Ophthalmology - Squint and Neuro-ophthalmology Flashcards Preview

Year 4 - SPM > Ophthalmology - Squint and Neuro-ophthalmology > Flashcards

Flashcards in Ophthalmology - Squint and Neuro-ophthalmology Deck (76):

What is a squint?

The true definition of a squint (or strabismus) is that one of the eyes is not directed towards the object under scrutiny. Note that if the eyes converge for close work, this does not indicate a squint.

Patients often use the word to describe narrowing of the gap between the upper and lower eyelids, usually carried out by patients to create a pinhole effect. This reduces the consequences of any refractive error and improves the clarity of the image.


Why is a squint important?

A squint:
1) may show impaired visual acuity
2) may itself cause ambylopia in a child
3) may be a sign of a life threatening condition

1) The eyes are kept straight by the drive to keep the image of the object being viewed in the centre of the macular area, where highest defintion and colour vision are located. The tone in the extraocular muscles is constantly being readjusted to maintain this. If the vision is impaired in one or both eyes, this constant readjustment cannot occur and one eye may wander. This could be caused by very treatable diseases, such as cataract or refractive errors.

2) Double vision due to misalignment of the eyes, or congenital cataracts may lead to suppression of vision in the affected eye and the visual pathways then fail to develop properly. This leads to ambylopia of the eye.

3) Squint is a common presenting complaint of a child with retinoblastoma. A squint can also be caused by a 6th nerve palsy resulting from a tumour causing raised ICP. Patients with myasthenia may also present with a squint and diplopia.


What features in the history are important in squints?

A family history of a squint is a strong risk factor in the development of a squint. Children with disorders of the central nervous system such as cerebral palsy have a higher incidence of squint.

Squint is more common in preterm infants. Problems during delivery and delayed development also increase the likelihood of squint. The parents visual problems should be ascertained, particularly large refractive errors.

The earlier the age of onset, the more likely the squint will need an operation. A constant squint has a worse visual prognosis than one that is intermittent.


What is the approach to examining a squint?

1) Check the visual acuity
2) Look at the position of the patients eyes - large squints will be obvious. Wide epicanthic folds may give the impression of squint, but children with wide epicanthic folds may still have squints
3) Look at the corneal reflections of a bright light held in front of the eyes - note the position of the reflections, they should be symmetrical (this test gives a rough estimate of the angle of deviation)
4) Cover test
5) Test eye movements in all directions
6) Examine the pupil with dilating and relaxing agents


Why is it important to check the visual acuity when examining a squint?

If the visual acuity does not correct with glasses or pinhole, occular disease or ambylopia must be suspected. This is particularly important in children, as the ambylopia or ocular problems must be treated immediately if sight is to be preserved.

Visual acuity in infants is difficult to assess. A history from the parents is useful to find out whether the baby looks at them and at objects. If the sight is poor in one eye, covering the good eye may make the child try to push it away.


What is the cover test?

This is technique used to examine a squint. Two types of cover test help to reveal a squint, especially if it is small and the examiner is unsure about the position of the corneal reflections.

(i) In the cover and uncover test, one eye is covered and the other is observed. If the uncovered eye moves to fix on the object there is a squint that is present all the time - a MANIFEST squint. The test should then be carried out on the other eye. A problem arises when the vision in the squinting eye is reduced, and the eye may not be able to take up fixation. This emphasises the need to test any patient with a squint. If the cover and uncover test is normal (no manifest squint) then the alternate cover test should be performed.

(ii) In the alternate cover test, the occluder is moved to and fro between the eyes. If the eye that has been uncovered moves, then there is a latent squint.


Why is it important to examine an eye with a pupil dilating agent (mydriatic) and a ciliary muscle relaxing agent (cycloplegic)?

Dilating pupils allows you to check for retinal disease, such as retinoblastoma and the cycloplegic eye allows a check for any refractive error. Adequate examination of the peripheral fundus and refraction require dilation of the pupil and special equipment. Cataracts and other opacities in the media, and the white reflex suggestive of retinoblastoma may be checked without dilating the pupil, and looking for the red reflex.


