Eye

The eyeball is approximately 25 mm in length and comprises three distinct layers. From outside in ( Fig. 8.1 ), these are the:

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  Outer fibrous layer: this includes the sclera and the clear cornea. The cornea accounts for two-thirds of the refractive power of the eye, focusing incident light on to the retina.

  
  
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  Middle vascular layer (uveal tract): anteriorly this consists of the ciliary body and the iris, and posteriorly the choroid.

  
  
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  Inner neurosensory layer (retina): the retina is the structure responsible for converting light to neurological signals.

Extraocular muscles

The six extraocular muscles are responsible for eye movements ( Fig. 8.2 ). Cranial nerve III innervates the superior rectus, medial rectus, inferior oblique and inferior rectus muscles. Cranial nerve IV innervates the superior oblique muscle and cranial nerve VI innervates the lateral rectus muscle. The cranial nerves originate in the midbrain and pons and then pass through the cavernous sinus ( Fig. 8.3 ).

Control of eye movements.

The direction of displacement of the pupil by normal contraction of a particular muscle can be used to work out which eye muscle is paretic. For example, a patient whose diplopia is maximal on looking down and to the right has either a weak right inferior rectus or a weak left superior oblique muscle.

Cavernous sinus (coronal view).

Neuroanatomy of cranial nerves III, IV and VI.

Refractive elements of the eye

The major refracting elements of the eye are the tear film, the cornea and the crystalline lens. The cornea possesses the greatest refractive power and is the main refracting element of the eye; the lens provides additional controllable refraction, causing the light to focus on to the retina. When light is precisely focused on to the retina, refraction is called emmetropia ( Fig. 8.4A ). When the focus point falls behind the retina, the result is hypermetropia ( Fig. 8.4B , long-sightedness). When rays focus in front of the retina, the result is myopia ( Fig. 8.4C , short-sightedness). These refractive errors can be corrected with lenses or with a pinhole ( Fig. 8.4D ).

Normal and abnormal refraction by the cornea and lens.

A Emmetropia (normal refraction). Cornea and lens focus light on the retina. B Hypermetropia (long-sightedness). The eye is too short and the image on the retina is not in focus. A convex (plus) lens focuses the image on the retina. C Myopia (short-sightedness). The eye is too long and the image on the retina is not in focus. A concave (minus) lens focuses the image on the retina. D Myopia corrected using a pinhole. This negates the effect of the lens, correcting refractive errors by allowing only rays from directly in front to pass.

Visual pathway

The visual pathway consists of the retina, optic nerve, optic chiasm, optic tracts, lateral geniculate bodies, optic radiations and visual cortex ( Fig. 8.5 ). Deficits in the visual pathway lead to specific field defects.

Visual field defects.

1, Total loss of vision in one eye because of a lesion of the optic nerve. 2, Bitemporal hemianopia due to compression of the optic chiasm. 3, Right homonymous hemianopia from a lesion of the optic tract. 4, Upper right quadrantanopia from a lesion of the lower fibres of the optic radiation in the temporal lobe. 5, Lower quadrantanopia from a lesion of the upper fibres of the optic radiation in the anterior part of the parietal lobe. 6, Right homonymous hemianopia with sparing of the macula due to a lesion of the optic radiation in the occipital lobe.

Pupillary pathways

The pupil controls the amount of light entering the eye. The intensity of light determines the pupillary aperture via autonomic reflexes. Pupillary constriction is controlled by parasympathetic nerves, and pupillary dilatation is controlled by sympathetic nerves.

For pupillary constriction, the afferent pathway is the optic nerve, synapsing in the pretectal nucleus of the midbrain. Axons synapse in both cranial nerve III (Edinger–Westphal) nuclei, before passing along the inferior division of the oculomotor nerve to synapse in the ciliary ganglion. The efferent postganglionic fibres pass to the pupil via the short ciliary nerves, resulting in constriction ( Fig. 8.6A ).

Pupillary innervation.

A Parasympathetic pathway. B Sympathetic pathway.

