Special senses
Smell, taste, vision, hearing and equilibrium
Each special sense has a receptor with its own transduction trick and a pathway whose lesions give recognisable deficits. CPSP asks how receptors convert stimuli, which nerves carry taste, why the fovea and rods behave as they do, where visual pathway lesions sit, how the cochlea maps pitch, and how vestibular signals produce nystagmus.
Smell
- Olfactory receptor cells are bipolar neurons in the roof of the nasal cavity, unusual in being replaced throughout life from basal stem cells. Odorants bind G protein-coupled receptors, raise cAMP and open cation channels.
- Axons pass through the cribriform plate to the olfactory bulb, which on coronal MRI lies in the olfactory sulcus under the frontal lobe. Smell reaches the piriform cortex and amygdala without a thalamic relay.
- Anosmia: head injury shears the filaments at the cribriform plate; nasal polyps stop odorants reaching the olfactory cleft; post-viral loss damages the epithelium. An olfactory groove meningioma gives anosmia, atrophy of the ipsilateral optic disc (compressed nerve) and papilloedema in the other eye.
- Flavour depends largely on smell, so anosmic patients say food is bland but still detect salt and sweet.
Taste
| Taste | Transduction |
|---|---|
| Salty | Sodium entry through ion channels |
| Sour | Hydrogen ions through ion channels |
| Sweet, bitter, umami (L-glutamate) | G protein-coupled receptors |
| Region | Nerve |
| Anterior two-thirds of tongue | Chorda tympani (facial), crossing the middle ear, so ear surgery can abolish taste with touch intact |
| Posterior third | Glossopharyngeal |
| Epiglottis and supraglottis | Internal laryngeal branch of the vagus |
- All taste fibres synapse first in the nucleus tractus solitarius, then the thalamus (VPM), then the gustatory cortex (area 43, insula and frontal operculum).
- Zinc deficiency (for example with penicillamine) disturbs taste.
Vision
- Myopia: image falls in front of the retina, corrected by a concave lens. Accommodation for near vision needs the parasympathetic-driven ciliary muscle.
- Phototransduction: light converts 11-cis retinal (from vitamin A) in rhodopsin to all-trans, cGMP falls, sodium channels close and the photoreceptor hyperpolarises. The retinal pigment epithelium recycles retinal and digests shed outer segments; its failure leaves drusen in macular degeneration.
| Feature | Rods | Cones |
|---|---|---|
| Location | Periphery; none in the fovea | Packed in the fovea |
| Sensitivity | Very high, dim light | Low, bright light, colour |
| Convergence | Many rods to one ganglion cell | One-to-one links in the fovea (acuity) |
| Red light | Insensitive, so red light preserves dark adaptation | Respond |
- A faint star vanishes when looked at directly because the fovea has no rods. Macular degeneration destroys reading and face recognition but spares navigation by peripheral vision.
- The inner retina is fed by the central retinal artery, the fovea by the choroid: in central artery occlusion the pale retina surrounds a cherry-red spot.
- The optic disc is the blind spot, enlarged by papilloedema. The optic nerve is CNS tissue myelinated by oligodendrocytes, so it is affected by multiple sclerosis: MRI shows nerve enhancement, the swinging light test shows both pupils dilate when light moves to the affected eye (afferent defect), and visual evoked potentials show a delayed P100 with near-normal amplitude.
| Lesion | Field defect |
|---|---|
| Lateral chiasm (tortuous carotid) | Ipsilateral nasal hemianopia |
| Central chiasm (pituitary) | Bitemporal hemianopia |
| Optic tract | Contralateral homonymous hemianopia |
| Temporal (Meyer) loop | Contralateral superior quadrantanopia |
| Cuneus (above calcarine sulcus) or parietal radiation | Contralateral inferior quadrantanopia |
| Occipital pole | Contralateral homonymous central scotoma |
Hearing
- The ossicles and the large drum-to-oval-window area ratio match air to cochlear fluid.
- Basilar membrane: stiff and narrow at the base (near the oval window): high frequencies; wide and floppy at the apex (helicotrema): low frequencies. Ménière disease affects low frequencies first. Noise damage gives a notch at 4 kHz.
- Endolymph is rich in potassium and sits at about +80 mV, generated by the stria vascularis; potassium entry depolarises hair cells.