How are paralytic squints managed?

Paralytic squints usually occur in adults. Underlying conditions such as raised ICP, compressive lesions, and diseases such as diabetes, hypertension and myasthenia and thyroid eye disease should be excluded.

If diplopia is a problem, one eye may need to be occluded temporarily, for example by a patch stuck to the patients glasses. Alternatively, temporary prisms can be stuck onto the glasses to eliminate diplopia. An operation on the ocular muscles may be indicated if the squint stabilises. If this is inappropriate or proves inadequate, permanent prisms may be incorporated into the glasses prescription. Botulinum toxin can also be used as part of the diagnostic or treatment process.


How can non paralytic squints be treated?

Non paralytic squints usually occur in children/ If the squint is caused by disease in the eye that is causing reduced vision and subsequent deviation of the eye (e.g. cataract) this needs to be treated.

Treatments for non paralytic squints include:
- spectacles
- occlusion
- orthoptic (visual exercises)
- surgery
- botulinum toxin


What are the 2 main indications for prescribing glasses to a child?

1) A child who is hypermetropic (longsighted) and has a convergent squint. If the child is hypermetropic, the ciliary muscle has to contract strongly during accommodation for the child to be able to focus on the near object. This excessive accommodation may cause overconvergence so that a squint occurs. This type of squint is called an accommodative convergent squint. The use of hypermetropic glasses relaxes the ciliary muscles and reduces the drive to converge

2) A child who has a refractive error, particularly if this is unilateral. Because of the refractive error the image on the retina will be indistinct. The visual pathways will then not develop properly (resulting in ambylopia). Children with a refractive error may not develop a squint until the vision is poor in one eye


At what age is occlusive therapy unlikely to correct a squint in a child?

After the age of about 7, occlusion therapy is unlikely to be helpful. Occlusion itself can also only be done for a short amount of time, as there is a danger of ambylopia in the good eye. The vision of the good eye must also be "blurred" with drops containing atropine.


After what age is ambylopia unlikely to be correctable?

The effectiveness of treatment in reversing ambylopia decreases as the child gets older. Once the child is about 8 or 9 years old the visual system is no longer flexible and ambylopia may not be reversed. However, the child may still need glasses to correct any refractive error.


A parent complains that her 2 year old infant has developed a turn in one eye. What is the differential diagnosis?

Non-paralytic squint
Paralytic squint


"My child's eye has a turn." What issues in the history support the diagnosis?

Squint or strabismus occurs in about 3% of children. Most cases present between the ages of 3 months and 4 years. Most childhood squints are non paralytic, but paralytic squints may still occur. Exclusion of underlying ocular, orbital and/or systemic disease is of the utmost importance.


"My child's eye has a turn." What additional features in the history would you seek to support a particular diagnosis?

The antenatal, perinatal and neonatal history, including prematurity, birth weight, birth trauma and developmental milestones, is important. Ask about family history of refractive errors, ambylopia ("lazy eye"), squint, congenital cataracts or retinoblastoma. Is there any history of previous occlusion therapy of one eye, or squint surgery?Are there any associated neurological symptoms - headache, clumsiness, drowsiness or vomiting?


"My child's eye has a turn". What clinical examination would you perform and why?

Inspect the child for abnormal head posture, dysmoprhic features or hydrocephalus. Examination of the red reflex is important. It is reduced or absent in cataract or corneal opacification. There may be leukocoria (white pupil) in cataract, retinoblastoma, or other posterior segment pathology. Examine extraocular movements for limitations of eye movements indicative of palsy of a rectus muscle. In children with convergent squints, full aBduction of each eye must be demonstrated to ensure that a cranial nerve VI palsy is not present. Dilated fundoscopy is essential as conditions such as retinoblastoma may present with strabismus.


"My child's eye has a turn." What investigations would you perform and why?

Cycloplegic refraction is mandatory. Ultrasound examination of the posterior segment is performed in cases of media opacity. In some cases, CT/MRI of the brain, eye and orbit may be indicated.


