Unit 13 — The Eye · Question Bank

I. Three Tunics (Wall of the Eyeball)

1. Fibrous tunic (external tunic) — outermost coat; two parts:

• Cornea: anterior 1/6; transparent, more convex; avascular; supplied by CN V1; forms most of the refracting power of the eye (~43 dioptres). Most pain-sensitive structure in the body.
• Sclera: posterior 5/6; white, opaque, dense fibrous tissue; maintains eyeball shape; pierced posteriorly by optic nerve fibres. At sclerocorneal junction = canal of Schlemm (scleral venous sinus).

2. Vascular tunic (middle tunic / uvea) — contains blood vessels and pigment cells:

• Choroid: posterior 2/3; rich in blood vessels; nourishes outer retina; absorbs excess light.
• Ciliary body: at sclerocorneal junction; contains ciliary muscle (accommodation) and ciliary processes (secrete aqueous humour); connected to lens via ciliary zonule.
• Iris: anterior circular diaphragm; central aperture = pupil; sphincter pupillae (parasympathetic) + dilator pupillae (sympathetic).

3. Retina (inner tunic) — optic part (light-sensitive) + blind parts (ciliary + iridial):

• Outer layer: pigment cell lamina (absorbs backscattered light).
• Inner layer: nervous cell layer — rods (peripheral, dim light), cones (foveal, colour/acuity), bipolar cells, ganglion cells (axons form optic nerve).
• Macula lutea: oval yellowish area; fovea centralis = cone-dense, highest acuity.
• Optic disc: nasal to macula, ~1.5 mm; optic nerve exit; blind spot; central artery/vein pierce here.

II. Contents of the Eyeball

• Aqueous humour: colourless, watery fluid filling anterior and posterior chambers; produced by ciliary processes; drains via iridocorneal angle → canal of Schlemm → ophthalmic veins. Nourishes lens and cornea; maintains IOP.
• Lens: transparent, biconvex, elastic, avascular; between iris and vitreous body; suspended by ciliary zonule from ciliary processes; shape changes for accommodation.
• Vitreous body: colourless, transparent, jelly-like; fills posterior cavity (lens → retina); supports retina against detachment.

Together with the cornea, these contents form the refractive media (all transparent and avascular): cornea → aqueous humour → lens → vitreous body.

Mnemonic: LR6SO4(AO3)

Lateral Rectus = CN 6  |  Superior Oblique = CN 4  |  All Others = CN 3

The Four Rectus Muscles (arise from common tendinous ring around optic canal)

• Medial rectus (CN III): turns pupil medially (adduction); testing — ask patient to look inward.
• Lateral rectus (CN VI): turns pupil laterally (abduction); testing — ask patient to look outward. CN VI palsy → convergent squint (esotropia), diplopia on lateral gaze.
• Superior rectus (CN III): turns pupil superomedially; also intorsion.
• Inferior rectus (CN III): turns pupil inferomedially; also extorsion.

The Two Oblique Muscles

• Superior oblique (CN IV): arises from common tendinous ring; passes through the trochlea (pulley on medial orbital wall) then inserts into sclera posterolaterally. Primary actions: depression, abduction, intorsion. When eye adducted = pure depressor. CN IV palsy → cannot look down-and-in; patient tilts head away to compensate (ocular torticollis).
• Inferior oblique (CN III): arises from floor of orbit (NOT common tendinous ring); turns pupil superolaterally; extorsion.

Levator Palpebrae Superioris (CN III)

Elevates the upper eyelid. CN III palsy → complete ptosis + dilated pupil (loss of sphincter pupillae) + eye deviated down and out (“down and out gaze”, divergent squint).

Clinical Testing Summary

• CN III palsy: eye “down and out,” ptosis, mydriasis (surgical third nerve = pupil involved, e.g. posterior communicating artery aneurysm).
• CN IV palsy: failure to depress adducted eye; head tilt toward opposite shoulder.
• CN VI palsy: medial squint; diplopia on ipsilateral lateral gaze; long intracranial course makes it vulnerable to raised ICP.

The Visual Pathway

• 1. Photoreceptors → ganglion cells: rods and cones transduce light → bipolar cells → ganglion cells; ganglion cell axons converge at the optic disc.
• 2. Optic nerve (CN II): exits via optic canal; carries all fibres from one eye (temporal + nasal retinal fibres).
• 3. Optic chiasma: nasal retinal fibres (carrying temporal field) cross to opposite side; temporal retinal fibres (carrying nasal field) remain ipsilateral.
• 4. Optic tract: each tract = temporal fibres from ipsilateral eye + nasal fibres from contralateral eye → carries contralateral half of the visual field.
• 5. Lateral geniculate body (LGB): thalamic relay nucleus; 6 laminae; retinotopically organised.
• 6. Optic radiations (geniculocalcarine tract): Meyer's loop (lower fibres, temporal lobe, carry upper field) + dorsal fibres (parietal lobe, carry lower field) → primary visual cortex (V1).
• 7. Primary visual cortex (V1): calcarine sulcus of occipital lobe (Brodmann area 17); upper field = below calcarine; lower field = above calcarine.

