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Flashcards in Posterior Deck (346):
1

What is the pathogenesis of retinal vein occlusion

compression at AV crossings --> degenerative venous changes --> hypercoagubility

2

What are the risk factors of retinal vein occlusion? (9)

hypertension
hyperlipidemia
diabetes
CVD
increased IOP/glaucoma
smoking
high BMI
CT disorders/sarcoidosis/lupus
vasculitis

3

Symptoms of BRVO? (5)

may be asymptomatic
onset often in morning
transient vision loss
metamorphopsia
VF defects

4

Signs of acute BRVO (6)

located in one quadrant
flame/dot-blot haemorrhages
CW spots
dilated, tortuous veins
oedema
ON swelling/hyperaemia

5

Signs of chronic BRVO (2)

venous collateral formation
vascular sheathing

6

What modalities should you use to investigate BRVO? (2)

Fluorescein angiography
OCT

7

BRVO complications (2)

macula oedema
vitreous haemorrhage

8

BRVO are urgently referred if acute and semi-urgently if chronic for a systemic work-up and consideration of what types of treatment? (3)

laser
intravitreal steroid
anti-VEGF Tx

9

What is the optometrists role in managing BRVO other than referral?

monitoring for signs of NV and assoc complications

10

What are the clinical features of CRVO? (7)

intra-retinal haemorrhage (all quadrants)
venous engorgement and tortuosity
optic disc swelling
CW spots
CMO
sudden painless loss of vision
presenting VA reduced

11

Pathogenesis of CRVO?

Compression of CRV at lamina cribosa either by thrombus or CRA

12

Ischaemic vs non-ischaemic CRVO

Ischaemic
- VA <6/60
- marked RAPD
- optic nerve swelling
- severe venous tortuosity
- risk of developing retinal and iris NV

Non-ischaemic
- more common
- VA >6/60
- minimal RAPD
- may convert to ischaemic

13

CRVO management? (4)

monitoring monthly for 1 year
thrombolytics
Laser chorioretinal anastomosis (L-CRA)
pan retinal photocoagulation

*possibly intra-vitreal anti-VEGFs

14

A person with CRVO has a better outcome when

present early and treated early

15

CRAO symptoms (3)

-painless vision loss over several seconds
-possible Hx of amaurosis fugax
-vision significantly reduced (<6/120) unless cilioretinal artery present

16

CRAO signs (4)

- VA <6/120 and RAPD in affected eye
- Within first few minutes retina may look normal
- ischaemic whitening of retina resulting in cherry-red spot at macula
- retinal arteriole thinning and attenuation with possible segmentation of blood flow

17

What is the level of urgency for CRAO?

ophthalmic emergency - urgent referral

18

Management for CRAO? (7)

- emergency referral
- digital ocular massage or with gonio
- reduction of IOP by paracentesis or pharmaceutically
- assessment of risk of GCA
- control of systemic disease (HT, diabetes, hyperchol)
- assessment of carotid and cardiac disease as source of emboli
- use of aspirin or warfarin

19

BRAO can occur secondary to what two things?

emboli
inflammation

20

Over 90% of BRAOs involve arteries in which area?

temporal retinal arteries

21

BRAO symptoms (2)

-acute, unilateral, painless loss of vision over several seconds
- visual field defect may be noticed

22

BRAO signs (4)

- VA <6/12 affected eye
- initially fundus looks normal within first few mins
- localised ishaemic whitening of retina in area fed by arteriole
- retinal arteriole thinning and attenuation with possible segmentation of blood flow

23

Management of BRAO (4)

- referral for assessment of systemic associations
- control of systemic disease as for CRAO
- assessment for carotid and cardiac disease as for CRAO
- majority of Px achieve 6/12 or better with conservative Tx

24

Which is more common: BRVO or CRVO?

BRVO

25

BRAO level of urgency?

urgent referral

26

Optic disc drusen is believed to be buried or superficial _______ material as a biproduct from which cells?

hyaline-like astrocyte

27

Optic disc drusen can often cause what two signs?

field defects
choroidal neovascular membranes

28

What tests are done for a definitive Dx of optic disc drusen? (2)

B-scan and FA

29

Optic disc drusen are associated with what condition?

Pseudoxanthoma elasticum

30

The most important thing with optic disc drusen is?

to rule out other conditions which involve the disc

31

Optic disc colobomas are typically located where and accompanies a field defect located where?

inferior nasal
superior

32

Optic disc and chorioretinal colobomas can develop into what?

serous macular detachment

33

Morning glory anomaly is what?

variant of ONH coloboma

34

With morning glory anomaly the disc is deeply escavated with what sort of tissue at the base?

glial

35

Optic disc pits are what?

atypical coloboma of ONH

36

What is management of Px with optic disc pit?

monitor carefully including home Amsler

37

With posterior coloboma conditions we need to be aware that these can develop what?

serous maculopathy

38

Which condition demonstrates the "double ring sign"

optic nerve head hypoplasia

39

Optic nerve head hypoplasia results in?

loss of NFL with variable VF defects

40

Which condition is associated with maternal infection or drug abuse, fetal alcohol syndrome, gestational diabetes and brain malformations?

optic nerve head hypoplasia

41

What condition can make the disc look raised with indistinct margins and have anomalous vascular branching patterns (not papilloedema, papillitis)

small optic disc

42

Which condition is characterised by an enlarged ONH with large cupping with the lamina often visible (DDx with glaucomatous cupping)

megalopapilla

43

High survival rates of retinoblastoma are associated with?

early detection

44

Retinoblastoma signs? (5)

- White mass projecting forwards or backwards from retina
- leukocoria
- strabismus
- intraocular inflammation
- increased IOP

45

Tx of retinoblastoma? (4)

- cryotherapy
- thermotherapy
- radiation therapy
- enucleation

46

What condition is characterised by a retrolental mass of persistent embryonic hyaloid system and primary vitreous?

persistent hyperplastic primary vitreous

47

Retinopathy of prematurity is characterised by?

abnormal retinal vasculature in premature infants and/or low birth wt

48

ROP can be associated with?

supplemental oxygen

49

What are the five stages of ROP?

