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Clinical Ophthalmology > Neuro 1.3 > Flashcards

Neuro 1.3 Flashcards

1
Q

Causes of a Raised Optic Disc

A
  • Not swollen but very similar appearance
  • Compression
  • Infiltration
  • Congenital optic neuropathies (Leber’s optic neuropathy)
  • Toxic optic neuropathies (methanol poisoning)
  • Traumatic optic neuropathy
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2
Q

Compression

A
  • Orbital masses may compress optic nerve and venous drainage
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3
Q

Compression - Symptoms

A
  • Monocular
  • Slow, compressive visual loss
  • VF loss - may be central or diffuse
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4
Q

Compression - Signs

A
  • Eyelid oedema
  • Proptosis
  • EOM involvement
  • Pupils - RAPD
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5
Q

Compression - Disc Appearance

A
  • If anterior lesion, get disc oedema (will appear oedematous but will be raised)
  • If intraorbital/intracanalicular (further back from ONH), get disc pallor
  • If vasculature not compromised, get ON dysfunction and atrophy despite no preceding disc oedema
  • If BV’s normal, may get dysfunction without raised appearance
  • If swollen or raised, may have simple oedema or visible signs of infiltration
  • Optociliary shunt vessels - smaller vessels that dilate up to try and provide blood supply to affected area
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6
Q

Compression - Management

A
  • Referral for hospital investigations
    • MRI and CT scans conducted if lesion suspected
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7
Q

Compressive Lesion Types

A
  • Optic nerve sheath meningioma
  • Optic nerve glioma
  • Melanocytoma
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8
Q

Optic Nerve Sheath Meningioma

A
  • ON sheath surrounds ON providing it with protection
  • ON sheath meningioma - Benign tumour
  • Proliferation of meningoepithelial cells lining the sheath of the ON
  • One third of ON tumours
  • Mean age - 40-50 yrs
  • More common in females (as are meningiomas elsewhere)
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9
Q

Optic Nerve Sheath Meningioma - Signs and Symptoms

A
  • Painless, slowly progressive monocular visual loss (95% of cases)
  • Proptosis (60-90% of cases)
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10
Q

Optic Nerve Sheath Meningioma - Disc Appearance

A
  • Optic oedema then atrophy (again after 4-6 weeks)
  • Optociliary shunt vessels
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11
Q

Optic Nerve Sheath Meningioma - Management

A
  • Observe if stable and no visual loss
  • Radiotherapy:
    • Stability or improvement in up to 94%
    • Complications:
      • Radiation retinopathy
      • Pituitary dysfunction
  • Surgery:
    • Biopsy or excision
    • Risk of ON trauma and visual loss
    • Considered if intracranial extension
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12
Q

Optic Nerve Glioma

A
  • Optic glioma are usually pilocyctic tumours
  • Most common primary tumour of ON
  • Most are slow growing and benign
  • Some are malignant and more rapidly progressing, causing blindness and death
  • 70% detected during first decade of life, 90% by second
    • Hence less likely if px over 20
  • Association with Neurofibromatosis 1 (NF1):
    • 10-30% of NF1 have optic gliomas
    • 10-70% with optic glioma have NF1
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13
Q

Optic Nerve Glioma - Symptoms

A
  • Proptosis - 94% (main presenting symptom)
  • Visual loss - 87%
  • OD pallor - 59%
  • OD oedema - 35%
  • Strabismus - 27%
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14
Q

Optic Nerve Glioma - Signs

A
  • RAPD
  • VF defect
  • Optociliary shunt vessels
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15
Q

Optic Nerve Glioma - Management

A
  • Observation if good vision and stable imaging appearance
  • Chemotherapy if severe visual loss
  • Radiotherapy has a risk of complications including pituitary dysfunction
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16
Q

Optic Nerve Melanocytoma

A
  • Typically a benign pigmented tumour of uveal tract
  • Composed of melanocytes and melanin, and don’t grow
  • Likes the lamina cribrosa of ONH
  • Rarely become malignant
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17
Q

Optic Nerve Melanocytoma - Presentation

A
  • Can get ON dysfunction if large but usually a coincidental finding
  • Black lesion with feathery edges
  • Typically small and don’t grow
  • Good to monitor with photographs to check if growing
    • Growth (if present) will be very slow
    • Would take pics every 6/12, not every week
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18
Q

Optic Nerve Melanocytoma - Complications

A
  • CRVO
  • Malignant transformation
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19
Q

Optic Nerve Melanocytoma - Management

A
  • Observation every 6-12 months
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20
Q

Infiltration

A
  • Infiltration/invasion of ON by NEOPLASTIC (abnormal growth of cells which replicate - can be benign or malignant replication) or inflammatory cells
  • Ocular involvement may be presenting feature of systemic disease
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21
Q

Infiltration - Symptoms

A
  • Progressive, severe visual loss over days to weeks
  • Associated with headache
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22
Q

Infiltration - Signs

A
  • Retrobulbar infiltration (infiltration behind ONH) - disc appears normal
  • Disc involvement - swollen appearance
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23
Q

Infiltrative Lesions

A
  • Leukaemia
  • Lymphoma
  • Granulomatous infiltration
  • Sarcoidosis, TB, syphilis
  • Metastases
    • Rare but most commonly from breast or lung cancer (can manifest in the eye)
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24
Q