"My child's eye has a turn." What treatment options are appropriate?

There is a very close relationship between visual function and ocular alignment in children, and many children with squint develop ambylopia.
- Conservative management: detection and treatment of refractive errors and ambylopia (occlusion therapy of the "good eye") are important
- Surgical treatment: ocular realignment by means of strabismus surgery can then be carried out if necessary
- Retinoblastoma may be treated with chemoreduction and focal therapy (laser photocoagulation and cryotherapy). In some cases, external beam radiotherapy may be needed.


A 60 year old patient presents with intermittent loss of vision in one lasting a few seconds, which then returns to normal. What is the likely diagnosis?

Amaurosis fugax (transient loss of vision)


What is amaurosis fugax?

This is reversible loss of vision lasting less than 24 hours. It is a subtype of TIA. The blindness or partial blindness usually lasts less than 10 minutes


What causes amaurosis fugax?

- thromboembolism
- vasospasm
- blood hyperviscosity
- vasculitis involving blood vessels that supply the visual pathway
- intermittent optic nerve compression with gaze-evoked amaurosis

The most common cause of amaurosis fugax is is atherosclerosis of the internal carotid or vertebrobasilar system. Amaurosis fugax resulting from involvement of the internal carotid artery system is unilateral.


What are the important features of a history of amaurosis fugax that support the diagnosis?

Visual loss lasting more than 10 minutes or not returning completely should alert one to the possibility of a retinal vascular occlusion. Ask about symptoms of giant cell arteritis such as headache, scalp tenderness, jaw claudication, anorexia and weight loss.


What investigations are most useful for a patient with amaurosis fugax?

An ESR should be requested to exclude possible vasculitis associated with giant cell arteritis, SLE or other autoimmune disorder. Carotid Doppler ultrasonography will determine the extent of carotid artery stenosis.


What treatment options are appropriate for amaurosis fugax?

After a single TIA, a patient has a stroke risk of 5% per annum and death of 5% per annum.
1) Medical treatment - patients with carotid artery stenosis may be treated with antiplatelet drugs such as clopidogrel. Anticoagulation with warfarin may be considered if a cardiac source of recurrent emboli is identified or if the symptoms persist despite antiplatelet drugs

2) Carotid endarterectomy - recommend if patient has suffered stroke or TIA in the carotid territory and are not severely disabled
- should only be considered if carotid stenosis > 70% according ECST* criteria or > 50% according to NASCET** criteria


A patient presents with intermittent loss of vision in both eyes and then her vision clears. What differentials would you consider?

Increased ICP
Pseudotumour cerebri (idiopathic intracranial hypertension)
Amaurosis fugax


A patient presents with intermittent loss of vision in both eyes and then her vision clears. What issues in the history would support the diagnosis?

Migraine is a common cause of visual disturbance in young patients.

External compression of blood vessels supplying the visual pathway may also cause transient loss of vision. In patients with papilloedema, pressure on blood vessels within the swollen optic nerve head may cause transient loss of vision in one or both eyes.

Amaurosis fugax resulting from involvement of the vertebrobasilar system may produce binocular visual obscuration. Episodes usually last less than 1 minute.


What are the features of migraine that may help to identify it as a cause of intermittent visual loss?

The transient visual loss is usually associated with fortification spectra or scintillating scotomata (coloured zig zag lines oscillating in brightness) usually lasting 15-20 mins but can last longer. If so, the diagnosis of migraine is likely.

A personal history or family history of migraine is helpful. In patients with migraine, ophthalmic examination and pupillary reflexes are usually normal.


What are the features of headache associated with raised ICP?

Raised ICP often causes a headache that is worse on waking, and exacerbated by bending, straining and coughing. Establish whether there is any history of head trauma and whether the headache follows the visual disturbance.


What are the features of pseudotumour cerebri that can help establish the diagnosis in patients with intermittent loss of vision?

