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Duke Elder > Neuro-Ophthalmology > Flashcards

Neuro-Ophthalmology Flashcards

1
Q

Revise autonomic control of pupil size

A
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2
Q

Pathway causing Miosis

A
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3
Q

Revise pupil reflex pathway

A
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4
Q

Pathway causing Mydriasis

A
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5
Q

Describe the Visual Pathway

A

Starts in the retina and projects into the occipital cortex. Lesions after the retina typically result in hemianopia and quadrantanopia. Lesions of the retina tend to result in scotomas

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6
Q

Describe the defects which can be produced by lesions along the visual pathway

A
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7
Q

List the 4 divisions of the optic nerve (CN2)

A

Divisions:

  • Intraocular: shortest and ends at the lamina cribrosa
  • Intra-orbital: longest and ends at optic foramen
  • Intracanalicular: through the optic canal into the middle cranial fossa
  • Intracranial: ends at the chiasm
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8
Q

Axons of the retinal ganglion cells wrap together to form what?

A

The optic nerve

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9
Q

Blood supply to the optic nerve

A

Intraocular → short posterior ciliary artery
Rest → ophthalmic artery (Pial vessels)

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10
Q

Where do axons travelling from the nasal part of the retina leave the optic nerve and decussate?

A

At the optic chiasm

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11
Q

Anatomical location of the optic chiasm

A

The chiasm sits anterior to the hypothalamus and superior to the pituitary gland

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12
Q

Describe the following defects of the chiasm

  • Willebrand’s knee
  • Middle Chiasmal Lesions
  • Posterior Chiasmal Lesions
A

Note:
Remember that the lower part of the retina is responsible for the upper part of the visual field, and the upper part of the retina sees the lower visual field

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13
Q

Optic Tract

A

There are 2 optic tracts, one for each hemisphere

  • They project from the chiasm to the LGN
  • They carry ipsilateral temporal axons and contralateral nasal axons
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14
Q

Defects produced by lesions of the optic tract

A

Lesions of the tract result in contralateral incongruous (asymmetrical) homonymous hemianopia.

I.e lesion of the right tract will result in left homonymous hemianopia

Lesions of the tract can also produce contralateral afferent RAPD because over half the fibres have already crossed at the chiasm

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15
Q

What are Optic Radiations

A

Projections from the LGN to the visual cortex. The radiations are divided into superior (Dorsal loop) and inferior (Meyer’s loop) projections

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16
Q

Compare the two loops of the optic radiations

A
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17
Q

In what area of the brain does cognitive visual perception occur?

A

The occipital cortex

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18
Q

List 2 lesions in the occipital cortex

What visual field defects would be produced?

A

Systemic hypoperfusion or back of head injury → homonymous hemianopia with central scotoma

Posterior cerebral artery occlusion → homonymous hemianopia with macular sparing (central vision spared)

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19
Q

What are Visual Streams

A
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20
Q

How far do the visual fields extend

A
  • 50° superiorly
  • 60° nasally
  • 70° inferiorly
  • 90° temporally
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21
Q

Revise scotomas

A
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22
Q

Revise the different types of field defect terminology

A
  • Scotoma: Area of visual loss surrounded by normal visual area
  • Absolute scotoma: No light seen at all
  • Relative scotoma: Brighter lights are seen
  • Homonymous: Same visual field quadrants are affected in both eyes
  • Hemianopia: 2 quadrants of vision loss
  • Quadrantanopia: 1 quadrant vision loss
  • Congruousness: the degree to which the defects are the same in both eyes, increases as you move posteriorly in the tract
  • Seidel scotoma: enlargement of blind spot
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23
Q
A

A Goldmann Perimeter. The clinician sits on the opposite side and moves the stimulus at the edges of the bowl.

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24
Q

What does the report from the Humphrey visual field test of the right eye show?

A

It shows a complete loss of the temporal visual field.

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25
Q

What is used to measure visual fields

A

Perimetry

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26
Q

Compare the 3 types of perimetry

A
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27
Q
A

A Humphrey visual field analyser. The patient looks into the bowl and static stimuli a presented at various locations of the field, the patient responds when they see a stimulus. This data is plotted automatically

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28
Q
A

Goldmann visual field record sheet

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29
Q

What conditions are associated with Red-Green loss

A

Optic nerve problems such as neuritis
(NOT glaucoma!)

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30
Q

What conditions are associated with Blue-Yellow loss

A

Macular problems such as AMD
And glaucoma!

