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(2) Tri B - Clinical opthalmology > Week 2 - Neuro 1.2 > Flashcards

Week 2 - Neuro 1.2 Flashcards

1
Q

What 3 things should be examined when suspecting optic atrophy?

A

• Comparison of colour of 2 discs
- Subtle Pallor; watch if pseudophakia
• Evaluation of surface vasculature of disc
- Thin or absent capillary net
• Assessment of retinal nerve fibre layer
- dropout may precede atrophy, loss of normal glistening appearance, most likely superior than inferior first

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2
Q

What is optic atrophy? And how long for it to appear? What separates unilateral from bilateral?

A

• Pale (chalky white) disc appearance with sharp margins
• Damage to retinal ganglion cells at any level
• Lesion in optic pathway anterior to lateral geniculate body
- Anterior to chiasm - unilateral; Posterior to chiasm - bilateral

• 4 to 6 weeks to appear from time of axonal damage

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3
Q

What are the two types of optic atrophy?

A

• Primary Vs secondary

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4
Q

What is Primary optic atrophy and its causes?

A

No adjacent swelling of ON head
Causes:
• Retrobulbar neuritis
• Compression by tumour or aneurysm

• Hereditary optic neuropathies
• Toxic and nutritional optic neuropathy

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5
Q

What is secondary optic atrophy?

A

Proceeded by swelling of ON head

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6
Q

How is Primary and Secondary optic atrophy managed?

A

Primary:
• Retrobulbar neuritis; needs scan for MS
• Compression by tumour or aneurysm; emergency referral
• Hereditary optic neuropathies; H&S to check if any in family has it, referral
• Toxic and nutritional optic neuropathy; Depends on problem, different for diet/drugs/alcohol, GP/referral
Secondary:
• Swelling of ON head; depends on cause or swelling on ON head

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7
Q

What is Optic Disc Oedema?

A

• Swelling of nonmyelinated nerve fibres from impaired axoplasmic flow
- Evidence of acute / evolving pathology
• Blurred disk margins

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8
Q

What terms can be used to describe the appearance on record card?

A

• Elevated appearance of nerve head
• Filling of cup
• Retinal vessels drape over disc margin
• Blurring of margin
• RNFL oedema - greyish appearance obscuring vessels
• Hyperaemia
• Retinal venous dilation and toruosity
• Peripapillary haemorrhages/exudates

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9
Q

What are the different types of peripapillary haemorrhages and exudates?

A

• Dot-Blot haemorrhages
• Flame shaped haemorrhages
• Exudates
• Cotton wool spots

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10
Q

What are the differences between the two retinal haemorrhages?

A

Flame shaped haemorrhages:
• from superficial pre-capillary arterioles
• in NFL
Dot-blot haemorrhages:
• from venous end of capillaries
• in middle retinal layers

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11
Q

What are the differences between the two main types of Oedema?

A

• Oedema
- Diffuse: caused by extensive leakage
- Localised: focal leakage
Between OPL and INL, may later involve IPL and NFL

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12
Q

What are hard exudates?

A

• Caused by oedema
- Chronic localised oedema
• Located at junction of normal and oedematous tissue
• Lipoprotein and macrophages
• Mainly in OPL
- Get spontaneously absorbed as oedema recovers

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13
Q

What are cotton wool spots?

A

• Accumulation of neuronal debris in NFL
• Disruption of axial flow of neurons

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14
Q

What are the 4 causes of optic oedema, and their subcategories?

A

• Papilloedema (acute and chronic)
• Ischaemia
- Arteritic anterior ischaemic optic neuropathy (AION)
- Non-Arteritic Anterior Ischaemic optic neuropathy (NAION)
- Posterior Ischaemic optic neuropathy
• Inflammation
- Optic Neuritis (demyelinating, infectious, non-infectious)
- Neuroretinitis
• Diabetic papillopathy

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15
Q

What is Papilloedema? What is physiological cause?

A

• Raised intracranial pressure
• Pressure is transmitted to the optic nerve
• Optic nerve sheath acts as a band to impede axoplasmic transport so there is a build up of material at the lamina cribrosa
• BILATERAL

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16
Q

What causes raises intracranial pressure?