Stage 1 - white line at demarcation of avascular zone
Stage 2 - development of ridge and abnormal vessels
Stage 3 - fibrovascular proliferation
Stage 4 - contraction of fibrovascular tissue and RD
Stage 5 - complete RD

WARP CD

50

What is this condition?
- single or grouped usually unilateral
- flat, well demarcated, dark
- tend to depigment over time
- can be grouped (bear tracks)
- can be atypical and associated with colon polyps

congenital hypertrophy of the RPE

51

When there are multiple, large, bilateral CHRPEs affecting several quadrants, what other condition needs to be considered?

familial adenomatous polyposis

52

What are myelinated nerve fibres?

persistent myelination of axons anterior to lamina cribosa

53

Which condition causes the fundus to later develop granularity pigmentary changes and vessel attenuation with other signs: sluggish pupils, nystagmus, strabismus, cataract, KC, abnormal ERG?

leber's congenital amaurosis

54

Splitting of the NFL from retina in periphery is called?

retinoschisis

55

What condition has hypoplasia of ONH and/or fovea with varying levels of reduced VA?

albinism

56

varying degrees of amelanosis is due to varying levels of what?

tyrosinase

57

What is management of albinism? (2)

- control glare and photophobia
- low vision aids

58

When examining a Px with albinism what should you keep in mind?

don't prolong fundoscopy

59

What is the condition when you are born with no fovea?

hypoplastic fovea

60

What is tilted disc syndrome?

ONH appears rotated about its axis

61

Tilted disc syndrome signs? (4)

- oval shape disc
- scleral crescent
- myopic astigmatism common
- bi-temporal VF defects possible

62

What is obliquely inserted disc?

ONH inserts through scleral canal at an oblique angle

63

Obliquely inserted disc signs (4)

- elevated nasally, buried temporally
- function normal (usually)
- often hyperopic
- usually bilateral

64

Glial remnants are common in premature babies and protrude into the vitreal cavity and they are remnants of what?

embryonic hyaloid artery and related glial tissue

65

Toxoplasmosis scars are _________ in location, focal, with pigmented borders and can re-activate causing _____

chorio-retinal
retinitis

66

Risk factors for ARMD (3)

- Age
- Smoking
- Race - higher incidence in Caucasians

67

Classification of ARMD including proportion of cases

atrophic - dry - 80-90%
exudative - wet - 10-20%

68

In atrophic AMD, atrophy of what three cell types occurs?

photoreceptors
RPE
choriocapillaris

69

What test is essential for diagnosis of ARMD?

OCT

70

Hard drusen are _____ in size (___um), discrete and usually does not necessarily signify ARMD

small
<50-60um

71

Soft drusen are _____ in size (___)um, have indistinct margins and is more associated with ARMD

larger
=/>60 microns

72

Soft drusen can develop and become two things which are?

confluent drusen
calcified

73

Drusen are accummulation of waste products from which layer of the PRs and are found in between what layers?

Outer segment
Bruch's and RPE

74

Generally it is agreed that a Px has AMD after what is compromised? This occurs due to the ___ no longer being intact and causing damage to the PRs at the macula

BCVA
Inner segment

75

reflective deposits between RPE and retina found in the peripheral retina often seen in association with drusen and a risk factor for ARMD are called?

reticular pseudodrusen

76

Symptoms of atrophic ARMD? (4)

- slowly decreasing BCVA
- deepening central scotoma
- usually bilateral but asymptomatic
- positive Amsler grid findings

77

Signs of atrophic ARMD (4)

- RPE atrophy and hyperpigmentation
- broadening of atrophy with progression
- visible choroidal vessels
- drusen and mottling

78

Use of fluorescein angiography with atrophic AMD shows what two things?

hyperfluorescence in areas of RPE atrophy
hyper or hypo fluorescence of drusen

79

Tx of atrophic ARMD? (3) ish

- none effective
- nutritional supplements may slow progression
- low vision aids when BCVA severely affected

80

Exudative ARMD signs? (4)

- often soft, confluent drusen
- serous maculopathy (sometimes with hard exudates)
- Sub-RPE or sub-retinal CNV
- Sub-retinal haemorrhage

81

Exudative ARMD symptoms (3)

- increased blurred vision
- metamorphopsia
- vision loss can be sudden due to sub-macular haemorrhage

82

Suspected cases of exudative ARMD should be urgently referred for what test which determines the exact location in relation to the retina?

FA

83

Exudative ARMD Tx starting from historical to current main Tx (3)

- Photodynamic therapy - inject VISUDYNE and laser applied to CNV
- Argon laser photocoagulation - destroys CNV however cannot be undertaken if CNV near or under macula. 50% recurrence rate.
- VEGF blockers

84

What are the 3 current VEGF blockers used to treat exudative ARMD?

1) bevacizumab (Avastin) - funded
2) ranibizumab (Lucentis) - restricted funding
3) aflibercept (Eylea) - better binding - not funded

85

Tx with anti VEGF usually starts with what regime? What else is also sometimes used in conjunction with anti-VEGFs?

monthly injections for 3 months then monitor for stability.
Intra-vitreal steroids

86

What conclusions came about from the AREDS studies?

- zinc and antioxidants modestly effective in slowing progression of some AMD
- adding lutein + zeaxanthin, DHA + EPA or both did not further reduce risk of progression

87

What sort of nutritional advice could you give to Px to reduce risk of ARMD?

- increase intake antioxidants - colored veges, omega 3 (fish), vitamin supplements

88

What other advice could you tell patients to reduce risk of ARMD (4)

- avoid smoking
- improve lifestyle
- home amsler grid
- UV eye protection

89

Compare and contrast type 1 and 2 diabetes

Type 1
- rapid onset in youth
- dependent on insulin
- 10% of diabetes
Type 2
- progressive
- variable dependence on insulin
- can be treated with diet, exercise, weight control, oral agents and insulin
- 90% diabetes

90

Factors that determine presence of DR

- duration of disease
- level of blood glucose (HbA1c)
- poor metabolic control
- HT
- pregnancy
- nephropathy
- elevated blood lipids
- smoking

91

HbA1c levels have been classified as a percentage and categorise people as not diabetic or at risk. What are the values?

Not diabetic <6%
At risk 6-7%

92

Diabetes can cause what changes to the cornea? (4)

- epithelial changes
- reduced sensation and tear production
- possibly thicken stroma
- early aging signs at endothelium

93

Diabetes can cause what changes to iris and ciliary body? (3)

- vacuoles of pigment epithelium
- pinhole trans-illumination defects
- rubeosis irides

94

Diabetes can cause what changes to lens? (4)

- snowflake cataract
- increased risk of age-related cataracts
- varying of refractive power
- more post op complications after cataract surgery

95

Diabetes can cause what changes to the vitreous? (2)

- haemorrhage
- possibly early PVD

96

Diabetes can also cause diplopia, ptosis and anisocoria through complications of which cranial nerves?

