Neuro-ophthalmology: Raised Optic Disc Flashcards

1
Q

What are the symptoms of orbital compressive lesions?

A
  • Monocular
  • Slow growing
  • Slow, compressive, visual loss
  • VF loss – may be central or diffuse – depends on exact location of lesion
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2
Q

What are the associated signs/symptoms of orbital compressive lesions?

A
  • Eyelid oedema
  • Proptosis – eye pushed forward from usual position
  • Extraocular muscle involvement – may get painful, restricted eye movements, diplopia
  • Pupils:
    o RAPD on affected side
  • Disc Appearance:
    o If anterior lesion  disc oedema – will be raised
    o If intraorbital/ intracanalicular, get disc pallor 4-6 weeks after it damaged the nerves
    o If vasculature (BVs) not compromised, get optic nerve dysfunction & atrophy w/o preceding disc oedema – may just get disfunction w/o raised disc
    o May have simple oedema or visible signs of infiltration (cells)
    o Optocilliary shunt vessels
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3
Q

Which hospital investigations are needed in suspect orbital compressive lesions?

A

MRI & CT scan

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4
Q

What is the management of orbital compressive lesion?

A
  • Unexplained sudden loss of vision = SAME DAY referral
  • Unexplained gradual loss of vision = URGENT referral
  • Optic disc pallor (suspected compressive lesion) = URGENT referral
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5
Q

What are the main types of orbital compressive lesions?

A
  • Optic nerve sheath meningioma
  • Optic nerve glioma
  • Melanocytoma
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6
Q

Describe optic nerve sheath meningioma (orbital compressive lesion)?

A
  • Benign tumour
  • Proliferation of meningoepithelial cells lining the sheath of the optic nerve
  • One third of optic nerve tumours
  • Mean age of presentation: 40-50yrs
  • Female > Male (as are meningiomas elsewhere)
  • Symptoms/Signs:
    o Painless, slowly progressive monocular visual loss (95% of cases)
    o Proptosis (60-90% of cases)
    o Disc Appearance:
     Optic oedema then atrophy
     Optocilliary shunt vessels
  • Treatment:
    o Observe if stable & no visual loss
    o Radiotherapy:
     Stability or improvement in up to 94%
     Complications:
  • Radiation retinopathy
  • Pituitary dysfunction
    o Surgery:
     Biopsy or excision
  • Risk of optic nerve trauma & visual loss
  • Considered if intracranial extension
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7
Q

Describe optic nerve glioma (orbital compressive lesion)?

A
  • Optic glioma are usually pilocyctic tumours
  • Most common primary tumour of optic nerve
  • Most are slow growing & benign
  • Some are malignant & more rapidly progressing, causing blindness & death
  • 70% detected during 1st decade of life, 90% by 2nd
  • Association w/ Neurofibromatosis 1 (NF1):
    o 10-30% of NF1 have optic gliomas
    o 10-70% w/ optic glioma have NF1
  • Presenting Symptoms:
    o Proptosis – 94%
    o Visual loss – 87%
    o Optic disc pallor – 59%
    o Disc oedema – 35%
    o Strabismus – 27%
  • Signs:
    o RAPD
    o Visual Field Defect
    o Optocilliary shunt vessels
  • Hospital Management:
    o Observation if good vision & stable imaging appearance
    o Chemotherapy when visual loss severe
    o Radiotherapy has a risk of complications including pituitary dysfunction
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8
Q

Describe melanocytoma (orbital compressive lesion)?

A
  • Really a pigmented tumour of uveal tract
    o The other two were not pigmented
  • Predilection of lamina cribrosa of ONH
  • Typically benign composed of melanocytes & melanin & don’t grow
  • Rarely become malignant
  • Presentation:
    o Optic nerve dysfunction if large but usually coincidental finding
  • Signs:
    o Black lesion w/ feathery edges
    o Typically small & don’t grow – monitor with photographs
  • Complications:
    o Central retinal vein occlusion – theses are taking up space & can comoress on vein causing it to occlude
    o Malignant transformation
  • Hospital tx:
    o Observation every 6-12 months
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9
Q

Describe infiltrative lesions causeing raised optic disc?

A

Infiltration/invasion of optic nerve by neoplastic (cells that replicate – either benign or malignant) or inflammatory cells
Ocular involvement may be presenting feature of systemic disease

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10
Q

What are the symptoms and signs of raised optic disc due to infiltrative lesions?

A

Symptoms:
* Progressive (progressively getting worse), severe visual loss over days to weeks
* Associated w/ headache due to pressure from infiltrative lesions
Signs:
* Retrobulbar infiltration – disc appears normal – disc can become pale after 4-6 weeks
* Disc involvement – swollen appearance

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11
Q

What are the causes of infiltrative lesions that could lead to raised optic disc?

A
  • Leukaemia
  • Lymphoma
  • Granulomatous infiltration:
    o Sarcoidosis, TB, syphilis
  • Metastases:
    o Rare but most commonly from breast or lung cancer
    o V useful to gather this info in H&S
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12
Q

What are the hospital investigations of raised optic disc due to infiltrative lesions?