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31
Q

List the extraocular muscles of the eye

A
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32
Q

List the 4 important rules/laws which apply to the Extraocular muscles of the eye

A
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33
Q

Origins of the extraocular muscles

A
  • All recti originate from the common tendinous ring (Annulus of Zinn).
  • SO originates from the lesser wing of sphenoid
  • IO originates from the orbital floor
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34
Q

Which extraocular muscle of the eye inserts closest and furthurest to the limbus

A
  • Medial rectus inserts closest to the limbus
  • Superior rectus inserts furthest away
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35
Q

Innervation to the extraocular muscles of the eye

A
  • CN6 → LR
  • CN3 → All other recti + IO
  • CN4 → SO
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36
Q

Actions of the extraocular muscles

A
  • Elevation → SR (Primary) + IO
  • Depression → IR (Primary) + SO
  • Adduction → MR (Primary) + SR + IR
  • Abduction → LR (Primary) + SO + IO
  • Intorsion → SO
  • Extorsion → IO
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37
Q

Where are the nucleus locations of the CN3,4, 6

A
  • CN3 → dorsal midbrain at the level of the superior colliculus
  • CN4 → dorsal midbrain at the level of the inferior colliculus
  • CN6 → ventral to 4th ventricle at pontine tegmentum near the paramedian pontine reticular formation
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38
Q

CN3 Pathway

A
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39
Q

CN4 pathway

A
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40
Q

CN6 pathway

A
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41
Q

When is CN4 most likley to be damaged

A

CN4 is most likely to be damaged by trauma because it has the longest course.

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42
Q

When is CN6 most likley to be damaged?

A

CN6 is most likely to be damaged by raised ICP because it travels within Dorello’s canal where it is tightly packed against hard bony structures.

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43
Q

Revise cavernos sinus anatomy

A
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44
Q

CN3 actions

A
  • Ipsilateral IO IR MR
  • Contralateral SR
  • Bilateral levator
  • Ipsilateral sphincter pupillae
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45
Q

CN4 actions

A

Contralateral SO

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46
Q

CN6 actions

A

Ipsilateral LR

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47
Q

What controls ‘gaze’

A

Your gaze is controlled at 3 levels:

  • supranuclear (initiates movement at the cortex)
  • Intra-nuclear (coordinates movement at the brainstem)
  • Infra-nuclear (efferent nerves to muscles)
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48
Q

List the 3 types of gaze

A
  1. saccades
  2. smooth pursuit
  3. vestibular ocular movements
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49
Q

Saccades

A

The horizontal gaze pathway can be tricky to grasp at first but is well worth learning because it is frequently tested.

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50
Q

Smooth pursuit

A

Slow tracking of moving objects

  • Initiated by the Parietal-occipital-temporal (POT) region, ipsilateral to the tracking direction
  • For example, right slow pursuit is initiated by the right POT
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51
Q

Vestibular ocular movements

A

Keep eyes stable with head movement

  • Initiated at brainstem level, does not involve the cortex

Tested by dolls head reflex

  • The eyes move when the head is moved to keep them looking in the same direction
  • If the dolls head reflex is intact, then the internuclear pathways must be intact
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52
Q

What is Nystagmus

A

Nystagmus is repeated, involuntary oscillation of the eyes. It can be physiological or pathological

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53
Q

What is physiological nystagmus

A

Occurs at extremes of gaze or by following fast-moving objects

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54
Q

Causes of pathological nystagmus

A
  • Upbeat → medullary lesions
  • Downbeat → Arnold-Chiari malformation
  • Vestibular → vestibular lesion causes nystagmus towards the lesion
  • Latent → horizontal nystagmus that starts when one eye is covered. Beats towards the covered eye. Associated with infantile esotropia
  • Convergence retraction nystagmus → bilateral convergence and retraction of the globe on attempted upgaze
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55
Q

Congential nystagmus may be caused by what?

A

Congenital nystagmus can be caused by bilateral cataracts and neurological disorders

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56
Q

What is Optic neuritis

A

Inflammation of the optic nerve, anywhere from the chiasm to the optic disc.

The most common cause is demyelination.