III
IV
VI

97

Non-proliferative signs of DR are related to loss of which type of cells?

pericytes

98

Signs of NPDR (8)

- microaneurysms
- macular oedema
- dot, blot, flame haemorrhages
- hard exudates
- intraretinal oedema
- CW spots
- IRMAs
- venous beading

99

PDR is associated with retinal _____ causing the formation of ________ and involves ______ growth factors

hypoxia
new vessels
vascular endothelial

100

Signs of PDR (4)

- NV
- fibrous tissue
- pre-retinal or vitreous haemorrhages
- tractional RD

101

Clinically significant macular oedema (CSMO) is defined as oedema within how many DD?

1/3

102

Macular oedema is defined as within?

2DD of centre of macula

103

Assessment of macular oedema requires _______ ______ and diagnosis requires _____

stereoscopic examination
OCT

104

CSMO is treated with? (2)

Anti-VEGFs
laser

105

What sort of examination is required for every diabetic Px?

DFE

106

What two tests are needed for detecting DR?

FA
OCT

107

Grade R0 (No DR) - clinical signs and outcome?

No abnormalities
For type 1 - re-screen at 2 years, adjusting for clinical modifiers
For type 2 - re-screen at 2-3 years, adjusting for clinical modifiers

108

Grade R1 (Minimal) - clinical signs and outcome?

<5 microaneurysms or dot haemorrhages
Re-screen at 2 years depending on clinical modifiers

109

Grade R2 (mild) - clinical signs and outcome?

>4 microaneurysms or dot haemorrhages
Exudates >2DD from fovea
Some blot and larger haemorrhages acceptable
If more than 20 microaneurysms or haemorrhages per photographic field, upgrade to R3
Outcome - Re-screen after 12 months

110

Grade R3 (moderate) - clinical signs and outcome?

Any features of mild
Blot or larger haemorrhages
Up to one quadrant of venous beading
Outcome - re-screen 6 months

111

Grade R4 (severe) - clinical signs and outcome?

One or more of:
- definite IRMA
- two quadrants or more of venous beading
- four quadrants of blot or larger haemorrhages

Outcome - review by ophthal within 6 weeks

112

Grade R5 (proliferative) - clinical signs and outcome?

One or more of:
- NV
- sub-hyaloid or vitreous haemorrhage
- traction RD or retinal gliosis

Outcome - urgent referral to ophthal

113

Adequate quality of photos for grading require a minimum field size of? When is it required to take a superior and inferior image also?

two 45 degree fields
type 1 diabetes or R3 and higher

114

Taking a quality diabetic photo should produce an overlap of at least how many degrees horizontally and vertically?

75 horizontally
45 vertically

115

Which form of treatment for DR reduces risk of VA loss and is more effective if undertaken before high risk features are present?

photocoagulation

116

Symptoms of vitreous inflammation (4)

- Floaters
- Ache ?
- Decreased VA (depending on maculopathy)
- Red eye (depending on location)

117

Signs of vitreous inflammation (7)

- vitritis
- vitreous opacities
- PVD
- retinitis/scarring
- CMO
- cataract
- RD

118

What in particular causes vitreous inflammation?

intermediate and posterior uveitis

119

Which vitreous opacity are calcium soaps suspended in the vitreous that do not usually affect vision, usually do not move and is associated with diabetes and vascular disease?

asteroid hyalosis

120

Which vitreous opacity is any part of the hyaloid system that can remain and can cause floaters. They are also known as Mittendorf's dot and Bergmeister's papilla

hyaloid remnants

121

Which vitreous opacity often results from NV or retinal tears?

intra-vitreal haemorrhage

122

Which vitreous opacity can result from:
trauma
intraocular surgery
intraocular inflammation
RD

pigment particles

123

Which vitreous opacity are cholesterol crystals which:
- tend to form and settle in liquefied vitreous
- can be stirred up with movement
- tend to occur following vitreal inflammation and haemorrhage

synchysis scintillans

124

Persistent hyperplastic primary vitreous is what?

failure of regression of embryonic hyaloid vascular system

125

PHPV is usually unilateral/bilateral, common/rare, causes __________ and often associated with what (4) conditions?

unilateral
rare
leukocoria
microphthalmia, cataract, glaucoma, RD (+ others)

126

Retinoblastoma originates from where?

any layer of the retina

127

There are two types of retinoblastomas which are?

endophytic - grows inwards towards vitreous
exophytic - grows outwards into subretinal space --> RD + haem

128

Retinoblastomas can cause? (4)

- leukocoria
- strabismus
- intra-ocular inflammation
- increased IOP

129

What symptoms are common during PVD?

flashes and floaters

130

PVD can cause what other three things

RD
retinal haemorrhage
macular traction syndrome (and possible macula hole)

131

Lattice degeneration represents areas of (1) and (2) which run circumferentially between what two structures (3/4)?

1) retinal thinning
2) capillary drop-out
3) ora serrata
4) equator

132

Snail track degeneration is likely a variant of what other condition?

lattice degeneration

133

Which two conditions can contain atrophic holes and which is less likely to cause RD?

lattice degeneration and snail track degeneration
snail track less likely to cause RD

134

What peripheral retinal condition is thought to be congenital (may be degenerative) is usually seen in the inferio/temporal quadrant is associated with areas of retinal thinning with loss of RPE with Bruch's membrane intact and is of NO CONSEQUENCE

Pavingstone degeneration

135

Which peripheral retinal condition is very common, tends to increase with age and is characterised by cysts in the NFL or OPL and can be a precursor to what condition?

cystoid degeneration
retinoschesis

136

Which peripheral retinal condition can be mistaken for a RD, is usually bilateral, is flat, sharply demarcated and considered to be due to abnormal vitreo-retinal traction or a prominent vireous base (of no consequence)

white without pressure

137

RPE degeneration and disorganisation of pigment granules in the perpheral retina is characteristic of which condition? This condition can also have what characteristic which makes it look similar to RP?

1) reticular (pigmentary) degeneration
(a condition of no consequence)
2) can have bone spickle apperanace

138

What is retinoschesis (incl what layer is involved)

Splitting of neuro-retina (outer plexiform layer)

139

Retinoschesis is often associated with what other condition?

cystic degeneration
(retinoschesis is a benign condition)

140

Which condition is caused by mutation of gene controlling ornithine keto-acid aminotransferase which leads to 2nd decade axial myopia, night blindness, cataract and CMO with poor prognosis for vision?

gyrate atrophy

141

What are vitreo-retinal adhesions (tufts)?

abnormal areas of localised attachment of retina to vitreous with white tuft appearance

142

Vitreo-retinal adhesions (tufts) require monitoring for what reason?

can cause retinal traction

143

Define a retinal detachment

separation of the photoreceptors from the RPE

144

RD can be classified as?