A
  • Send to ophthalmology
  • MRI of brain & orbits
  • CSF analysis – looking at papilloedema type causes
  • Screening tests for inflammatory/ infective/ neoplastic disorders
  • Early identification allows life-saving tx
  • Palliative care may improve vision if poor prognosis
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13
Q

What is the management of raised optic disc due to infiltrative lesions?

A
  • Unexplained sudden loss of vision = SAME DAY referral
  • Unexplained gradual loss of vision = URGENT referral
  • Optic disc pallor (suspected compressive lesion) = URGENT referral
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14
Q

Describe Leber Hereditary Optic Neuropathy?

A
  • Hereditary (inherited) condition characterised by bilateral optic atrophy
  • Affects maternal mitochondrial DNA
  • Males, 10-30 years
    May cause a raised optic disc
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15
Q

What are the symptoms and signs of Leber Hereditary Optic Neuropathy?

A
  • Ask about family hx
  • Acute, severe, painless visual loss (<6/60)
  • Central/ centrocecal visual loss
  • RAPD when monocular involvement but both eyes become involved relatively quickly
    o Will not get an RAPD when bilateral
  • Disc Appearance:
    o Normal in up to 40%
    o Hyperaemia & elevation of disc
    o Thickening or peripapillary retina
    o Peripapillary telangiectasia – dilation of smaller BVs & can look like spiders legs
    o Tortuosity of medium sized retinal vessels
    o Eventual optic atrophy in affected area
  • Hospital Management:
    o MRI scan to exclude a treatable cause
    o Once diagnosed no tx (because it is hereditary) & visual loss usually permanent
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16
Q

Describe toxic optic neuropathies (nutritional optic neuropathy)?

A
  • Typical hx is of alcohol &/or tobacco excess w/ neglect of diet (B vitamins & thiamine)
    o Toxic effect of the alcohol/tobacco excess with reduction in the nutritional component of diet
  • Can get neuropathy in well-nourished individuals w/ pernicious anaemia (cannot metabolise iron properly) or vitamin B12 deficiency
  • Other causes:
    o Methanol intoxication – component of industrial solvents, antifreeze, fuel
    o Amiodarone – tx of cardiac arrhythmias
    o Tamoxifen – prevention & tx of breast cancer
    o Ethalbutamol tx for tuberculosis
    o Isoniazid – tx for tuberculosis
    o Isotretinoin – tx for acne
     Hard to stop these treatments due to the conditions they are for
17
Q

What are the symptoms of toxic optic neuropathies (nutritional optic neuropathy)?

A
  • Chronic (gradual & progressive) or acute – depending upon cause
  • Bilateral & symmetrical
  • Painless visual loss
  • Dimness of vision – like they’ve walked into a cloud
18
Q

What are the signs of toxic optic neuropathies (nutritional optic neuropathy)?

A
  • Affects central vision w/ central/caecocentral scotoma
  • Minimal findings on initial presentation:
    o Optic disc can be normal/mild pallor/ hyperaemia
     In a small group of pxs w/ hyperaemic discs, could get small splinter haemorrhages on disc edge
    o Mild depression on Amsler fixation target
    o Reduced colour vision
  • Months-years after presentation:
    o Papillomacular bundle dropout
    o Temporal disc (side of disc that leads onto macula) pallor followed by optic atrophy
19
Q

What is the hospital management of toxic optic neuropathies (nutritional optic neuropathy)?

A
  • Investigations of exclusion:
    o Fluorescein angiography
    o Blood testing
    o Electrophysiology
    o MRI imaging
  • Tx:
    o Reversal of inciting cause
     Can often be difficult:
  • If someone has addiction to alcohol or tobacco then that is hard to stop
  • If someone is on medication for a condition – hard to stop this too – can sometimes substitute with other meds (if available)
    o Can get reversal of ocular signs if optic atrophy has not supervened
     Optic atrophy is a sign of permanent damage – if hasn’t happen yet then there is the potential for reversal
20
Q

Describe traumatic optic neuropathy - including direct and indirect?

A
  • Optic nerve damage from trauma to head/orbit/globe
    o Px should tell you in H&S
  • Direct traumatic optic neuropathy:
    o Avulsion of nerve from laceration by bone fragments/ FBs
     Nerve has dislocated or gone out of its position
    o Direct compression from haemorrhage
  • Indirect traumatic optic neuropathy:
    o Nothing has directly happened to the nerve
    o Shear forces on nerve
    o Shear forces on vascular supply – blockage of BVs which can cause a raised optic disc
21
Q

Describe the signs of traumatic optic neuropathy?

A
  • Highly variable depending on type of trauma
  • Visual loss:
    o Immediate
    o Severe – no perception of light
  • RAPD – if monocular
  • Optic Disc:
    o Depends on physical location where it has happened
    o If posterior pathology may appear normal
    o Eventual atrophy
  • Neuroimaging:
    o Assesses extent of injury & co-morbidity – as often cannot see it from the front
22
Q

What is the hospital management of traumatic optic neuropathy?

A
  • Neuroimaging to assesses extent of injury and co-morbidity
    o Often do not present to community ophthalmology as normally have other broken bones
  • Therapy controversial
  • Prognosis poor if the injury is severe
  • Intravenous steroids
    o Anti-inflammatory and neuroprotective (protect the nerves)
  • Increased risk of mortality when combined with other head injuries
  • Consider when isolated injury with no other evidence of head injury