Drug history!
Tetracycline, steroid use or withdrawel, nalidixic acid, nitrofurantoin, danazol, ciclosporin and vitamin A in excess are all associated with pseudotumour cerebri, as is obesity.


A patient presents with intermittent loss of vision in both eyes and then her vision clears. What investigations would be most useful and why?

Request FBC and ESR to exclude anaemia and possible autoimmune disorder or hyperviscosity syndrome. Visual field analysis may detect an enlarged blind spot.

Neuroimaging may be indicated to exclude a SOL, hydrocephalus or dural sinus thrombosis.

In patients with pseudotumour cerebri, the CSF opening pressure is often >200mmHg but the CSF composition is normal. Lumbar puncture should always be performed with extreme caution in patients with papilloedema.


What is the management of pseudotumour cerebri?

weight loss
diuretics e.g. acetazolamide
topiramate is also used, and has the added benefit of causing weight loss in most patients
repeated lumbar puncture
surgery: optic nerve sheath decompression and fenestration may be needed to prevent damage to the optic nerve. A lumboperitoneal or ventriculoperitoneal shunt may also be performed to reduce intracranial pressure


How is migraine treated?

Management of migraine is divided into acute and prophylaxis.

- first-line: offer combination therapy with an oral triptan and an NSAID, or an oral triptan and paracetamol
- for young people aged 12-17 years consider a nasal triptan in preference to an oral triptan
- if the above measures are not effective or not tolerated offer a non-oral preparation of metoclopramide* or prochlorperazine and consider adding a non-oral NSAID or triptan

- prophylaxis should be given if patients are experiencing 2 or more attacks per month. Modern treatment is effective in about 60% of patients.
- NICE advise either topiramate or propranolol 'according to the person's preference, comorbidities and risk of adverse events'. Propranolol should be used in preference to topiramate in women of child bearing age as it may be teratogenic and it can reduce the effectiveness of hormonal contraceptives


What is diplopia?

Diplopia means "double vision" and can be classified as either monocular or binocular (i.e. affecting one or both eyes).

Monocular diplopia that occurs in an elderly patient, with reduced vision, monochromatic haloes, night time glare or an altered red reflex is due to age related cataracts and cataracts.


Binocular diplopia occurring with restricted eye movements/ vertical diplopia, and an infraorbital distribution of hypoanaesthesia is most likely caused by what?

Orbital floor fracture is the most common orbital fracture. It can result from blunt trauma to the orbit (blow out fracture). There may be limited upgaze causing vertical diplopia, enophthalmos and anaesthesia in the distribution of the infraorbital nerve. Patients should be advised not to blow their nose. Orbital and facial CTs should be obtained. Maxillofacial and ophthalmology referrals should be made.


What are the features of diplopia caused by thyroid eye disease or orbital space occupying lesion?

Patients tend to present with binocular diplopia that is subacute or progressive. There is proptosis, restricted eye movements and reduced visual acuity.


What is the pathogenesis of thyroid eye disease? How should it be investigated?

Lymphocytes infiltrate the orbital connective tissue, fat and extraocular muscles. The cytokines released by lymphocytes stimulate fibroblasts to secrete connective tissue. Crowding of the ‘closed box’ like orbital compartment causes protrusion of the eye and potential optic nerve compression. Within 2 years of the active inflammation, fibrosis and scaring of the orbital contents ensues.

Investigation is with TFTs and MRI (shows thickening of the ocular muscles).


Binocular diplopia that can have an almost hourly variation in severity and is made worse by fatiguability is likely to be caused by what?

Myasthenia gravis.


What are the features of the a 3rd nerve palsy?

The affected eye is down and out
The pupil may or may not be dilated and non reactive (depending on the cause)


What are the causes of the 3rd nerve palsy?

1) Ischaemic vascular disease
- usually secondary to hypertension or diabetes

2) Vasculitis

3) Intracranial compressive lesions (e.g. aneurysm, haematoma secondary to trauma, malignancy, pituitary apoplexy)

CN III palsy is uncommon. 1/3 of patients with a posterior communicating artery aneurysm have a CNIII palsy.


