structure Captopril is not a prodrug; enalapril is.
- Its potassium-sparing action Raised potassium does not explain this.
- Its blockade of AT1 receptors ACE inhibitors do not block AT1 receptors.
A man has brief episodes of an unpleasant smell of burning rubber followed by lip-smacking and impaired awareness. Where is the seizure focus?
Answer: Medial temporal lobe
Olfactory pathways project, without a thalamic relay, to the primary olfactory cortex in the uncus and piriform cortex, the amygdala and the entorhinal cortex of the medial temporal lobe. Focal seizures arising here can begin with olfactory or gustatory auras (unpleasant smells such as burning rubber), epigastric rising sensation, déjà vu or fear, followed by impaired awareness and automatisms such as lip-smacking (temporal lobe epilepsy, often from hippocampal sclerosis or tumour). MRI is needed to exclude a structural lesion. Occipital seizures cause visual phenomena; motor cortex seizures cause jerking that may march (Jacksonian).
Uncinate fits
- Olfactory cortex: uncus, piriform, amygdala
- No thalamic relay for smell
- Aura: unpleasant smell, déjà vu, epigastric rising
- Then automatisms (lip-smacking), impaired awareness
- Cause: hippocampal sclerosis, tumour → MRI
Remember A phantom burning smell points to the temporal lobe.
Why the other options are wrong
- Occipital lobe Visual aura.
- Primary motor cortex Clonic jerking.
- Cerebellum Not a seizure focus.
- Spinal cord Not a seizure focus.
A 66-year-old man with a left thalamic infarct has lost touch, pain and position sense over the right side of his body and face. His sense of smell is normal on both sides. Which of the following explains why smell is spared?
Answer: Smell reaches the cortex without a thalamic relay
Olfactory receptor neurons synapse on mitral and tufted cells in the olfactory bulb, whose axons run in the olfactory tract directly to the piriform cortex, amygdala and entorhinal cortex. Unlike all other senses, smell does not need a thalamic relay to reach the primary cortex, although some fibres later pass through the mediodorsal thalamus to the orbitofrontal cortex. A thalamic infarct therefore abolishes somatic sensation but spares conscious smell. The ventral posteromedial nucleus relays face sensation and taste.
Olfactory pathway
- Bulb mitral cells
- Olfactory tract to piriform cortex
- No thalamic relay needed
- Links to amygdala, memory
Remember Smell is the only sense that skips the thalamus.
Exam trap Thalamic strokes may affect taste through VPM, but smell is preserved.
Why the other options are wrong
- Olfactory fibres cross in the optic chiasm Olfactory fibres do not pass through the chiasm.
- Smell is relayed through the hypothalamus only The hypothalamus receives olfactory input but does not relay conscious smell.
- The olfactory tract runs in the internal capsule The olfactory tract does not run in the internal capsule.
- Each olfactory bulb projects to the cerebellum The cerebellum has no role in smell.
A 30-year-old nurse loses her sense of smell suddenly during a mild COVID-19 illness without nasal blockage, and it returns over 6 weeks. Which of the following best explains this pattern?
Answer: Infection of olfactory supporting cells
SARS-CoV-2 enters cells through ACE2 and TMPRSS2, which are expressed by the sustentacular (supporting) cells of the olfactory epithelium rather than by the olfactory neurons themselves. Infection and inflammation of these cells disrupts the environment the neurons need, so smell is lost suddenly without nasal blockage. Because the neurons are largely spared and the epithelium regenerates from basal cells, most patients recover within weeks. A minority have prolonged loss or distorted smell.
COVID-19 anosmia
- Virus targets sustentacular cells
- Neurons largely spared
- Sudden loss without blockage
- Most recover in weeks
Remember Support cells fall, smell fails, then recovers.
Exam trap Smell training can help those with prolonged loss.
Why the other options are wrong
- Permanent death of the olfactory bulb Recovery in weeks argues against permanent central damage.
- Swelling blocking air flow to the cleft There was no nasal blockage.
- Damage to the chorda tympani Carries taste from the tongue, not smell.
- Infection of the piriform cortex Cortical infection is not the usual mechanism.
A 64-year-old man is referred to the neurology OPD with a slight tremor of his right hand, slowness and a softer voice over a year. His wife says he lost his sense of smell about six years ago and has acted out dreams at night for longer. Smell testing confirms marked hyposmia. Which of the following best explains his early loss of smell?
Answer: Early Lewy pathology in the olfactory bulb
In Parkinson disease, α-synuclein aggregates (Lewy bodies and neurites) appear early in the olfactory bulb and anterior olfactory nucleus and in the dorsal motor nucleus of the vagus, years before they reach the substantia nigra. Hyposmia therefore affects most patients and often precedes motor signs, along with REM sleep behaviour disorder and constipation. Nigral dopamine loss produces the motor features later. Levodopa does not cause the smell loss.
Prodromal Parkinson disease
- Early olfactory bulb α-synuclein
- Hyposmia years before tremor
- REM sleep behaviour disorder
- Constipation from vagal nucleus involvement
Remember Lost smell plus dream enactment: think early Parkinson.
Exam trap Normal smell argues against Parkinson disease in a patient with tremor.
Why the other options are wrong
- Dopamine loss in the substantia nigra Nigral loss causes the motor signs, which came later.
- Side effect of levodopa treatment He is not yet treated, and levodopa does not cause hyposmia.
- Atrophy of the nasal mucosa with age Age reduces smell gradually but not this much in six years.
- Olfactory nerve compression by the frontal lobe There is no frontal mass.
Where this sits in the CPSP syllabus
- Paper 1: Special senses, Smell and taste
- Surgery & Allied, Paper 2: Special senses, Smell and taste
- Medicine & Allied, Paper 2: Special senses, Smell and taste
Read next
Drug dose pages
Doses, cautions and practical tips for drugs in this chapter.