- with retinal break (rhegmatogenous)
- without retinal break (non-rhegmatogenous)
- tractional
- exudative/serous

145

Retinal breaks can be classified as? (3)

- U or V shaped with apex pointing to post pole
- operculated (flap completely torn off)
- dialyses (tears away from ora)

146

Most retinal breaks are located where on the retina?

superio-temporal

147

What are risks for retinal breaks? (7)

- PVD
- vitreous traction
- lattice degeneration
- snail track degeneration
- white without pressure
- retinoschisis
- retinal traction

148

PVD's are generally assoc with no complications but they can cause what two things

retinal break
vitreous haemorrhage

149

Following cataract surgery and YAG capsulotomy in myopia there is a higher risk of what?

RD

150

Risk factors for rhegmatogenous RD (6)

- retinal holes/tears
- myopia
- FHx
- RD other eye
- Hx of trauma
- Hx of intraocular surgery

151

Symptoms of rhegmatogenous RD (3)

- photopsia
- floaters
- VF defect

152

Sign of rhegmatogenous RD (5)

- Shafer's sign
- Tear/s or hole/s in retina
- RAPD if extensive RD
- decreased IOP if RD is large
- mild anterior uveitis possible

153

How can you tell the difference between a recent and longstanding rhegmatogenous RD? (3 each)

Recent
- affected retina appears opaque or gray
- tends to move with eye movements
- loss of visibility of underlying structures
Longstanding
- retina thins = some viewing of underlying structures possible
- high water mark of pigmentation forms at boundary
- intraretinal cysts may develop

154

Compare and contrast a rhegmatogenous RD vs retinoschisis (write on paper - 9 points for each)

RD
- looks whitish initially, semitransparent later
- surface folds
- tends to undulate on eye movements
- retinal break present
- pigmented demarcation line when longstanding
- speed of enlargement variable
- can invade posterior pole
- symptoms common
- usually treated

Retinoschisis
- usually transparent
- smooth, taut surface
- no movement
- inner and outer breaks possible
- rarely has pigmented demarcation line
- enlarge very slowly
- rarely invades posterior pole
- usually asymptomatic unless affects post pole
- not usually treated unless inner and outer breaks

155

Non-rhegmatogenous RDs can be due to what two things?

proliferative retinopathy
proliferation of (epi) retinal membranes

156

How does a tractional RD (without retinal break) compare to a rhegmatogenous RD? (3 main points)

tends to be slower onset and without flashes and floaters
affected retina not usually mobile

157

Describe exudative RD

exudation from choriocapillaris into subretinal space (fluid passes through RPE) causing detachment

158

What are the causes of exudative RD? (6)

- central serous retinopathy
- subretinal NV
- choroidal tumours (75%)
- posterior scleritis
- severe hypertension
- systemic corticosteroids

159

Symptoms of exudative RD (3)

- no flashes usually, might be present in acute presentation
- absolute scotoma at site of lesion
- metamorphopsia if central

160

Signs of exudative RD (4)

- no retinal breaks
- smooth surface
- RD can be deep and fluid may be seen to move with gravity
- underlying cause may be seen (e.g. choroidal tumour)

161

What is polypoidal choroidal vasculopathy?

network of branching inner choroidal vessels ending with polyp-like extensions which occupy the sub-retinal space and can cause fluid build up and haemorrhage

162

Polypoidal choroidal vasculopathy is considered a unique form of _____ and has an appearance of ____, ____-like elevations and is diagnosed with what two tests?

CNV
sharp, dome-like elevations
OCT and FA

163

How do you manage CSR if:
- first episode
- recurrent

- if first episode monitor up to 3 months and refer if non-resolving
- consider referral for recurrent cases

164

What do you have to rule out for CSR?

other causes of serous detachments e.g. choroidal melanoma, ARMD

165

What modality is required to confirm Dx of CSR?

OCT

166

In all cases of flashes and floaters what must we do?

Rule out retinal breaks, RD, PVD

167

Comment on time for surgery for macula-off RD (2)

- Eyes treated up to 3 days have better outcomes than eyes treated after. No difference within the first 3 days.
- should NOT postpone surgery for macula-off detachments

168

Drug induced maculopathy can be caused by what 6 drugs?

- Chloroquine and hydroxychloroquine
- phenthiozines
- tamoxifen
- vigabatrin
- methanol

169

Cystoid macular oedema is characterised by ______ accumulations of fluid with _________ formations, typically in a _____ pattern.

- intracellular accumulations of fluid
- microcystic formations, typically in a stellate pattern

170

CMO symptoms and signs (5)

- often asymptomatic in early stages
- metamorphopsia
- reduced vision
- prolonged photostress recovery
- subtle macular changes, increasingly obvious with progression

171

Definitive Dx of CMO requires what modality

OCT or FA

172

CMO is associated with what conditions? (6)

- post-ocular surgery
- retinal vascular disorders
- intraocular inflammation
- retinal degeneration (RP, cellophane maculopathy, tumours)
- idiopathic
- drug related (epinephrine)

173

What is the prognosis and Tx for CMO? (5 for Tx)

- often self-limiting within 3 months
- referral to consider:
NSAIDS
steroids
anti-VEGFs
CAIs
laser

174

Vitreomacular traction syndrome can cause what symptoms? (4)

metamorphopsia
decreased VA
micropsia
photopsia

175

Pxs who get macular holes are usually? (2)

over 60
female

176

Macular holes are considered to be caused by? (2)

vitreal traction forces and/or cystic formation

177

Macular holes are usually unilateral and there is a __ yr risk of development in the other eye with no ___ with a chance of __-__%

5 year risk
PVD
20-30%

178

Describe stage 1 macular hole (5)

- loss of foveal depression
- radial traction lines possible
- metamorphopsia/distortion
- VA might remain good
- appearance of yellow spot possible (xanthophyll)

179

Describe stage 2 macular hole (3)

- VA drops to 6/12-6/30
- foveal hole or tear develops
- cuff of subretinal fluid

180

Describe stage 3 macular hole (6)

- further vitreo-foveal separation
- enlargement of hole
- positive Watzke-Allen test
- operculum may be visible
- white/yellow deposits may be visible in hole
- VA 6/30-6/60

181

Describe stage 4 macular hole (3)

- Full thickness hole with PVD
- operculum might be mobile
- central absolute scotoma

182

What is prognosis of stage 1 macular hole vs stage 2 or 3?

