Vision and hearing pathways

What it normally does

• Split each retina down the middle. The half nearer the nose (nasal retina) looks out at the outer half of the world (temporal field) and its fibres cross at the optic chiasm. The half nearer the temple (temporal retina) looks at the inner field and stays on its own side. So there are three zones: in front of the chiasm a nerve carries one eye only; at the chiasm the crossing fibres of both eyes are bundled together in the middle; behind it every fibre carries the opposite half of the visual world from both eyes at once.

  Gives the three-step rule that localises almost every field defect: loss in one eye only is in front of the chiasm, loss of both outer fields is at the chiasm, and loss of the same side of the field in both eyes is behind it.

• The map stays orderly all the way back, but it is upside down and it splits. Fibres from the lower retina (which see the upper field) swing forward around the temporal horn before turning back (Meyer loop); fibres from the upper retina (lower field) run straight back through the parietal white matter. Both end in the calcarine cortex of the occipital lobe, where the macula is given a huge area at the occipital pole, and that pole is fed by both the posterior and the middle cerebral artery.

  Explains why a temporal lobe lesion knocks out the contralateral UPPER quadrant and a parietal one the contralateral LOWER quadrant, and why an occipital stroke can spare central vision (macular sparing).

• The pupil light reflex is a separate loop that never reaches the cortex. Light in one eye runs up the optic nerve, and the pupil fibres leave the optic tract BEFORE the lateral geniculate to reach the pretectal nucleus in the midbrain, which drives BOTH Edinger-Westphal nuclei; parasympathetic fibres then ride on the outside surface of the third cranial nerve to constrict both pupils — the lit one (direct) and the other one (consensual).

  Explains the relative afferent pupil defect of a damaged optic nerve, why a cortically blind patient still has brisk pupils, and why a compressing third nerve lesion (posterior communicating aneurysm, uncal herniation) involves the pupil early — the superficial parasympathetic fibres are squeezed first — whereas a microvascular diabetic third nerve palsy typically spares it.

• Sound has to cross from air into fluid, and fluid resists — most of the energy would simply bounce off. The ear canal, eardrum and three ossicles fix that by funnelling a large drum area onto a small stapes footplate, plus a small ossicular lever, worth roughly 20-30 dB (impedance matching, the conducting apparatus). Inside the cochlea, hair cells turn the travelling wave into nerve impulses — high frequencies at the base, low at the apex — and the eighth nerve carries the signal in. Above the cochlear nucleus the pathway runs up both sides of the brainstem.

  Explains the two mechanisms of deafness — the sound cannot get in (conductive) or the cochlea and nerve cannot code it (sensorineural), with mixed loss when both are present at once — why a tuning fork on the skull separates them, and why a hemisphere stroke never makes anyone deaf in one ear.

What goes wrong

• Pituitary tumour compressing the optic chiasm← from “Split each retina down the middle. The half ne…”

  The pituitary sits directly under the chiasm. A tumour growing up out of the sella presses first on the fibres crossing in the middle — the nasal retinal fibres from both eyes — and those fibres carry the outer half of each field. Pressure comes from below and reaches the inferonasal crossing fibres first, and those carry the UPPER temporal field, so the upper outer quadrants go first and the loss then spreads down into a full bitemporal hemianopia. (A craniopharyngioma pressing from above does the reverse, taking the lower fields first.)

  A defect that respects the VERTICAL midline is chiasmal or behind it; one that respects the HORIZONTAL midline (altitudinal) is retinal or optic nerve vascular disease. Bitemporal hemianopia means image the pituitary and measure prolactin.

  You would find: Both outer fields fade, so the patient clips door frames and cars on both sides and misses people approaching from either side. On confrontation with a red pin the defect stops dead at the vertical midline. Look for the hormone story alongside it: amenorrhoea and galactorrhoea in a prolactinoma, acromegalic features, or the sudden headache and collapse of pituitary apoplexy.

• Optic neuritis← from “The pupil light reflex is a separate loop that…”

  Inflammatory demyelination of one optic nerve, often the first presentation of multiple sclerosis in a young adult. Conduction in that nerve slows and partly blocks, so fewer impulses reach the visual cortex and fewer reach the pretectal nucleus — the afferent limb of the light reflex is weakened on that side only.

  A relative afferent pupil defect means optic nerve or massive retinal disease — never cataract, never a refractive problem, never a functional one. Vision usually recovers over weeks; the risk that matters afterwards is MS, so the MRI is for the brain, not just the nerve. Bilateral, severe or poorly recovering optic neuritis should also prompt testing for MOG and aquaporin-4 antibodies rather than being assumed to be MS.