Visual Field Defects

• Optic nerve lesion: complete monocular blindness (ipsilateral).
• Optic chiasma lesion (e.g. pituitary tumour): bitemporal hemianopia.
• Optic tract / LGB / radiation / cortex lesion: contralateral homonymous hemianopia (both eyes lose the same half-field).
• Meyer's loop lesion (temporal lobe): contralateral superior homonymous quadrantanopia (“pie in the sky”).
• Parietal radiation lesion: contralateral inferior homonymous quadrantanopia (“pie on the floor”).
• Cortical lesion with macular sparing: homonymous hemianopia with central vision preserved (macular cortex has dual blood supply).

I. Lacrimal Gland

Located in the lacrimal fossa in the superolateral orbital cavity (under the frontal bone). Its ducts (~12) open into the lateral part of the superior conjunctival fornix. Tears contain lysozyme (antibacterial), immunoglobulins, and moisture for the ocular surface. Innervated by parasympathetic fibres via the facial nerve (CN VII) → pterygopalatine ganglion → lacrimal gland (reflex and emotional tearing).

II. Drainage Pathway of Tears

• Step 1: Tears secreted from lacrimal gland → spread across conjunctival sac by blinking → flow medially by capillary action to the lacrimal lake (medial canthus).
• Step 2: Absorbed via lacrimal puncta (tiny openings on the medial margin of each eyelid, upper + lower) → enter lacrimal ductules (superior + inferior, ~10 mm each).
• Step 3: Lacrimal ductules empty into the lacrimal sac (lodged in the lacrimal groove on the medial orbital wall; superior end = blind, inferior = continues as nasolacrimal duct).
• Step 4: Nasolacrimal duct (~18 mm; runs in bony nasolacrimal canal) → opens into the inferior nasal meatus under the inferior nasal concha (under Hasner's valve).

III. Nasolacrimal Duct Obstruction

• Congenital: failure of Hasner's valve to open at birth (most common cause of watery eye in neonates); usually resolves spontaneously by 12 months; treatment = massage, topical antibiotics, probing if persistent.
• Acquired: chronic dacryocystitis (infection of lacrimal sac), nasal polyps, trauma, nasal surgery. Symptoms: epiphora (overflow of tears onto the cheek), mucopurulent discharge, recurrent conjunctivitis.
• Surgical treatment: dacryocystorhinostomy (DCR) — creates a new drainage passage directly from the lacrimal sac to the nasal cavity bypassing the blocked duct.

I. Aqueous Humour Production

Aqueous humour is produced by the ciliary processes of the ciliary body (by active secretion and ultrafiltration from ciliary capillaries) into the posterior chamber (space between iris and lens). Normal production rate ~2–3 μL/min; normal IOP ~10–21 mmHg.

II. Circulation and Drainage

• Posterior chamber → pupil → anterior chamber (between cornea and iris).
• Anterior chamber angle (iridocorneal angle) → trabecular meshwork → canal of Schlemm (scleral venous sinus) → aqueous collector channels → episcleral veins → ophthalmic veins.
• A small amount also drains via the uveoscleral (suprachoroidal) route.

III. Glaucoma

Definition: A group of conditions characterised by raised intraocular pressure (usually) leading to progressive optic nerve damage (cupping of the optic disc) and visual field loss, eventually causing blindness if untreated.

Types:

• Primary open-angle glaucoma (POAG): most common; iridocorneal angle is open but trabecular meshwork is functionally impaired → reduced aqueous outflow → gradually rising IOP. Painless, insidious; peripheral field loss first (arcuate scotoma) → tunnel vision → central vision last to go. Most common cause of irreversible blindness worldwide.
• Acute angle-closure glaucoma (AACG): iridocorneal angle is physically closed by the iris bowing forward (pupil block). Precipitated by mydriasis (dim light, anticholinergic drugs). Presents as acute ocular emergency: sudden severe eye pain, headache, nausea, halos around lights, hard red eye, corneal oedema, fixed mid-dilated pupil. Requires urgent treatment (IV acetazolamide, pilocarpine, laser iridotomy).

IV. Mechanism of Optic Nerve Damage

Raised IOP → direct mechanical compression of the lamina cribrosa (scleral sieve through which ganglion cell axons pass) + impaired axoplasmic transport + reduced blood flow in the optic nerve head → ganglion cell death → optic disc cupping (cup:disc ratio >0.6 is suspicious) → irreversible visual field loss.

V. Treatment Principles

• Reduce aqueous production: beta-blockers (timolol), carbonic anhydrase inhibitors (acetazolamide).
• Increase drainage: prostaglandin analogues (latanoprost, uveoscleral route), pilocarpine (miotic, opens angle).
• Surgical: trabeculectomy (creates fistula to subconjunctival space), laser trabeculoplasty.