30-50% of stage 1 holes arrest and spontaneously resolve whereas less than 10% of stage 2 or 3 holes resolve

183

Tx of macular holes? (4)

refer to retinal specialist to consider:
- vitrectomy
- vitreous peeling
- gas tamponade
- face down therapy

184

Epiretinal membranes/cellophane retinopathy/macular pucker is due to?

proliferation of glial cells from retina

185

Epiretinal membranes can be idiopathic or secondary. Secondary causes can be from? (6)

- chronic RD
- secondary glaucoma
- chorio-retinitis
- DR
- ocular surgery
- laser photocoagulation

186

When should you consider referral for epiretinal membrane and what will the ophthal likely do?

when vision 6/12
membrane peel

187

Signs of degenerative myopia? (6)

- RPE atrophy
- lacquer cracks
- CNV
- subretinal haemorrhagse
- Foerster-Fuchs spot
- macular hole

188

What condition is characterised by orange peel effect seen at and temporal to the macula where cracks in thickened Bruch's membrane radiate from the disc?

angioid streaks

189

Characteristics of optic disc pits (4)

- congenital
- serous maculopathy in ~50% cases
- metamorphopsia
- VF defects

190

direct sun gazing causes bilateral VA loss, chromatic changes in vision, metamorphopsia and causes foveo-macular retinitis. This condition is called?

Solar maculopathy

191

Stargardt disease is _______ in inheritance is a __lateral condition and causes reduced _____ vision from about ____ years old to about 6/___ or less

autosomal recessive
bilateral
central
10
6/60

192

Fundus flavimaculatus can occur with or without Stargardt and has what characteristics? (4)

- yellow white flecks (disruption of RPE)
- accummulation of lipofuscin
- variable effect on vision
- 50% have Stargardt

193

Best Disease is _____ in inheritance and reduces vision from about ___ years of age. It is characterised by what appearance?

autosomal dominant
10 yrs old
egg-yolk appearance due to lipofuscin accummulation

194

Name the prostaglandins for glaucoma Tx (3)

latanoprost (Hysite)
travaprost (Travatan)
Bimatoprost (brand name same)

195

Name the beta-blockers for glaucoma Tx (4)

Betaxolol (Betoptic)
levobunolol (Betagan)
Timolol (same)
Timolol XE (Timolol gel)

196

Name the sympathomimetics (a2 agonists) for glaucoma Tx (2)

brimonidine (Alphagan)
apraclonidine (Iopidine)

197

Name the carbonic anhydrase inhibitors for glaucoma Tx (3)

acetazolamide (Diamox)
Brinzolamide (Azopt)
Dorzolamide (Trusopt)

198

Name the combination meds for glaucoma Tx (6)

Latanoprost + timolol (Xalacom)
Travaprost + timolol (DuoTrav)
Brimonidine + timolol (Combigan)
Brinzolamide + timolol (Azarga)
Dorzolamide + timolol (Cosopt)
Bimatoprost + timolol PF (Ganfort)

199

Glaucoma is an ____ _________ caused by chronic destruction of ______ cells with characteristic atrophy and functional loss with or without IOP elevation.

optic neuropathy
ganglion

200

A visual field loss may only be detected after how many ganglion cells are lost?

20-40%

201

Mechanical theory of glaucomatous optic neuropathy

- IOP damages neurons at lamina
- compression/rearrangement of lamina cribrosa sheets
- distortion/enlargement of lamina pores
- altered lamina and ECM
- results in axoplasmic stasis
- necrosis

202

Vascular theory of glaucomatous optic neuropathy

1. ischaemia due to blood flow abnormalities or elevated IOP reduces perfusion
2. autoregulation of blood flow in ON arteries abnormal
3. slows axoplasmic flow
4. damages optic nerve/peripapillary region

203

What conditions are associated with POAG

- systemic hypotension
- decreased cardiac output or BP drop at night
- migraine/vasospasm
- diabetes
- acute loss of blood
- chronic vascular obstruction
- hyperviscosity diseases

204

What is the apoptosis theory of glaucomatous optic neuropathy?

1. elevated IOP decreases axoplasmic flow
2. Decreases effect of BDNF for ganglion cell survival
3. initiates apoptosis response

205

What two main factors are thought to be responsible for optic nerve injury/insult in glaucoma which leads to cell death --> excitotoxicity + decreased NTFs --> apoptosis

elevated IOP
decreased blood flow

206

Define target pressure

the pressure at which the clinician expects the loss to be no greater than the age related rate

207

What is the relation between IOP and corneal thickness?

0.3mmHg per 10um (Goldmann is calibrated for 515um)

208

How can you mechanically increase outflow through the TM?

cholinergic agonists e.g. Pilocarpine

209

What effect do steroids have on outflow?

steroid respones --> increase GAGs in TM --> increased outflow resistance

210

What are the two main routes for aqueous outflow including outflow capacity %

1. Canalicular/TM 85-95%
2. Extracanalicular/uveo-scleral outflow 5-15%

211

What glaucoma drug increases outflow by acting on the CB and how?

Prostaglandins (e.g. Latanoprost) by decreasing CT density in CB and making it more porous

212

Glaucoma patients with big diurnal spikes in IOP are best treated with what kind of drug?

Outflow drugs e.g. prostaglandins

213

What are the avenues of treatment for glaucoma? (3)

1. lowering IOP
2. treating vascular diseases
3. countering apoptosis/promoting neuroprotection

214

What are the predictive factors for glaucoma (according to OHTS)? (6)

- age (older)
- race (african higher iop)
- CD ratio (vertical more relevant)
- IOP
- corneal thickness
- increased or asymmetric PSD

215

Which glaucoma drug is a potential neuroprotective drug?

Brimonidine
- impairs apoptotic pathways
- upregulates anti-apoptotic genes
- reduced excitatory aa release
- increased neuroprotective agents
BUT lack of clear evidence

216

What are the risk factors for POAG? (7)

- FHx
- Ethnicity (african americans>caucasians>asians)
- Age
- IOP
- Vascular conditions (hypo/hyperT, diabetes, reynauds, migraine)
- Myopia
- Obesity

217

Comment on the characteristics of NTG (6)

- more sensitive to ON damage
- more splinter haemorrhages
- ONH cupping larger and steeper at time of Dx
- frequent inferotemporal displacement of cup
- higher incidence of inferior focal rim compromise or notching
- slower progressive VF loss

218

Pseudoexfoliation glaucoma is characterised by what 2 things which can lead to what?