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57
Q

Classification of optic neuritis

A
  • Papillitis: Inflammation of the optic disc. Typically presents in post-viral children with flame haemorrhages and an oedematous optic nerve
  • Retrobulbar neuritis: disc is spared but the segment behind the eyeball is affected. The disc looks normal in this acute setting. More common in adults
  • Neuroretinitis: The disc and retina are both involved. Occurs in Lyme disease and cat scratch
58
Q

Disc Structure

A
  • High myopes have larger discs and hyperopes have smaller discs
  • Axons travel within the neuroretinal rim of the disc, not at the centre. The centre of the disc is vascular and contains the central retinal vessels
  • Macular fibres are responsible for central vision and count for over 1/3 of the axons of the disc, this is why optic neuropathies commonly cause central/paracentral scotomas
59
Q

What causes cat scatch disease

A

Bartonella Henselae, transmitted by cats

60
Q

Compare typical vs atypical optic neuritis

A
61
Q

Compare the clinical manifestations of optic nerve disease vs macular disease

A
62
Q

Papilloedema

A

Papilloedema is swelling of the optic disc directly from raised intracranial pressure. Disc oedema is the generic term for a swollen optic disc.

63
Q

What effect does acute papilloedema have on vision

A

Causes an enlarged blind spot

63
Q

What effect does acute papilloedema have on vision

A

Causes an enlarged blind spot

64
Q

What effect does chronic papilloedema have on vision

A

Results initially in the loss of the inferior nasal quadrant of vision

65
Q
A

Fundus image of a patient with papilledema. There are multiple haemorrhages and the disc margin is blurred.

66
Q

How can Anterior Ischemic Optic Neuropathy (AION) be classified?

Compare these

A

Arteritic or Non-arteritic

67
Q

Pathology of MS

A

T-cell mediated type 4 autoimmune neurodegenerative disorder of myelin in the central nervous system, which leads to inflammation and sclerosis.

68
Q

Classification of MS

A
  • Relapsing remittent - Episodes of MS which come and go
  • Primary progressive - The episode lasts >1 year and gets worse continually with time
  • Secondary progressive - Like relapsing remittent but the baseline condition is worse after each episode
69
Q

Presentation of MS

A

Classically presents in women in their 20s with optic neuritis.

70
Q

Investigations for MS

A

Diagnosis is based on episodes of neurological dysfunction in the history alongside CNS lesions, disseminated across time and space respectively.

71
Q

List/ Discuss 3 Other Optic Nerve Disorders

A
72
Q

Describe the following 3 pupil abnormalities

  • Marcus-Gunn Pupil
  • Argyll-Robertson Pupil
  • Adie’s Pupil
A
73
Q

What is Holmes-adie syndrome?

A

Aldie pupil + decreased lower limb reflexes

74
Q

What is Horner Syndrome

A

Horner syndrome is a triad of: ptosis, anhidrosis and miosis.

It is caused by a lesion in the sympathetic pathway to the head and neck.

75
Q

Lesions of first, second and third order neurons in Horners

A
  • First order : lesions of brain and spinal cord
  • Second order : Pancoast tumour and neck trauma
  • Third order: no anhidrosis. Caused by cavernous sinus lesions and internal carotid dissection
76
Q

Why is there no anhydrosis in third order Horner syndrome

A

Because the secretomotor fibres that supply the sweat glands of the face leave this pathway before the third-order neuron.

Therefore, a lesion of the third neuron will not affect sweat gland function.

77
Q

How can the lesion in Horners be localised

A

Administration of various topical medications bilaterally helps localise which order neuron is likely to be affected, and then relevant imaging of the high yield sites are conducted for diagnostics.

78
Q

Horners Syndrome - Topical Cocaine

A
  • Used to confirm horner syndrome, a lesion somewhere along the sympathetic chain
  • It blocks noradrenaline reuptake → enhances sympathetic effect and causes mydriasis in normal people
  • In Horner syndrome, the sympathetic pathway is broken so the Horner pupil will not dilate to Cocaine, but the normal one will
79
Q

Horners Syndrome - Topical Apraclonidine

A
  • Used to confirm Horners
  • Apraclonidine is an alpha agonist that causes mydriasis in normal people
  • In Horner syndrome, the sympathetic pathway is broken and the effector muscles at the end of the pathway are hypersensitive. When Apraclonidine is administered, the Horner eye dilates even more than the normal eye.
  • The principle underlying this test is denervation hypersensitivity
  • Remember that medications are applied bilaterally, to both eyes.
80
Q