- Inner hair cells send most afferent signals; outer hair cells contract and amplify, producing the otoacoustic emissions used in newborn screening.
- Tuning forks: sensorineural loss (right vestibular schwannoma) gives Rinne positive on both sides and Weber to the good ear; conductive loss gives Rinne negative and Weber to the affected ear. In otosclerosis the patient hears better in noise because speakers raise their voices.
- Pathway: cochlear nuclei, superior olive, lateral lemniscus, inferior colliculus, medial geniculate body, primary auditory cortex (Heschl gyrus). Bilateral projections mean a one-sided cortical lesion does not cause deafness.
Equilibrium
- Semicircular canals detect rotational (angular) acceleration through endolymph moving the cupula. Utricle and saccule maculae, loaded with otoconia, detect linear acceleration and head tilt.
- Nystagmus is named by its fast phase. After spinning to the right and stopping, the fast phase is to the left. Right vestibular neuritis gives a fast phase to the left, away from the weak side.
- Caloric test: cold water in the ear normally produces nystagmus with the fast phase away from that ear. In brainstem death no eye movement occurs because the reflex arc (vestibular nuclei through the medial longitudinal fasciculus to III and VI nuclei) is lost.
- Benign paroxysmal positional vertigo: loose otoconia in a canal (usually posterior), brief spells on lying back. A cholesteatoma eroding the lateral semicircular canal causes vertigo on pressing the tragus.
- Motion sickness: mismatch between vestibular and visual signals.
- The lateral vestibular nucleus drives extensor (antigravity) muscles through the lateral vestibulospinal tract; a lesion between the red nucleus and vestibular nuclei releases it, giving decerebrate (extensor) posturing.
Remember High notes at the base, low notes at the apex of the cochlea.
Exam trap Utricle and saccule sense linear acceleration and tilt; the canals sense rotation.
Exam trap The fast phase of nystagmus after a sudden stop beats opposite to the direction of spin.
Test yourself on this topic
5 of the 47 questions in our bank on this topic. Choose an answer to see why every option is right or wrong.
A 66-year-old man has a small infarct confined to the right cuneus, the part of the occipital lobe above the calcarine sulcus. Which visual field defect will he have?
Answer: Left inferior homonymous quadrantanopia
The primary visual cortex lines the calcarine sulcus. The upper bank (cuneus) receives fibres from the upper retina, which sees the lower visual field, and the lower bank (lingual gyrus) receives the lower retina, which sees the upper field. Each hemisphere represents the opposite half of the field. A right cuneus lesion therefore causes a left inferior homonymous quadrantanopia.
Calcarine cortex
- Upper bank (cuneus): upper retina
- Upper retina sees the lower field
- Lower bank (lingual): upper field
- Each side sees the opposite half
Remember Cuneus lesion, lower field lost on the opposite side.
Exam trap Do not forget the inversion: the upper bank of the cortex sees the lower field.
Why the other options are wrong
- Left superior homonymous quadrantanopia Would follow a lesion of the right lingual gyrus, below the calcarine sulcus.
- Right inferior homonymous quadrantanopia Would need a left-sided lesion.
- Bitemporal hemianopia Results from chiasmal compression.
- Left homonymous hemianopia with macular loss Would need the whole right visual cortex, and the macula is often spared.
A 30-year-old woman with a single episode of right optic neuritis a year ago now has numbness in both legs. Visual acuity has recovered fully. Which visual evoked potential finding in the right eye best supports earlier demyelination?
Answer: Delayed P100 with near-normal amplitude
Visual evoked potentials are recorded over the occipital cortex while the patient watches a reversing checkerboard. The main positive wave, P100, appears about 100 ms after the stimulus. Demyelination slows conduction along the optic nerve without destroying most axons, so the P100 is delayed while its amplitude is fairly preserved. The delay often persists after vision recovers, revealing a previous, clinically silent lesion.
VEP in demyelination
- Checkerboard reversal stimulus
- P100 at about 100 ms
- Demyelination: delayed P100
- Amplitude preserved
Remember Myelin loss slows the signal; axon loss shrinks it.
Exam trap Normal acuity does not mean a normal optic nerve; the VEP delay often persists.
Why the other options are wrong
- Absent response with no recordable wave An absent response suggests severe axonal loss or no visual input.
- Normal latency with much reduced amplitude Reduced amplitude with normal timing points to axonal loss or compression.