For pupillary dilatation, the sympathetic pathway originates in the hypothalamus, passing down to the ciliospinal centre of Budge at the level of T1. Fibres then pass to, and synapse in, the superior cervical ganglion before joining the surface of the internal carotid artery and passing to the pupil along the nasociliary and the long ciliary nerves ( Fig. 8.6B ).

Common presenting symptoms

Start the ophthalmic history with open questions. This builds rapport with the patient by allowing them to describe the condition in their own words, and provides clues for more directed questions later.

The visual system has its own set of presenting symptoms, which prompt specific sets of questions. The most common are described here.

Altered vision

Vision may be altered by an intraocular disease that leads to a change in the optical or refractive properties of the eye and prevents incident light rays from being clearly focused on the retina. Alternatively, it may result from extraocular factors associated with damage to the visual pathway, which runs from the optic nerve to the occipital lobe (see Fig. 8.5 ).

Establish whether the change in vision is sudden or gradual, as these will have their own specific set of differential diagnoses ( Box 8.1 and Fig. 8.7 ; Box 8.2 and Fig. 8.8 ).

8.1

Common causes of an acute change in vision

Cause	Clinical features	Cause	Clinical features
Unilateral
Giant cell arteritis	• Painless loss of vision • Age > 50 years • Weight loss • Loss of appetite, fatigue • Jaw or tongue claudication • Temporal headache • Pale or swollen optic disc • RAPD	Vitreous haemorrhage	• Painless loss of vision • Risk in proliferative diabetic retinopathy • History of flashing lights or floaters may precede haemorrhage in posterior vitreous detachment • Poor fundus view on examination • Reduction or loss of the red reflex • Usually no RAPD if retina is intact
Central retinal vein occlusion	• Acute, painless loss of vision • May have RAPD if severe • Greater risk if hypertensive • Haemorrhages, exudates and tortuous retinal veins ( Fig. 8.7A )	Wet age-related macular degeneration	• Sudden painless loss of central vision • Age > 55 years • Increased risk in smokers • Haemorrhage at the macula ( Fig. 8.7E )
Retinal detachment	• Painless loss of vision • Association with flashing lights or floaters • History of a curtain coming across vision • Myopic patients at greater risk • RAPD if macula is involved • Pale raised retina usually with a retinal tear ( Fig. 8.7B )	Anterior ischaemic optic neuropathy	• Painless loss of upper or lower visual field • Increased risk in vasculopaths • Examination may reveal optic disc swelling
Central retinal arterial occlusion	• Acute, painless loss of vision • Carotid bruit may be heard • RAPD • Increased risk in vasculopaths • Examination: pale retina with a cherry red spot at the fovea ( Fig. 8.7C )	Optic neuritis/retrobulbar neuritis	• Visual reduction over hours • Usually aged 20–50 • Pain exacerbated by eye movement • RAPD • Reduced colour sensitivity • Swollen optic disc in optic neuritis ( Fig. 8.7F ) or normal appearances in retrobulbar neuritis
Corneal disease	• Usual association with pain • Foreign body sensation • Corneal opacity may be visible (e.g. Fig. 8.7D )	Amaurosis fugax	• Painless loss of vision for minutes • History of cardiovascular disease • May have associated atrial fibrillation or carotid bruit • Normal ocular examination
Bilateral
Giant cell arteritis	• Painless loss of vision • Age > 50 years • Weight loss • Loss of appetite, Fatigue • Jaw or tongue, claudication • Temporal headache • Pale or swollen optic disc	Cerebral infarct	• May have associated headache and/or neurological signs • Usually specific field defects dependent on how the visual pathway is affected ( Fig. 8.5 ) • Normal fundus examination • If post chiasmal visual pathway affected, bilateral visual field abnormalities
Raised intracranial pressure	• Headache • Often asymmetric • Pulsatile tinnitus • Swollen optic discs	Migraine	• Gradually evolving usually bilateral visual loss • Vision loss is usually preceded by visual aura • Normal ocular examination • Ocular examination: normal • Vision usually returns to normal after hours

 

RAPD, relative afferent pupillary defect (p. 162).