How can I tell if my patient has a 3rd nerve palsy?

Droopy eyelid, double vision. Patients will often present with a droopy eyelid and not complain of diplopia because the affected eye will be covered. As the ptosis resolves the diplopia may become apparent to the patient.

History should rule out potentially fatal pathology so ask about trauma and symptoms of raised intracranial pressure (sudden onset severe, headache, vomiting, LOC).


What are the important examination findings in a 3rd nerve palsy?

Ptosis. The affected eye appears "down and out" (depressed and abducted). The pupil may or may not be dilated and non reactive. Diplopia in primary gaze may be elicited on elevation of the closed eyelid.


Why do patients with a 3rd nerve palsy have diplopia and ptosis?

Diplopia is secondary to unopposed action of the lateral rectus and superior oblique muscles (the only ones not supplied by the occulomotor nerve).

Ptosis occurs because of loss of supply to levator palpebrae superioris.


Why does the cause of the 3rd nerve palsy determine if the pupil is dilated or not?

The blood supply to the CNIII is formed of two components. The pial vessels supply the superficial fibres of the nerve where the parasympathetic pupillary fibres traverse. Typically diabetic or hypertensive microvascular disease only affects the blood supply to the central part of the third nerve which carries fibres to the ocular muscles. Microvascular disease can therefore affect the third nerve but not give rise to a dilated pupil – (a medical CNIII palsy or ‘partial, pupil sparing’ CNIII palsy). An extrinsic compressive lesion would unselectively affect the CNIII and thus cause a ‘complete’ or ‘surgical’ CNIII palsy with pupil and motor signs.


What investigations should be considered in a patient with a 3rd nerve palsy?

Consider urgent MRA, BP, glucose, ESR and fasting lipids.


How do I manage a patient with a 3rd nerve palsy?

Management of diabetes, hypertension and other vascular risk factors. Otherwise depends on the underlying cause. Diplopia may require patching of the affected eye or the prescription of glasses with prisms.

Urgent neurosurgical intervention if an intracranial lesion is present.


An elevated eye with limited depression, vertical diplopia worse on downgaze and a compensatory head tilt are features of which cranial nerve palsy?

4th nerve palsy


What are the causes of a 4th nerve palsy?

Congenital (although may not present until adulthood)
Head injury
Microvascular disease secondary to diabetes, hypertension or atherosclerosis
Rarely: aneurysms, tumours, vasculitis

4th nerve palsies are uncommon.


What is the history associated with a 4th nerve palsy?

Vertical diplopia. Squint, head tilt (may be noticed from photographs in congenital cases). Sudden onset/ recent symptoms associated with head trauma.


What are the important examination findings in a 4th nerve palsy?

Ipsilateral hypertropia (manifest vertical squint), limited depression of the affected eye. Diplopia worse on downgaze. Contralateral head tilt.


What is the pathogenesis of 4th nerve palsy?

CNIV is a long nerve that arises from the dorsal aspect of the brain. The trunk of the nerve passes over the rigid edge of the tentorium. It is therefore susceptible to minor head trauma causing ‘stretch’ of the nerve. Bilateral CNIV palsy occurs in cases of such intracranial pathology. CNIV supplies the superior oblique which is responsible for depression (when the eye is adducted) and intorsion of the eye (when the eye is abducted) explaining the compensatory head tilt.


What investigations are required in a case of 4th nerve palsy?

Consider neuroimaging in acute cases. BP, FBC, ESR, lipids, glucose


How should I manage a 4th nerve palsy?

Treat the underlying cause. Patches/ prisms. Squint surgery.
Diplopia can become persistent.

Medical causes have a high rate of spontaneous recovery. Definitive surgical management is often needed in traumatic cases due to low rates of spontaneous recovery.


What are the characteristic features of a 6th nerve palsy?

The affected eye has limited abduction and horizontal diplopia. The head is turned towards the affected side to compensate.

CNVI is THE most common affected ocular motor nerve.