- Shortened P100 latency Demyelination slows conduction; it never speeds it.
- Normal response in both eyes Would not support a previous right optic neuritis.
A 26-year-old woman has painful blurred vision in the left eye from acute left optic neuritis. What does the swinging light test show?
Answer: Both pupils dilate when the light moves to the left eye
In left optic neuritis the afferent signal from the left eye is weaker. Light in the right eye causes strong constriction of both pupils, because each pretectal nucleus projects to both Edinger-Westphal nuclei. When the light swings to the left eye the weaker input lets both pupils dilate slightly: a relative afferent pupillary defect. The efferent (oculomotor) pathway is intact, so the pupils are equal in size at rest.
RAPD
- Weaker afferent input from one eye
- Swing to it: both pupils dilate
- Pupils equal at rest
- Optic nerve or extensive retinal disease
Remember RAPD is an afferent problem; anisocoria is an efferent problem.
Exam trap Cataract does not cause an RAPD, because light still reaches the retina.
Why the other options are wrong
- The left pupil is fixed and dilated in all light A fixed dilated pupil is an efferent (third nerve) problem.
- Only the right pupil reacts to light in the left eye Both pupils always react together, as the reflex is consensual.
- Both pupils constrict more when the left eye is lit Weaker input gives less, not more, constriction.
- The left pupil fails to constrict to near vision The near response is unaffected in optic neuritis.
A 30-year-old man with a long-standing foul ear discharge from an attic cholesteatoma has brief vertigo whenever he presses on his tragus. At surgery the bony prominence on the medial wall of the attic and aditus is eroded. Which part of the inner ear has been exposed?
Answer: Lateral semicircular canal
The lateral (horizontal) semicircular canal forms a bony bulge on the medial wall of the aditus and attic, right where a cholesteatoma expands. It is therefore the commonest site of a labyrinthine fistula. When the bone is eroded, pressure changes in the ear canal move the perilymph and stimulate the canal, causing vertigo and nystagmus: the fistula sign. The cochlea lies further forward and medial, behind the promontory.
Labyrinthine fistula
- Lateral canal bulges into the aditus
- Eroded by attic cholesteatoma
- Pressure causes vertigo, nystagmus
- Positive fistula sign
Remember Tragal pressure vertigo in cholesteatoma: lateral canal fistula.
Exam trap Removing cholesteatoma matrix from a fistula can cause total deafness; the surgeon must know beforehand.
Why the other options are wrong
- Basal turn of the cochlea Lies behind the promontory, deeper and further forward.
- Posterior semicircular canal Lies posteriorly, deep in the petrous bone, away from the attic.
- Superior semicircular canal Lies on the roof of the petrous bone; its dehiscence is usually not from cholesteatoma.
- Endolymphatic sac Lies on the posterior surface of the petrous bone, near the dura.
After falling backwards and striking his head, a man complains that he cannot see the centre of what he looks at to the left. He has a contusion limited to the tip of the right occipital pole. Which field defect is most likely?
Answer: Left homonymous central scotoma
In the primary visual cortex the macula is represented at the occipital pole, over a large area of cortex, while the peripheral field is represented further forward along the calcarine sulcus. A lesion confined to the right occipital pole damages the macular representation of the left half-field of both eyes, giving a left-sided homonymous central (paracentral) scotoma with intact peripheral vision. Posterior cerebral artery strokes, in contrast, may spare the macula because the pole has MCA collateral supply.
Macular cortex
- Macula maps to the occipital pole
- Large cortical area for central vision
- Pole lesion: homonymous central scotoma
- Periphery is anterior along calcarine
Remember Pole injury hits the centre; PCA infarct may spare it.
Exam trap Because both eyes are affected, covering one eye does not make the central scotoma go away.
Why the other options are wrong
- Left homonymous hemianopia sparing the macula This is the pattern of a PCA infarct with pole sparing, the opposite of this lesion.
- Right central scotoma in one eye Cortical lesions are homonymous; a single-eye scotoma points to the eye or optic nerve.
- Left superior quadrantanopia Results from a temporal (Meyer loop) or lingual gyrus lesion.
- Bitemporal peripheral field loss Results from chiasmal compression.
Where this sits in the CPSP syllabus
- Diagnostic Radiology, Paper 2: Nervous system and special senses, Smell, taste, vision, hearing and equilibrium
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