- amyloid-like material in AC and TM
- iris transillumination near pupil margin
- material can lead to peripupillary ischaemia and PS leading to pigment release and further TM blocking

219

What signs might you see with a patient with pigmentary glaucoma? (4)

- spoke wheel iris transillumination
- krukenbergs spindle
- pigment deposit in TM
- Sampaolesi line

220

Which groups of people are at higher risk of steroid responsive glaucoma?

- diabetic
- high myopic
- CT damage
- children

221

Name as many secondary open angle glaucomas as you can (7)

pseudoexfoliation
pigmentary
steroid responsive
intraocular inflammatory
neovascular
lens-associated
traumatic

222

Describe characteristics of sub-acute PACG (3)

- intermittent pain/halos
- precipitated at night or with dilation
- frequent recurrence

223

Describe characteristics of chronic PACG (2)

- eye quiet with usually mildly shallow angles
- gonio shows narrow angle with broad areas of PAS

224

What are the risk factors for PACG? (4)

- shallow AC
- plateau iris
- large lens
- iridocorneal syndromes

225

Name 4 types of secondary ACG

- intraocular inflammatory
- subluxated lens
- neoplasm of iris/CB
- phacomorphic (secondary to hyper/mature cataract)

226

What ocular signs do we need to consider when diagnosing glaucoma? (9)

- abnormal NRR
- laminar pore slits
- cup size for ON size
- peripapillary atrophy
- retinal fibre layer loss
- CD ratio >0.5
- CD ratio asymmetry >0.2
- non-central insertion of CRA
- compromised AC

227

What are the five rules (5+1) of ONH evaluation for glaucoma?

- disc size
- ISNT (looking more at notching or vert elongation)
- disc haems
- RNFL dropout
- PPA
- changes to BVs e.g. baring, bayoneting

228

Give the 5 stages of Tubingen classification of glaucomatous defect (maybe write physically)

Stage 0
- increased short term fluctuations in arcuate region (nasal step)
- review
Stage 1 (mild)
- relative defect - local loss in arcuate defect, nasal step
- act
Stage 2 (mild-moderate)
- absolute defect
- act
Stage 3 (moderate)
- ARCUATE DEFECT - joins blind spot
- act
Stage 4 (moderate-severe)
- multiple arcuate defects
- peripheral break through threat to fixation
Stage 5 (severe)
- end stage glaucoma
- act

229

What is the target IOP for stage 1-2 (Tubingen)

<23

230

What is the target IOP for stage 3 (Tubingen)

<22

231

What is the target IOP for stage 4 (Tubingen)

<21

232

What is the target IOP for progressive glaucomatous defects

<17

233

What do we do to the IOP level for 60 and 70yo respectively

60yo - drop 1 IOP level
70yo - drop 2 IOP levels

234

How is field loss in LTG/NTG different from POAG? (4)

- more frequent damage within 5 degrees of fixation
- higher probability in superior hemifield
- field loss is steeper sided and more dense in NTG
- more localised

235

Is SWAP useful in glaucoma diagnosis?

probably picks up glaucoma earlier because it picks up on different GCs but the test is difficicult to do and takes a long time

236

What are the three R's to assess the results of threshold VF tests?

reliability
region affected
repeatibility

237

What is the mean deviation (MD) in a VF test?

average deviation from age-matched normals

238

What is the PSD in VF test?

average slope (drop off from hill of vision)

239

What is the GHT in VFs?

uses 5 mirror image clusters of points

240

what is the total deviation in VF test?

compares average sensitivity to normal

241

What is the pattern deviation in VF test?

total deviation corrected for diffuse loss

242

What % of FP is considered unreliable in VF?

>33%

243

What % of fixation losses is considered unreliable in VF?

>20%

244

What % of FN is considered unreliable in VF?

>33%

245

Scotomas are characterised by which reliability indices?

high FN
high fixation loss

246

Detection of local defects is the hallmark sign of POAG - what is important in regards to VF testing for reliability

repeat fields to confirm reliability
2-6 weeks later

247

Definition of progression in glaucoma

if structural and/or functional changes, associated with the disease, are verifiably detected on clinical examination and/or testing

248

VF progression is judged with what analysis?

event or trend analysis

249

How many VF tests do you need to establish baseline?

2

250

How many VF tests do you need to do per year to establish progression?

2 per year, within 2 years

251

What is the problem with FDT compared to SAP in VF testing?

FDT provides poor progression data

252

What is the gold standard glaucoma examination required under NHMRC guidelines? (5)

Must do all of the following:
IOP
gonio
VF
optic disc images
RNFL images

253

What is the suggested glaucoma work-up? (12)

- Case Hx
- BCVA
- Pupils
- Monocular CV
- Gonio
- Pachy
- Anterior segment
- Tono (GAT)
- dilation
- VF (threshold)
- NFL assessment
- ONH analysis

254

Dry eye is a _________ disease of the ______ ______ characterised by a loss of _________ of the tear film, and accompanied by ocular ________, in which tear film _______ and ________, ocular surface ________ and damage, and ___________ abnormalities play _______ roles.

Dry eye is a multifactorial disease of the ocular surface characterised by a loss of homeostasis of the tear film and accompanied by ocular symptoms, in which tear film instability and hyperosmolarity, ocular surface inflammation and damage, and neurosensory abnormalities play etiological roles.

255

The tear film has 4 main functions which are?

- optical
- mechanical
- nutritional
- defensive

256

What four things can cause aqueous deficient dry eye (ADDE)?

- Sjogren Syndrome
- Non-Sjogren Syndrome (congenital, age)
- Lacrimal gland obstruction
- Hyposecretion due to lacrimal function unit (LFU) failure

257

Evaporative dry eye (EDE) can be classified into two groups by?

- lid related (obstructive MGD)
- ocular surface related (Vit A deficiency, mucin/glycocalyx deficiency, iatrogenic)

258

What sort of triaging questions would you use when diagnosing dry eye? (3)

How severe is the eye discomfort?
Do you have any mouth dryness or enlarged glands?
How long have your symptoms lasted and was there any triggering event?
Is your vision affected and does it clear on blinking?
Are the symptoms or any redness much worse in one eye than the other?
Do the eyes itch, are they swollen, crusty or any discharge?
Do you wear CLs?
Have you been diagnosed with any general health conditions or taking any meds?