Common causes of an acute change in vision.

A Central retinal vein occlusion. B Retinal detachment. Elevation of the retina around the ‘attached’ optic disc; the retina may even be visible on viewing the red reflex. C Central retinal arterial occlusion. D Herpes simplex virus keratitis. E Wet age-related macular degeneration. F Swollen optic nerve head in acute optic neuritis.

8.2

Common causes of a gradual loss of vision

Cause	Clinical features
Refractive error	• No associated symptoms • Normal ocular examination • Vision can be improved by pinhole ( Fig. 8.4D )
Glaucoma	• Usually bilateral but asymmetric loss of visual field • Cupped optic discs on examination
Cataract	• Gradual clouding of vision • May be associated with glare • Usually seen in the elderly • Examination: clouding of the pupil and altered red reflex (see Fig. 8.8A and B )
Diabetic maculopathy	• History of diabetes • Central vision reduced or distorted • Haemorrhages and exudates at the macula on examination ( Fig. 8.17A )
Compressive optic neuropathy	• Gradual unilateral loss of vision • Pale optic disc on examination ( Fig. 8.8D )
Retinitis pigmentosa	• Gradual bilateral symmetric loss of peripheral visual field • Nyctalopia (poor vision in dim light) • Family history • Examination: bone spicule fundus, attenuated blood vessels and waxy optic disc ( Fig. 8.8E )
Dry age-related macular degeneration	• Gradual loss of central vision • Usually bilateral • Examination: drusen, atrophy and pigmentation at the macula ( Fig. 8.8C )

 

Common causes of a gradual loss of vision.

A Cataract. B Altered red reflex in the presence of cataract. C Dry age-related macular degeneration. D Compressive optic neuropathy. Optic nerve sheath meningioma causing optic disc pallor and increased disc cupping with sparing of the outer optic nerve rim. E Retinitis pigmentosa, with a triad of optic atrophy, attenuated retinal vessels and pigmentary changes. The latter typically start peripherally in association with a ring scotoma and symptoms of night blindness.

Vision may be not just reduced but also distorted. This results from disruption to the normal structure of the macula, the central part of the retina. The most common cause is macular degeneration but it may also frequently stem from an epiretinal membrane, vitreous traction or central serous retinopathy.

Flashes and floaters result from disturbance of the vitreous and the retina, occurring most commonly in posterior vitreous detachment. This is usually found in older patients as the vitreous gradually degenerates and liquefies, causing it to peel off from the retina. The vitreous is attached to the retina in certain regions; in these regions the vitreous either detaches with traction, resulting in flashing lights, or detaches by tearing the retina, releasing retinal pigment cells. Patients will see either of these as floaters.

Haloes are coloured lights seen around bright lights. They occur with corneal oedema and are most commonly associated with angle-closure glaucoma.

When patients present with a change in vision, ask:

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  Did the change in vision start suddenly or gradually?

  
  
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  How is the vision affected (loss of vision, cloudy vision, floaters, distortion)?

  
  
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  Is it one or both eyes that are affected?

  
  
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  Is the whole or only part of the visual field affected?

  
  
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  If partial, which part of the visual field is affected?

Red eye

The eye is covered in a network of vessels in the conjunctiva, episclera and sclera. Ciliary vessels are also found around the cornea. Dilatation or haemorrhage of any of these vessels can lead to a red eye. Additionally, in uveitis, acute angle-closure glaucoma and corneal irritation the ciliary vessels around the cornea become more prominent (a ‘ciliary flush’). The appearance is distinct from conjunctivitis, in which there is a relative blanching of vessels towards the cornea.

Ask:

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  if the eye is painful or photophobic

  
  
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  if vision is affected

  
  
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  if there has been any recent trauma

  
  
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  whether the eye is itchy

  
  
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  whether there is any discharge

  
  
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  whether there has been any recent contact lens wear or foreign body exposure.

Box 8.4 summarises the features of the common causes of a red eye on history and examination.

8.4

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