Horners Syndrome - Topical Hydroxyamphetamine

A
  • Used to distinguish 3rd order lesions from the others (postganglionic or preganglionic). The ganglion in question is the superior cervical ganglion; it sits at the carotid bifurcation
  • Hydroxyamphetamine releases noradrenaline from the 3rd order neuron endings (postganglionic) to the dilator pupillae muscle which causes pupil dilation. If there is a 3rd order lesion, the pupil will not dilate. If there is no lesion, or a lesion of 1/2 order, the pupil will dilate
81
Q

Horners Syndrome - Topical Dilute Adrenaline

A
  • Used to distinguish 3rd order lesion from the others (postganglionic or preganglionic). The ganglion in question is the superior cervical ganglion; it sits at the carotid bifurcation
  • Adrenaline activates postsynaptic effector terminals to bring about the sympathetic response - pupil dilation. In Horner syndrome there is denervation hypersensitivity in these receptors, especially in 3rd order disease. If there is a 3rd order lesion, significant dilation is seen. Preganglionic Horner syndrome does not dilate as much.
82
Q

What 2 topical medications can be used to diagnose Horners

A

Cocaine and Apraclonidine

83
Q

What 2 topical medications can be used to localise 3rd order disease in Horners

A

Hydroxyamphetamine and dilute adrenaline

84
Q

Painful Horner syndrome is what until proven otherwise?

A

Carotid dissection until proven otherwise!

Urgent carotid angiogram is needed

85
Q

How are CN3 lesions characterised

A

Medical or surgical

Medical lesions characteristically spare the pupil (i.e pupil reflexes are intact and there is no anisometropia).

86
Q

How do medical vs surgical CN3 lesions differ

A

Medical

  • Much more common than surgical type
  • Typically caused by microvascular complications of diabetes and hypertension
  • The pupil will react to light

Surgical

  • Characteristic surgical causes include posterior communicating artery aneurysm and uncal hernia
  • The pupil will not react to light
87
Q

Why is the pupil only affected in surgical causes of CN3

A

The pupil is affected in surgical causes because they violently compress the pupillomotor fibres which run within CN3.

Microvascular problems are unlikely to affect these superficial fibres because of the rich blood supply via pial vessels.

Hence the pupil reflexes are spared in medical CN3 lesions.

88
Q

Presentation of CN3 lesion

A
  • Ptosis
  • Ophthalmoplegia with only abduction preserved
  • Down and out eye
  • Dilated pupil (in surgical type)
89
Q

Investigation for CN3 lesion

A
  • Urgent CT angiography in acute surgical third nerve palsies to rule out posterior communicating artery aneurysm
  • Medical cases should still get neuroimaging and workup for vascular risk factors, but this is far less serious in comparison.
90
Q

What is Weber’s stroke syndrome

A

CN3 palsy + contralateral hemiparesis

91
Q

CN4 Lesion causes

A

CN4 lesions are typically either congenital, traumatic or microvascular (most common)

92
Q

Presentation of CN4 lesion

A

Patients present with vertical diplopia and hypertropia (superior displacement of the eye)

93
Q

What special test is used to identiy CN4 lesion

A

Parks Test / Park-Bielschowsky 3 step test

  1. Find the hypertropic eye in the primary position
  2. Evaluate how the diplopia changes with horizontal gaze direction
  • Image separation is worse in contralateral gaze direction
  • I.e if the left eye is affected, diplopia is worse on right gaze
  1. Evaluate how diplopia changes with head tilt
  • Image separation is worse on ipsilateral head tilt
  • I.e if the left eye is affected, diplopia is worse on left head tilt.
94
Q

Most common cause of CN6 lesion

A

The most common cause is microvascular disease resulting in nerve ischemia.

95
Q

Presentation of CN6 lesion

A
  • Presents with horizontal diplopia and esotropia (the affected eye is deviated inwards).
  • Abduction is severely limited
96
Q

What is Gradenigo Syndrome

A
  • A classic syndrome of otitis + CN6 palsy
  • CN6 travels very close to the auditory structures so an infection in the ear can result in CN6 palsy.
  • Characteristically caused by pathology at the petrous apex of the temporal bone
97
Q

What is Internuclear Ophthalmoplegia (INO)

A

Internuclear refers to communication between CN6 (Pons) nucleus and the contralateral CN3 (midbrain) nucleus. This communication is by the medial longitudinal fasciculus (MLF). A lesion of the MLF results in internuclear ophthalmoplegia.