What causes a 6th nerve palsy?

Microvascular disease secondary to diabetes or hypertension, basal skull fractures, raised intracranial pressure, demyelination, vasculitis, tumours.


What can be associated with a 6th nerve palsy?

May be associated with raised ICP (a "false localising sign"). Pontine gliomas in children give rise to this lesion. Posterior fossa tumour resection.


What are the important features of a 6th nerve palsy?

Double vision on the horizontal plane, worse on looking in the direction of the affected muscle. Squint. Symptoms of raised intracranial pressure should be excluded.


How do I know my patient has a 6th nerve palsy?

On examination there is esotropia (manifest convergent squint) of the affected eye; worse when looking into the distance than near. Limited abduction. Head turn, towards the affected side. Cranial nerve examination should be performed with particular attention to hearing and the corneal reflex.


What is the pathology of a 6th nerve palsy?

CNVI supplies the lateral rectus hence the esotropia and limited abduction. The head turns towards the affected side to reduce the consequential diplopia.

The nerve is prone to stretching over the petrous tip in cases of raised intracranial pressure or tumours which can cause the brainstem to become displaced inferiorly. This can give rise to a falsely localizing sign in that a patient may appear to have an isolated CNVI palsy but actually have life-threatening intracranial pathology.

Pontine gliomas can present with this sign. Acoustic neuromas may damage the 6th nerve although CNVI palsy alone will rarely be a presenting feature.


How should a patient with a 6th nerve palsy be investigated?

BP, FBC, glucose, lipids, ESR. Low threshold for neuroimaging in the young or if there is no resolution within three months in adults. Multiple cranial nerve signs should prompt urgent MRI.


What would CNIII, IV and VI palsies, impaired ophthalmic and maxillary divisions of CNV sensation, proptosis, painful ophthalmoplegia and a non reactive mid dilated pupil suggest?

Cavernous sinus syndrome - a syndrome caused by a lesion that give rise to a mass effect within the cavernous sinus.


What causes cavernous sinus syndrome?

Cavernous sinus tumours (primary or metastatic), cavernous sinus thrombosis (may be due to infection with staphylococcus aureus or strep pneumoniae), cavernous sinus aneurysm, carotid-cavernous fistula.
Inflammatory causes - Tolosa Hunt syndrome


What risk factors are associated with cavernous sinus syndrome?

Increased age - cavernous sinus aneurysms, trauma; can cause carotid-cavernous fistula
Wegener's granulomatosis
Facial infection


What are the important features in the history of cavernous sinus syndrome?

Reduced vision, protrusion of the eye, red eye, diplopia, painful eye movements, headache. Concurrent infection of the face, sinuses or dentition. Symptoms are usually unilateral but may be bilateral.


What are the features on examination of cavernous sinus syndrome?

May be systemically unwell (e.g. fever and tacchycardia)

1) Multiple cranial nerve palsies:
- II - reduced vision, RAPD and decreased colour perception - if there is orbital involvement
- III, IV and VI - painful ophthalmoplegia and ptosis
- V1-2 (ophthalmic and maxillary divisions) reduced/ absent sensation including corneal reflexes

2) Specific additional signs:
- pulsating exophthalmos, conjunctival/ lid oedema - direct carotid-cavernous fistula
- visual field defect, endocrinological signs - pituitary tumours
- local and systemic signs of infection, meningism, papilloedema - cavernous sinus thrombosis


What is the pathology of cavernous sinus syndrome?

The cavernous sinuses are paired intracranial venous structures bounded by the sphenoid bone and temporal bone that communicate with the ophthalmic veins. Traversing through the cavity are important structures including the internal carotid artery, CNIII, CNIV, CNV1-2, CNVI. Mass effect or thrombosis within
the cavity therefore leads to the signs described above. Tolosa Hunt syndrome is an ideopathic inflammation of the walls of the cavernous sinus. The pituitary gland lies medial to the cavernous sinus thus pituitary tumour or apoplexy can impinge on the structures within it.


What investigations should I perform if I suspect cavernous sinus syndrome?