259

What sort of risk factor questions could you ask when diagnosing dry eye?

- smokin
- diet
- CL wear
- General health
- Medications
- Environment
- Screen/computer use

260

What three diagnostic tests can you do for dry eye diagnosis?

TBUT (non-invasive via keratoscope or NaFl)
Osmolarity
Ocular surface staining

261

What is the diagnostic criteria for osmolarity of tears to diagnose hyperosmolarity?

>308mOsm/L
OR
inter-eye difference >8mOsm/L

262

What is the diagnostic criteria for ocular surface staining?
(number of corneal punctate spots, conjunctival spots, lid margin width)

Corneal punctate spots >5
Conjunctival spots >9
Lid margin >2mm length and 25% width

263

What are the diagnostic tear volume tests for aqueous deficient dry eye disease? (3)

tear meniscus height
Shirmer test
Phenol red test

264

What are the diagnostic tests for evaporative dry eye disease? (5)

- MG assessment (expressibility and oil flow)
- Meibography
- Interferometry
- Blink and lid closure
- Lid margin keratinisation

265

What are the three main things to consider when managing dry eye?

- protect eyes from environment
- retain or supplement the tears
- look after the eyelids

266

What are the methods for tear conservation?

- tear retention (reducing tear evap) with goggles
- punctal occlusion

267

When is punctal occlusion contraindicated? (2)

not aqueous deficient dry eye
dry eye due to eyelid disease

268

What therapeutic is good for reducing bacterial load for the lids?

Fusidic acid 1% (active against gram +ve)

269

What other alternative therapy has been shown to be good for reducing bacterial load?

manuka honey

270

What is the current recommendation for treating demodex?

lid hygiene with tea tree lid cleanswer daily for 4-6 weeks

271

What are three methods for altering the composition of the oils for MGD?

- systemic anti-inflammatory therapy
- essential fatty acids
- artificial supplementation (lipid based drops)

272

Treatment with tetracyclines (e.g. low dose doxycycline for 2-3 months) does what?

laters meibum composition by improving lipid quality and irritation symptoms and dry eye signs

273

Doxycycline is contraindicated in? (2)

growing children and pregnancy

274

Is increasing omega-3 or omega-6 anti-inflammatory?

omega-3

275

The two main anti-inflammatory therapies for dry eye are?

- topical glucorticoids
- non-glucocorticoid immunomodulators (cylcosporine, NSAIDs, tarcolimus)

276

TD-OCT vs SD-OCT (5 points each - write)

TD-OCT
- A-scan generated sequentially, 1 pixel at a time
- moving reference mirror
- 400 scans/sec
- low resolution
- slower than eye movement
SD-OCT
- entire A-scan generated at once
- stationary reference mirror
- 26000 scans/sec
- high resolution
- faster than eye movement

277

In OCT which lesions are hyper-reflective? (3)

hard exudates
blood
scars

278

In OCT which lesions are hypo-reflective? (2)

serous fluid
hypo-pigmented lesions of RPE

279

What is the technique in OCT where A-scans are done anterior to posterior (instead of a cross-section)

en-face

280

Define optic neuropathy

any pathological condition of the optic nerve

281

Define optic neuritis

inflammation of the optic nerve

282

Define optic atrophy

loss of neurons within the optic nerve due to cell death

283

Define papilloedema

bilateral elevation of the optic nerve heads secondary to raised intracranial pressure

284

What sort of cinical signs could you expect to find with optic nerve dysfunction? (6)

- reduced VA
- VF defects
- impaired CV (red/green defects)
- decreased brightness sensitivity
- decrease CS
- afferent pupillary defect

285

How would the optic nerve appear with optic atrophy and why?

optic nerve pallor (pale or white coloration) due to astrocytes which fill the spaces where axons died

286

There are many causes of optic atrophy, name 3? (6)

- papillitis
- compression (tumours, aneurysms)
- Leber's
- Toxic/nutritional optic neuropathies (alcohol)
- Ischaemia
- chronic papilloedema

287

What are signs of true disc swelling? (5)

- blurred NFL
- disc vessels partially/fully obscured
- cup retained
- dilated retinal veins
- flame-shaped haemorrhages

288

In which optic neuritis does the optic disc look normal? This optic neuritis is also the most common in adults and is frequently associated with what other condition?

retrobulbar optic neuritis
multiple sclerosis

289

What is neuroretinitis?

papillitis with inflammation of retinal NFL and exudates at macula in a star pattern

290

What are the 4 causes of optic neuritis?

- demyelinating (most common)
- parainfectious (following viral infection/immunisation)
- infectious (cat scratch fever, syphillis, Lyme disease)
- non-infectious (sarcoidosis, SLE)

291

What are symptoms of optic neuritis? (6)

- decreased VA (minimal to NLP)
- decreased CV
- decreased CS
- VF abnormalities (vary)
- pain around eye (esp with eye movements)
- Uhthoff's phenomenon (diff perception of motion between each eye)

292

Describe the two signs of optic neuritis

1. fundus appearance of optic disc
- two thirds have normal appearance
- one third show papillitis
- exudates in pattern of macular star uncommon with demyelinating
2. RAPD on affected side

293

Describe the course of vison loss with optic neuritis (3)

- variable levels of monocular vision loss progressing over 7-10 days
- vision tends to recover after 2 weeks, mostly complete after 1 month
- 90% achieve 6/12 or better

294

Management of optic neuritis? (2)

- most do not require Tx
- corticosteroids may speed up recovery but does not influence final visual outcome (only prescribed under special circumstances)
- MRI for prognosis

295

Risk factors for NAION

- age (55-70)
- structural crowding of the ONH
- predisposing systemic conditions

296

Name predisposing systemic conditions for NAION (8)

- HT
- diabetes
- hypercholesterolemia
- sudden hypotensive events
- cataract surgery
- sleep apnoea
- erectile dysfunction medications

297

Signs of NAION? (6)

- sudden, painless monocular vision loss
- RAPD
- VF defects (typically inf altitudinal)
- dyschromatopsia (red/green)
- diffuse or sectorial hyperaemic disc swelling
- presence of known factors

298

Management of NAION? (4)

- urgent referral
- no definitive treatment
- address systemic predispositions
- rule out GCA (ESR and CRP estimation)

299

AAION is caused by ____ and has strong association with what condition?