A

• Relates to Cerebrospinal fluid - CSF
- produced in centre of brain; choroid plexus, to provide cushion/buffer for brain
- occupies subarachnoid space
- if problem along that pathway; this will raise the CSF, causing papilloedema

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17
Q

What can cause a disruption of CSF and therefore raised intracranial pressure?

A

• Intracranial mass
• Hydrocephalus (dilation of ventricles)
• Central nervous system infection e.g Meningitis
• Trauma
• Infiltration e.g. leukaemia, sarcoidosis
• Benign intracranial hypertension

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18
Q

What is Benign intracranial hypertension?

A

• Raised ICP in the absence of an intracranial mass, lesion or hydrocephalus and normal CF constituents
• Not life threatening but permanent, often severe, visual damage (fields more than VA)

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19
Q

What is the most common symptom of papilloedema, especially in the early stages?

A

• Occasionally asymptomatic

• Headaches
- “muzzy headed” at start, then develop into extreme pain; hospital at 6 weeks
- Characteristic in morning, waking up px
- generalised or localised
- Worse when pressure increases: moving head, bending over, coughing etc
• Very rarely is a headache absent

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20
Q

Apart from headaches, what are other systemic symptoms of papilloedema?

A

• Nausea and vomiting
- Often projectile
- May partially/temporarily relieve headache
- Could occur at time of headache onset or earlier (up to few months)

• Deterioration of consciousness
- From slight (drowsy) to dramatic

• Pulsatile tinnitus

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21
Q

What are the visual symptoms of papilloedema?

A

• Visual symptoms often absent
• Transient visual loss
• Horizontal diplopia (6th nerve palsy)
• Constriction of visual field
• Altered colour perception
• Reduced VA in later stages

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22
Q

What are the four stages if Papilloedema?

A

• Acute/early
• Acute/established
• Chronic
• Atrophic

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23
Q

What are the symptoms and examinations if acute/early papilloedema?

A

• Symptoms
- Headache
- Nausea and vomiting
- Vision normal and no visual symptoms

• Examination
- VA usually normal
- Colour vision usually normal
- Pupil responses normal

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24
Q

How might the disc appear in acute/early papilloedema and what terms might describe it?

A

• Hyperaemia
• Dilatation of capillary net
• Oedematous retinal nerve fibre layer seen as obscuration of disc edge and vessels
• Mild elevation

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25
Q

What absent spontaneous venous pulsation?

A

• If SVP present, papilloedema unlikely
• absence of SVP does not confirm papilloedema as 20% of normal individuals don’t have this
• Loss of previous SVP more indicative of papilloedema

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26
Q

What are the symptoms and examinations of acute/established papilloedema?

A

Symptoms
As early stage but includes:
• Transient visual disturbance, lasting seconds

Examination
As early stage but includes:
• Visual fields: enlargement of blind spot

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27
Q

How does the fundus appear for acute/established papilloedema?

A

As early, but includes:
• Severe hyperaemia
• Moderate elevation, enlarged optic nerve head and retinal folds
•Peripapillary flame shaped haemorrhages and cotton wool spots
• Hard exudates in macular fan with temporal part missing

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28
Q

What are the symptoms and examinations of chronic papilloedema?

A

Symptoms
• Vision variable, fields restricted

Examination
• Gradual deterioration in optic nerve function
• VA variable
• Visual fields:
- nasal loss
- arcuate defect
- generalised depression
• central loss a late finding

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29
Q

What is the disc appearance of chronic papilloedema?

A

• Pale due to axonal loss
• Marked elevation of discs
• Absence of cotton wool spots and haemorrhages
• Optociliary shunt vessels / collateral vessels
- Pre-existing venous channels
- Chronic central retinal vein obstruction
- Refractile bodies at disc due to chronic lipid rich exudation
• High water marks

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30
Q

What are the symptoms/examinations and optic disc appearance of Atrophic Papilloedema

A

(secondary optic atrophy)

• Symptoms/examination
VA, fields etc severely reduced

• Optic disc appearance
Pale/grey optic nerve
Possibly mild elevation, indistinct margins

31
Q

Management if Papilloedema?

A

• Same day referral to ophthalmologist
• Treatment of cause

32
Q

What are the differential diagnosis for raised discs?