98
Q

Normal MLF Function

A
  • Normally, the MLF coordinates the CN6 and CN3 to permit horizontal gaze
  • The 2 muscles needed for horizontal gaze are CN6 (innervates LR) and CN3 (innervates MR)
  • The MLF connects the CN6 nucleus to the contralateral CN3 nucleus
  • E.G the RIGHT MLF connects the LEFT CN6 nucleus to the RIGHT CN3.
99
Q

Identifying The Lesion INO

A
100
Q

Bilateral INO (WEBINO/EBINO)

A

Bilateral internuclear ophthalmoplegia (INO) occurs when both MLF are diseased. It is also called WEBINO or EBINO. ‘WE’ stands for wall-eyed in WEBNIO. ‘E’ stands for Exotropic in ‘EBINO’. WEBINO is an outdated term as it conveys a negative image.

101
Q

Findings of Bilateral INO

A

In the primary position, both eyes are slightly deviated outwards, hence wall-eyed/exotropic.

On attempted LEFT gaze
* abducting nystagmus of the LEFT eye
* unable to adduct the RIGHT eye

On attempted RIGHT gaze
* abducting nystagmus of the RIGHT eye
* unable to adduct LEFT eye

102
Q

One and Half Syndrome

A

The ‘one’ refers to horizontal gaze palsy. This is caused by a lesion of the CN6 nucleus/PPRF. For example, a RIGHT CN6 nucleus lesion will stop the function of the right CN6 and the LEFT MLF. This means that neither eye will move on attempted RIGHT gaze. But LEFT gaze would be completely normal.

The ‘half’ refers to INO.

103
Q

Findings of One and Half Syndrome

A

The Pontine paramedian reticular formation (PPRF) and the CN6 nucleus are separate entities but are very closely associated, and can be considered as one entity for image below.

104
Q

List 2 other Gaze abnormalities

A
105
Q

Myasthenia Gravis

A

Myasthenia gravis is an autoimmune disorder of the neuromuscular junction. It is relevant in ophthalmology because it affects the eyelid/eye muscles.

106
Q

Pathology of Myasthenia Gravis

A

Anti-acetylcholine antibodies target the postsynaptic acetylcholine receptors at the neuromuscular junction, causing fatigability.

  • Repetitive movements worsen fatigue and weakness.
  • Because the eyelid muscles are used extensively throughout the day, ptosis and diplopia towards the end of the day is a classic sign.
107
Q

Lambert-Eaton syndrome

A

Another disease of the neuromuscular junction, but it affects the presynaptic calcium channels. Fatigue improves with muscle use.

108
Q

Presentation of Myasthenia Gravis

A
  • Ptosis which is worse at the end of the day
  • Diplopia is worse after extended reading or TV watching
  • Respiratory depression (Myasthenic crisis)
109
Q

Investigations for Myasthenia Gravis

A
  • Autoantibodies: Anti-AChR and Anti-MUSK
  • Repetitive nerve stimulation shows decrease in action potential amplitude
110
Q

Why is a CT thorax indicated in Myasthenia Gravis

A

A CT thorax is indicated in these patients because a thymoma can cause myasthenia gravis.

In these cases, thymectomy can cure the disease

111
Q

Management of Myasthenia Gravis

A

Acetylcholinesterase inhibitors such as pyridostigmine are used in long term management

Steroids are used in myasthenic crisis

112
Q

Myotonic Dystrophy

A

An autosomal dominant disorder is characterised by the failure of muscle relaxation after contraction.

113
Q

Pathology of Myotonic Dystrophy

A

Caused by trinucleotide expansion of CTG on the DMPK gene (chromosome 19)

114
Q

Presentation of Myotonic Dystrophy

A
  • Presents by the 2nd decade of life
  • Bilateral ptosis, cataracts(Christmas tree) and ophthalmoplegia.
  • Muscle weakness with delayed relaxation (myotonic grip)
  • Frontal baldness, testicular atrophy and cardiomyopathies
115
Q

Investigation for Myotonic Dystrophy

A

Diagnosis made by DNA testing

116
Q

Kearns-Sayre Syndrome

A

A rare cause of chronic progressive external ophthalmoplegia of mitochondrial inheritance. This is ultra-rare and has only been included for completeness, and to demonstrate that general myopathies often affect the extraocular muscles

117
Q

Presentation of Kearns-Sayre Syndrome

A
  • Can present at birth, most cases manifest well before the 2nd decade of life
  • Bilateral ptosis and ophthalmoplegia
  • Pigmentary salt and pepper retinopathy
  • Cardiac conduction defects
118
Q

Compare Neurofibromatosis (1&2) vs Tuberous Sclerosis

A
119
Q

Inheritance of Neurofibromatosis and Tuberous Sclerosis

A

Autosomal Dominant

120
Q

Types of Strabismus

A

There are 2 broad types of strabismus (tropias and phorias):

  • A tropia is when the eyes are always deviated (manifest deviation)
  • A phoria is a more subtle deviation which is hidden by binocular fusion, and becomes apparent when this is broken during testing.
121
Q

What is Strabismus

A

Strabismus is caused by abnormalities in extraocular muscle function. It can be treated with prism lenses or surgery, depending on the extent of the deviation.