  You would find: Pain on moving the eye for a day or two, then vision in that one eye dims over days; colours look washed out (red desaturation) and acuity is far worse than the eye looks. Swinging torch test: when the light swings from the good eye to the bad one, both pupils dilate instead of constricting (relative afferent pupil defect). The disc is often normal early — the patient sees nothing and the doctor sees nothing, because the lesion is behind the globe (retrobulbar).

• Homonymous hemianopia and quadrantanopia after stroke← from “The map stays orderly all the way back, but it…”

  Behind the chiasm each side carries the opposite half of the world from both eyes, so any lesion there takes the same half of the field out of each eye. Occlusion of the posterior cerebral artery infarcts the calcarine cortex and produces a full contralateral homonymous hemianopia, often with central vision spared because the occipital pole also draws blood from the middle cerebral artery. A middle cerebral branch stroke in the temporal lobe hits Meyer loop and takes the contralateral upper quadrant (pie in the sky); in the parietal lobe it takes the contralateral lower quadrant.

  Congruous (identical in both eyes) and complete points occipital; incongruous and quadrantic points optic radiation — temporal for upper, parietal for lower. Macular sparing means occipital. A homonymous hemianopia (and usually a homonymous quadrantanopia) fails the Austroads visual field standard for an unconditional private licence, and the patient has a legal duty to notify the driver licensing authority — so ask about the licence at the first consultation.

  You would find: Sudden onset. The patient bumps into things consistently on one side and loses the start or the end of a line when reading. Confrontation shows the identical defect in both eyes and it stops at the vertical midline. Pupils react normally, because the reflex arc leaves the tract before the lateral geniculate and the midbrain loop is untouched — that is what tells you the blindness is retrogeniculate. Do not confuse the field defect with visual NEGLECT: a patient with hemianopia alone knows the field is missing and turns the head to scan, while the patient who eats only half the plate or shaves half the face and denies anything is wrong has parietal neglect, which can occur with or without a field defect.

• Conductive hearing loss: otitis media with effusion and chronic suppurative otitis media← from “Sound has to cross from air into fluid, and fl…”

  Anything that blocks or stiffens the conducting apparatus — wax or debris occluding the canal, fluid or pus behind the drum, a perforation, or a stapes footplate fixed by abnormal new bone (otosclerosis) — stops sound energy being delivered efficiently across the air-to-fluid step. The energy never reaches the cochlea, which is working perfectly. A tuning fork on the skull bypasses the whole broken conducting chain and reaches the cochlea directly — and with no competing air-borne background noise it sounds louder in the blocked ear.

  Weber goes TO a conductive loss and AWAY from a sensorineural one. Persistent middle ear disease during the years a child is learning language shows up later as speech delay, an inattentive child at the back of the classroom, and poorer schooling — so examine the ears of every Aboriginal and Torres Strait Islander child at every opportunity, not only when they complain.

  You would find: Weber test lateralises TO the bad ear; Rinne is negative on that side (bone conduction beats air conduction). The patient's own voice sounds loud to them (autophony). A flat (type B) tympanogram, a dull retracted drum, or a perforation with discharge. Loss is typically 20-40 dB and cannot go beyond about 60 dB, because at that point bone conduction takes over. In Aboriginal and Torres Strait Islander children this starts within the first months of life, is often bilateral and persistent, and rates of chronic suppurative otitis media in some remote communities are among the highest reported anywhere in the world — far above the 4% prevalence the WHO calls a massive public health problem.

• Sensorineural hearing loss← from “Sound has to cross from air into fluid, and fl…”

  The hair cells or the eighth nerve stop coding sound. High frequencies go first because those hair cells sit at the base of the cochlea, where every travelling wave passes and where the cochlea is most vulnerable: ageing (presbycusis), loud noise, ototoxic drugs, or a schwannoma growing on the vestibular nerve at the internal acoustic meatus. Bone conduction is now no better than air, because both routes end at the same broken cochlea.

  No drug restores a dead hair cell. Management is a hearing aid, and a cochlear implant when aids no longer help — which is why the pharmacology on this page is mostly about not causing it in the first place.

  You would find: Weber lateralises AWAY, to the good ear; Rinne stays positive (air beats bone) but everything is quieter. The classic complaint is not volume but discrimination — fine one to one, hopeless in a noisy pub. The audiogram slopes down at high frequency, or shows a 4 kHz notch after years of noise exposure. Unilateral or clearly asymmetrical loss with tinnitus and unsteadiness means image the internal acoustic meatus with MRI. Sudden sensorineural loss over hours to days is an emergency, not a wax problem — it needs same-day assessment, because steroid treatment works best when started early.

What we give, and how it works

Open a drug to see what it binds, what that does to the cell, and what you then see in the patient.