A

• Compression
• Infiltration
• Congenital optic neuropathies (Leber’s optic neuropathy)
• Toxic optic neuropathies (methanol poisoning)
• Traumatic optic neuropathy

33
Q

What other conditions could cause APPEARANCE of a raised disk (optic neuropathy without swelling)

A

• Optic disc drusen
• Tilted optic disc
• Myelinated nerve fires
• Hypermetropic crowded disc

34
Q

What Intraocular diseases could cause APPEARANCE of a raised disk (optic neuropathy without swelling)

A

• Central retinal vein occlusion
• Posterior uveitis
• Posterior scleritis
• Hypotony

35
Q

What is anterior ischaemic optic neuropathy? (AION)

A

• Most common optic neuropathy over 50 years
• Represents ischaemic damage to optic nerve head

36
Q

What is the carotid artery and its divisions?

A

• comes from heart
• External carotid artery supplies face
• Internal carotid artery supplies brain/eyes etc

37
Q

What are the divisions of the internal carotid?

A

• Ophthalmic artery divides into multiple branches:
- Central retinal artery
- posterior ciliary artery : PCA, feeds choroid. Around 6-12 in total.

38
Q

What type of vision loss do you get with anterior ischaemic optic neuropathy? (AION)

A

Visual loss (both types)
• Painless, monocular visual loss over hours to days
• Altitudinal defects most common
• Reduced central vision
Relative afferent pupillary defect
Optic disc oedema present from onset

39
Q

What are the two subtypes of Anterior ischaemic optic neuropathy?

A

• Arteritic anterior ischaemic optic neuropathy (AAION)
• Non-Arteritic Anterior ischaemic optic neuropathy (NAION)

40
Q

what is Arteritic anterior ischaemic optic neuropathy (AAION) caused by?

A

• 5-10% of AION cases
• Occurs in older patients

• Caused by Giant Cell Arteritis (GCA)
- Inflammatory and thrombotic occlusion of short posterior ciliary arteries causing optic nerve head infarction

41
Q

What percentage of (AAION) have systemic symptoms, and how is it related to GCA?

A

• Variable, no systemic symptoms in 20%
• Giant Cell Arteritis
Granulomatous necrotizing arteritis
Affects large and medium sized arteries, especially:
• superficial temporal artery
• ophthalmic artery
• posterior ciliary artery
• proximal vertebral artery
- 5-10% of GCA have AAION

42
Q

What are the AAION systemic symptoms?

A

• Usually 60-80years old
• Tender, hardened, non pulsatile temporal artery
• Scalp tenderness, especially on brushing hair
• Jaw claudication (pain on speaking or chewing, almost pathognomonic)
• Proximal muscle weakness (typically shoulders), may occur 1st

43
Q

What affects on health might AAION cause to a patient?

A

• Reduced appetite
- Unexplained weight loss
- Unexplained lethargy, malaise, depression

As a result of all the systemic conditions

44
Q

What are the visual symptoms of AAION?

A

• Sudden, profound, visual loss
- Usually unilateral (initially)
• May be proceeded by transient visual obsurcations, flashing lights
• Periocular pain

45
Q

What will you find during the fundus examination AAION?

A

• Severe visual loss
• Pale swollen disc
• Cotton wool spots (retinal ischaemia)
• Over 1-2 months, swelling resolves leaving optic atrophy

46
Q

How is AAION managed in practice?

A

• If in community, immediate (same day) referral to ophthalmologist
• Treatment aimed at preventing blindness of 2nd eye

47
Q

How is AAION managed in ophthalmology?

A

• Immediate therapy is essential
• Confirmed with immediate blood results (
• Temporal artery biopsy confirms diagnosis

• Usually overnight stay in hospital, High dose systemic steroids (IV usually)
• Blood tests aid in tapering of steroids which is done in response to serial blood tests and symptoms
• Patients may remain on oral steroids for years (average 1-2yrs)

48
Q

What is the prognosis of AAION?

A

• Visual loss usually permanent
• Prompt administration of steroids may allow partial visual recovery In 25% of cases 2nd eye affected despite treatment, this could be within days

49
Q

What is Non-Arteritic Anterior Ischaemic Optic Neuropathy (NAION) and its risk factors?