Urgent neuroimaging: MRI/MRA/MRV. CT of the orbit/nasal sinuses. FBC, blood cultures, ESR. Lumbar puncture for cytological analysis.


How do I manage cavernous sinus syndrome?

Urgent referral to the appropriate speciality.
Tumours – radiotherapy, resection.
Cavernous sinus thrombosis – antibiotics, drainage of site of primary
Inflammatory causes (e.g. Tolosa hunt syndrome) – systemic steroids.
Cavernous sinus aneurysms, carotid-cavernous fistulas – endovascular neurosurgical intervention.


Outline the visual pathway

The nasal retinal receives light from the temporal visual field and the temporal retina receives light from the nasal visual field. Photoreceptors within the retina act as the first-order neurones in the visual pathway. These then synapse with bipolar cells (second-order neurones) which synapse with ganglion cells (third-order neurones). The optic nerve contains axons from these ganglion cells.

The fibres of the optic nerve converge at the optic chiasm and here fibres from the nasal retina cross over. Fibres from the temporal retina remain uncrossed. The optic tracts commence posterior to the chiasm and connect to the lateral geniculate body.
The axons of the lateral geniculate body travel via the optic radiations in the temporal and parietal lobes to the primary visual cortex in the occipital lobe.


Where would the lesion be located to cause ipsilateral blindness with a normal contralateral visual field?

Optic nerve
Causes include optic neuritis, ischaemic optic neuropathy, chronic papilloedema


What causes a bitemporal hemianopia?

Lesions affecting the optic chiasm.
If they spread up from below (for example, pituitary tumours), the defect is worse in the upper field.
If they spread down from above (for example, craniopharyngioma), the lesion is worse in the lower quadrants.
Lesions at the optic chiasm may show a phenomenon where two identical coloured objects are shown to one eye in the left and right halves of the visual field but one appears to be brighter and sharper than the other. For example, with a right hemianopia the left hemifield is brighter than the right.


What visual field defect do lesions of the optic tract cause?

Homonymous hemianopia.
Left homonymous hemianopia means visual field defect to the left, i.e. Lesion of right optic tract
Fibres in the optic tracts gradually rotate until the fibres reach the geniculate body, so lesions in the tract before the geniculate body (i.e. optic tract) may produce incongruous defects.

Lesions in the main optic radiation or optic peduncle cause complete (left or right) homonymous hemianopia without macular sparing. This is seen in stroke and middle cerebral artery lesions.


What visual field defect do lesions in the temporal radiation cause?

Lesions in the temporal radiation cause upper quadrantic homonymous hemianopia, commonly with macular sparing - eg, tumours. Think that your temples are at the top.


What visual field defect do lesions in the parietal radiations cause?

Lesions in the parietal radiation cause inferior quadrantic homonymous hemianopia without macular sparing.


How does the area of the visual cortex correspond to the type of visual field defect observed?

Lesions in the anterior visual cortex (common) produce a contralateral homonymous hemianopia with macular sparing - eg, posterior cerebral artery occlusion.
Lesions in the macular cortex produce homonymous macular defect - eg, blunt injury to the occiput.
Lesions of the intermediate visual cortex produce an homonymous arc scotoma, with sparing of both macula and periphery. This is seen in a distal posterior cerebral artery occlusion.


What visual field defect occurs if both occipital lobes are affected?

If both occipital lobes are injured then the patient is in a state of cortical visual impairment. The patient is unable to process visual information and behaves in a similar fashion to someone who develops a peripheral visual loss. However, some patients still try to behave as if they have vision. This state of unawareness of cortical visual loss is called Anton's syndrome.


What driving advice should be given to patients with a visual field defect?

Patients with a newly diagnosed significant visual field defect should not drive until this has been formally assessed. Patients must inform the DVLA which will then organise for them to have a very specific visual field test (Estermann's visual field test), carried out by one of their approved optometrists. The approved optometrist then reports back to their medical officers, who make the final decision regarding whether a person is safe to drive.

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