122
Q

Types of Tropias and Phorias

A

Further classified according to the direction of eyeball deviation

  • Exotropia - outwardly turned (Divergent squint)
  • Esotropia - inwardly turned (Convergent squint)
  • Hypertropia - upwardly turned
  • Hypotropia - downwardly turned

The same terminology applied to phorias

123
Q

Most common form of childhood strabismus

A

Esotropia

124
Q

Esotropia is associated with what?

A

Hypermetropia

125
Q

How can Esotropia be classified

Compare these

A

Accommodative

  • Fully accommodative → Esotropia resolves with correction of hypermetropia
  • Partially accommodative → Esotropia partially resolves with cycloplegic hypermetropic correction and also needs treatment for amblyopia
  • Convergence excess → Esotropia for only nearly vision caused by high convergence. Manage with bifocal glasses or squint surgery

Non-accommodative

  • Infantile Esotropia is the commonest non-accommodative type
126
Q

Exotropia is typically associated with what

A

Myopia

127
Q

How can Exotropia be classified

Compare these

A

Intermittent vs Constant

Intermittent
* More common
* Exotropia which worsens based on distance or near gaze.
* Near exotropia is relatively common in in the adolescent population

Constant exotropia
* Presents in infants as a result of gross abnormalities in ocular motility

128
Q

What is responsible for stereopsis?

A

Binocular vision is also responsible for stereopsis (depth perception).

You need inputs from both eyes to perceive depth.

129
Q

Special Tests for Strabismus

A
  • Titmus, TNO, Lang, synoptophore → Stereopsis
  • worth 4-dot, Bagolini glasses and synoptophore → Sensory fusion
  • Prism cover test → Motor fusion (alignment)
130
Q

Hirschberg Test

A

Allows the clinician to identify tropias

  • A light from an ophthalmoscope is shone, and the corneal light reflex is located.
  • In orthophoria, the cornea light reflex should be right over the centre of the pupil.
  • In tropias, the corneal light reflex is deviated.

I.e In a right exotropia:
The corneal light reflex of the right eye will be more medial to the pupil. Demonstrating outward deviation of the eyeball.

131
Q

Cover Test

A
132
Q

What are Restriction Syndromes

A

Extraocular muscle action can be mechanically restricted for various reasons. This can lead to strabismus.

133
Q

List 2 types of Restriction Syndromes

A
  • Duane Syndrome
  • Brown Syndrome
134
Q

Duane Syndrome

A

Thought to be caused by aberrant co-innervation of both the LR and MR by CN3

  • This makes the globe retract during adduction.
  • Systematically associated with Goldenhar syndrome
  • There are 3 types based on additional features:

1: esotropia + abduction deficit
2 : exotropia + adduction deficit
3: esotropia + abduction and adduction deficits

Duane type 1 is the commonest

135
Q

Brown Syndrome

A

Limited elevation when adducted

  • Upgaze causes a characteristic clicking sensation
  • Caused by mechanical restriction of the superior oblique
  • Can be found congenitally or after trauma
136
Q

Strabismus Surgery techniques and outcome

A
137
Q

Amblyopia

A

The visual pathways develop in childhood by the age of 8. Any visual problems during this age can lead to abnormal visual development, which is then permanent throughout life. This is why strabismus and amblyopia are so important in paediatrics.

138
Q

Pathology of Amblyopia

A
  • Anything that affects vision in childhood can potentially lead to amblyopia
  • Common causes include strabismus and refractive error
  • Other causes include ptosis and congenital cataract
139
Q

Management of Amblyopia

A
  • Occlusion therapy - the good eye is occluded with an eye patch to allow the amblyopic eye to develop properly and catch up
  • Atropine penalisation - atropine is topically administered to the good eye, thereby reducing its visual acuity, and allowing the amblyopic eye to develop properly

Duke Elder (12 decks)

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