A

• 90% of AION cases
• Occlusion of short posterior ciliary arteries causing infarction of optic nerve head
• Typically in 55-70yrs (average 60yrs), younger compared to AAION
• Structural “crowding” of the disc when cup is small/absent

Common risk factors include:
• diabetes
• hypertension
• high cholesterol
• smoking

50
Q

What are NAION symptoms?

A

• Sudden, painless loss of vision
• Unilateral
• Visual impairment on wakening (nocturnal hypotension?)
• Lack of systemic symptoms

51
Q

What do you find during the examination of NAION?

A

• VA: Moderate to severe reduction in VA in most px 30% have normal or slightly reduced VA
• Visual fields: Commonly inferior altitudinal defect
• Dyschromatopsia: Proportional to amount of VA loss
Most px have no further visual loss although in a small number, visual loss continues for about 6 weeks

52
Q

What would you find during the Fundus examination of NAION?

A

• Disc oedema diffuse or segmental
• Disc hyperaemic with focal telangiectasia on disc surface
• Often a few peripapillary splinter-shaped haemorrhages

• Atrophy within 3-8 weeks of onset
• Contralateral eye usually small with absent cup - “disc at risk”

53
Q

How is NAION managed?

A

• In community, difficult to differentiate from other causes of swollen disc and AAION
• Treat underlying cause
• Prophylaxis ? Aspirin is frequently given but does not appear to reduce risk in fellow eye

54
Q

What is the NAION prognosis, progression and risk factors for progression?

A

• Most px: no further visual loss, some Px visual loss continues for about 6 weeks
• Some recovery (e.g. 2 lines) in 31% at 2 years

• Chance of other eye being affected is 15% over 5yrs

• Risk factors for other eye are:
- poor VA in 1st eye
- diabetes
• Pseudo-Foster Kennedy syndrome if contralateral eye affected
- Unilateral disc swelling with contralateral optic atrophy in absense of mass compressing nerve

55
Q

What are the differences in Arteritic vs non/arteritic for:

age, sex, associations, VA, Disc, ESR, CRP, fluorescein angiography, prognosis and treatment?

A

• age: Mean 70 vs 60 yrs
• sex : F > M vs F=M
• associations: Headaches, tenderness vs none
• VA: 60% of cases - <6/60 vs >6/60
• Disc: Pale vs hyperaemic disc odema
• ESR: Mean 70 vs mean 20-40
• CRP: Elevated vs normal
• prognosis: Rarely improves vs 31% improves
- Fellow eye >50% vs 10-20%
• treatment: systemic steroids vs none

56
Q

What is posterior ischaemic optic neuropathy and its causes?

A

• Much rarer than AION
• Obstruction of plial artery/capillary plexus leading to ischaemia to retrolaminar part of the optic nerve
Causes:
• After surgical procedure, e.g. of spine
- Arteritic (similar to AAION)
- Non-arteritic (similar to NAION)

Diagnosis after ruling out other causes (compression, inflammation)

57
Q

What are 3 causes optic neuritis?

A

• Infection of the optic nerve
• Inflammation of the optic nerve (non-infectious)
• Demyelination of the optic nerve (most common)

58
Q

What are some causes of infection of optic nerve? (optic neuritis)

A

• local infection e.g. sinus, syphillis, Lyme disease, Herpes zoster, cat-scratch disease
• viral infection e.g. chicken pox, whooping cough, glandular fever, measles, mumps
• Following an immunisation

59
Q

What are some causes of inflammation of optic nerve? (non-infectious)

A

• Sarcoid
• Autoimmune

60
Q

What is Demyelination of optic neuritis and some causes?

A

• Demyelination disrupts nerve conduction within brain, brainstem and spinal chord sparing peripheral nerves

Causes:
• Multiple sclerosis (most common)
• Isolated optic neuritis with no other demyelination, but that may subsequently develop
• Devic disease or Schilder disease, both rare and bilateral optic neuritis

61
Q

What other symptoms may brain stem demyelination lesions cause?

A

• cranial nerve palzies
• gaze palsies
• facial nerve palsies
• nystagmus

62
Q

What is multiple sclerosis (MS) and its statistics with optic neuritis?