giant cell arteritis
systemic polymyalgia rheumatica

300

Signs of AAION (3)

- sudden, profound unilateral vision loss and can be accompanied by periocular pain and/or preceded by TVO and flashing lights
- systemic symptoms of GCA (headache, scalp tenderness, jaw claudication)
- pale "chalky white" oedematous disc

301

What is the gold standard method of diagnosing GCA?

temporal artery biopsy

302

With a blood test, what would you expect to see with AAION?

elevated ESR and CRP

303

Management for AAION? (2)

- immediate referral
- systemic steroids for GCA - IV methylprednisolone 3 days followed by long taper of oral prednisolone

304

What is PION?

ischaemia of the retrolaminar optic nerve

305

PION occurs in specific scenarios which are? (3)

- operative - especially spinal surgery w/ resultant bilateral poor vision
- arteritic
- non-arteritic (similar prognosis to NAION but not assoc with small discs)

306

Parainfectious optic neuropathy is associated with?

various viral infections e.g. measles, mumps, chickenpox, rubella

307

Parainfectious optic neuropathy usually occurs in ____ and is characterised by ______, ______ vision loss, _-_ weeks after exposure and usually present with bilateral _____

children
acute, severe
papillitis

308

Treatment for paraninfectious optic neuropathy?

none required in most cases (spont visual recovery)
- consider intravenous steroids if vision loss severe bilaterally or affecting only seeing eye

309

Infectious optic neuropathy is a DIRECT result of?

infection by various organisms

310

Give some examples of what can cause infectious optic neuropathy (3)

- sinus-related
- cat-scratch fever
- syphillis
- Lyme disease
- crytococcal meningitis
- varicella zoster

311

How is infectious optic neuropathy treated?

appropriate anti-infective

312

Sarcoid optic neuropathy causes what three things to the optic nerve?

- compression
- infiltration
- ischaemia

313

Signs of sarcoid optic neuropathy?

- often presents like MS
- "lumpy" disc possible
- granulomatous uveitis (mutton fat KPs) common

314

Tx of sarcoid optic neuropathy?

systemic steroids for ON involvment
topical/periocular steroids for uveitis

315

Characteristics of Leber's hereditary optic neuropathy (6)

- caused by mutation of maternally inherited mitochondrial dna
- males>females (9:1)
- usually teens to early twenties
- unilateral acute/subacute, painless, severe loss of central vision
- second eye involved within weeks/months of first

316

Signs of Leber's hereditary optic neuropathy (5)

- hyperaemia/elevation of optic disc
- thickening of peripapillary retina
- peripapillary telangiectasia
- tortuosity of arterioles
- optic disc atrophy

317

Tx Leber's hereditary optic neuropathy and prognosis?

- no effective Tx
- very poor prognosis (most permanent bilateral 6/60 or worse)

318

What is the most common inherited hereditary optic neuropathy characterised by bilateral progressive acuity loss and tritanopia

dominant optic atrophy (DOA)

319

Nutritional optic neuropathy usually occurs with people who are _____, ______, ______ and experience ______, bi/unilateral vision loss with acquired _________.

alcoholics, smoke in excess, poor diets
progressive bilateral
dyschromatopsia

320

Toxic optic neuropathy is commonly caused by (2)

methanol and ethylene glycol

321

radiation optic neuropathy is probably a result of radiation induced what?

vascular occlusion

322

What are the causes of increased intracranial pressure? (5)

- intracrainal lesions (tumour, haem)
- ventricular system obstruction
- impairment of CSF absorption
- severe systemic HT
- idiopathic (pseudotumour cerebri)

323

On refill write out the four different stages of papilloedema

Early
- mildly elevated hyperaemic discs
- loss of spontaneous venous pulsation
- vision normal

Established
- moderately elevated hyperaemic discs
- venous engorgement, peripapillary haemorrhages and CW spots
- TVOs + possible reduced VA

Chronic
- marked elevated discs
- lack of CW spots or haemorrhages
- variable VA and VF constriction

Atrophic
- slightly elevated, dirty grey discs
- VA severely impaired

324

Symptoms of papilloedema? (5)

- possibly none initially
- headache
- nausea and vomiting
- changes in vision (TVOs, horizontal diploplia, VA)
- deterioration of consciousness

325

What are the goals for management of papilloedema?

goal is to relieve headache and prevent vision loss

326

idiopathic intracranial hypertension is normally seen in?

- obese women of child bearing age
- associated with certain medications or sleep apnoea

327

Which portion of the occipital lobe is responsible for central macula vision?

most posterior portion

328

Which portion of the occipital lobe is responsible for peripheral vision?

mid-occipital portion

329

Which portion of the occipital lobe is responsible for extreme temporal vision on the contra-lateral side

anterior most portion

330

A lesion in the anterior occipital lobe causes?

monocular temporal crescent defect in contra-lateral eye

331

A lesion in the mid-occipital lobe causes?

macula sparing congruous homonymous hemianopia

332

A lesion at the posterior tip of the occipital lobe causes?

congruous homonymous central defect

333

What is amaurosis fugax

sudden onset monocular vision loss

334

What things should you check for a Px reporting amaurosis fugax? (5)

- neck pain or Hx of neck injury
- symptoms of GCA
- emboli on funduscopy
- pupils
- CV

335

Any patient with any form of homonymous hemianopia must have what done?

MRI

336

What is the most common cause of homonymous VF loss?

Migraine

337

What is migraine aura?

neurological symptoms that precede, accompany or more rarely follow a migraine headache

338

Symptoms of aura can be positive or negative. Name a few positive symptoms

- scintillating scotomas
- fortification spectra
- flashes
- heat waves
- kleidoscope effects
- fragmented vision

339

Symptoms of aura can be positive or negative. Name a few negative symptoms

- homonymous hemianopia
- tunnel vision
- cortical blindness
- transient monocular vision loss

340

What is retinal migraine

repeated episodes of monocular visual disturbances incl scintillations, scotomata or blindness assoc with migraine headache

341

DDx for migraine aura (3)

- photopsia from vitreous traction
- TIAs from retinal emboli
- transient visual obscurations

342

DDx of migraine HA

- arteriovenous malformation
- HZO
- trigeminal neuralgia

343

Tx and management of migraine?

avoidance of triggers
medications

344

Migraine without aura vs tension type headaches?

finish this card for before exams

345

Characteristics of a cluster headache?

finish this card for exams

346

Characteristics of Charles Bonnet Syndrome

finish this card for exams