A

• MS is an inflammatory, demyelinating disease of the central nervous system (CNS)
• Multiple exacerbations characterised by variable CNS involvement
- Exacerbations are separated in time and anatomical location

• Optic neurotis : 15-20% MS px
• 50% of those with MS with get optic neuritis
• If have optic neuritis, over 10yrs MS risk is 38%

63
Q

What is optic neuritis and its symptoms?

A

• Infection, inflammation or demyelination of the optic nerve

Symptoms:
• Monocular visual impairment
• Subacute: develops over several days to 2 weeks
• Discomfort, exacerbated by eye movements which precedes visual loss in majority of cases
• Globe tenderness

64
Q

What visual, field and fundus defects can be found during examination of optic neuritis?

A

Visual:
• VA 6/18-6/60 (or worse)
• RAPD
• Reduced colour vison / red desaturation
• Reduced contrast sensitivity

Field defects:
• Generalised depression
• Nerve fibre bundle defects
• Central loss

Fundus examination
• Normal in most cases (retrobulbar neuritis)
• Could get swollen disc

65
Q

What are symptoms/signs of neuroretinitis? (type of optic neuritis)

A

• Acute loss of vision (usually painless)
• Disc edema which is diffuse, spreads to involve around fovea at plexiform layer
• Star pattern of exudates at macula

66
Q

What are some causes if neuroretinitis?

A

• Demyelination rare
• 66% secondary to cat-scratch disease
• Syphilis
• Lyme disease
• Viruses

67
Q

How is optic neuritis managed? (in practice and in hospital)

A

• In community, difficult to differentiate from other causes of swollen disc

• Most need no medical treatment
• Intravenous steroids followed by oral course speed recovery by 1 - 2 weeks
• Oral steroids alone associated with increased recurrence rate
• Corticosteroids have no long term effect on visual outcome

• If relapsing-remitting MS, immunomodulatory therapy for reducing morbidity

68
Q

If a patient has optic neuritis, and is suspected for MS, how is it managed?

A

• If suspect MS, MRI scan:
• Look for periventricular white matter lesions
Assesses risk of future MS
• No lesions: 25% risk at 15 years
• >1 lesion: 72% at 15 years
• Overall risk if no scan: 50%

Unresolving cases with other signs should raise suspicion of other underlying cause
•Blood tests - inflammatory markers, infective serum tests
• CSF
• Chest X-ray

69
Q

What is the prognosis of optic neuritis?

A

• Recovery between 1 month- 6 months
- 75% recover to 6/9 or better
• May be permanent loss of colour perception and contrast sensitivity
- due to Optic atrophy after optic neuritis

• Pseudo-Foster Kennedy syndrome
- If contralateral eye affected

70
Q

What is diabetic papillopathy and its causes/associations?

A

• Optic disc swelling in diabetic patient
• Diagnostic and therapeutic challenge
• Rare

• Pathogenesis unclear: Caused by capillary damage?

• Associations with small cup/disc ratio and rapid reduction in glycemia
• Vascular leakage and edema of the nerve fibres
Causes:
• Chronic ischaemia and secondary nerve swelling

71
Q

What are the symptoms and what is found during the examination techniques of diabetic papillopathy?

A

Symptoms:
• Usually asymptomatic or with mild symptoms

Examination:
Va:
• Unilateral
• VA 6/12 or better
• Mild or no RAPD
Visual field:
• Enlargement of blind spot
• Constriction or altitudinal loss in severe cases frequently found

72
Q

What is found during the fundus examination of diabetic papillopathy?

A

• Mild disc edema with hyperaemia
• Telangiectasis (dilated capillaries) which could be confused with neovascularisation (new blood vessels)

73
Q

How is diabetic papillopathy managed and what’s its prognosis/risk to develop into?

A

Management:
• In community, difficult to differentiate from other causes of swollen disc
• Little evidence that treatment is successful
Possibly corticosteroids/steroids

Prognosis:
• Visual prognosis good: 6/12 or better
• May take 6 months or longer for oedema to resolve
• 5 to 15% progress to non-arteritic ischaemic optic neuropathy

(2) Tri B - Clinical opthalmology (10 decks)

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