Infiltration - Management

A
  • Urgent referral to ophth

Hospital Investigations:
- MRI of brain and orbits
- CSF analysis
- Screening tests for inflammatory/infective/neoplastic disorders

  • Early identification allows life-saving treatment
  • Palliative care may improve vision if poor prognosis
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25
Q

Inherited Optic Neuropathies - Leber’s Hereditary Optic Neuropathy

A
  • Hereditary condition characterised by bilateral optic atrophy
  • Affects maternal mitochondrial DNA
  • More common in males aged 10-30
26
Q

Leber’s Hereditary Optic Neuropathy - Signs and Symptoms

A
  • Ask about FH
  • Acute, severe, painless visual loss (<6/60)
  • Initially monocular but both involved quickly
  • Central visual loss
  • RAPD when monocular involvement but NOT when BE affected
27
Q

Leber’s Hereditary Optic Neuropathy - Disc Appearance

A
  • Normal in up to 40%
  • Hyperaemia and elevation of disc
  • Thickening of peripapillary retina
  • Peripapillary telangiectasia
  • Tortuosity of medium sized retinal vessels
  • Eventual optic atrophy
28
Q

Leber’s Hereditary Optic Neuropathy - Management

A
  • MRI scan to exclude a treatable cause
  • Once diagnosed, there is no treatment and visual loss usually permanent
29
Q

Toxic Optic Neuropathies

A
  • Typical history - alcohol/tobacco excess with neglect of diet (B vitamins & thiamine)
  • Can get neuropathy in well-nourished individuals with pernicious anaemia (can’t metabolise ion properly) or vitamin B12 deficiency

Other causes:
- Methanol intoxication (component of industrial solvents, antifreeze, fuel)
- Amiodarone (treatment of cardiac arrhythmias)
- Tamoxifen (prevention and treatment of breast cancer)
- Ethalbutamol treatment for TB)
- Isoniazid (treatment for TB)
- Isotretinoin (treatment for acne)

30
Q

Toxic Optic Neuropathies - Symptoms

A
  • Chronic (gradual & progressive) or acute, depending on the cause
  • Bilateral and symmetrical
  • Painless loss of vision
  • Dimness of vision (like walking into a cloud)
31
Q

Toxic Optic Neuropathy - Signs

A
  • Affects central vision with central scotoma
  • Minimal findings on initial presentation:
    • OD can be normal/mild pallor/hyperaemia
  • In a small group of px’s with hyperaemic discs, could get small splinter haemorrhages on disc edge
    • Mild depression on Amsler fixation target (general dimming)
    • Reduced CV
  • Months-years after presentation:
    • Papillomacular bundle dropout
    • Temporal disc pallor followed by optic atrophy
32
Q

Toxic Optic Neuropathy - Management

A
  • Investigations of exclusion:
    • Fluorescein angiography
    • Blood testing
    • Electrophysiology
    • MRI imaging
  • Reversal of inciting cause (can be difficult - alcohol/tobacco abuse, med subs)
  • Can get reversal of ocular signs if optic atrophy has not happened
    • Optic atrophy is a sign of permanent damage, the nerves are damaged and the disc has gone pale, if that hasn’t happened there is potential to reverse the problem
33
Q

Traumatic Optic Neuropathy

A
  • ON damage from trauma to head/orbit/globe
  • Direct traumatic optic neuropathy
    • Avulsion of nerve (nerve has dislocated and gone out of its position) from laceration by bone fragments/FB’s
  • Direct compression from haemorrhage (blood from trauma can directly affect ONH)
  • Indirect traumatic optic neuropathy - something hasn’t physically happened to the nerve/gone into the nerve
    • Shear forces on nerve (shear force - 2 forces pulling in opposite direction)
    • Shear forces on vascular supply
34
Q

Traumatic Optic Neuropathy - Examination

A
  • Visual loss
    • Immediate loss
    • Severe - no perception of light
  • RAPD
  • Optic disc
    • If pathology is posterior, OD may appear normal
    • Eventual atrophy
  • Neuroimaging
    • Assesses extent of injury and co-morbidity
35
Q

Traumatic Optic Neuropathy - Management

A
  • Neuroimaging to assesses extent of injury and co-morbidity
  • Prognosis poor
  • Intravenous steroids
    • Anti-inflammatory and neuroprotective
  • Increased risk of mortality when combined with other head injuries
  • Consider when isolated injury with no other evidence of head injury
36
Q

Causes of APPEARANCE of a Raised Optic Disc

A
  • Optic disc drusen
  • Tilted optic disc
  • Myelinated nerve fibres
  • Hypermetropic crowded disc
  • Intraocular disease
    • Central retinal vein occlusion
    • Posterior uveitis
    • Posterior scleritis
    • Hypotony
37
Q

Optic Disc Drusen

A
  • Calcified nodules within ONH
  • 0.34% - 2% of population
  • Bilateral in 75%
  • Unclear pathophysiology - impaired ganglion cell axonal transport (debris from axonal flow deposited in ONH)
  • Buried in childhood, more prominent with age
  • Most px’s asymptomatic
38
Q

Optic Disc Drusen - Examination

A
  • Possible RAPD if monocular/asymmetric
  • Visual fields
    • VF loss in 75-87%
    • Enlarged blind spot/arcuate defect
    • Fibres branch from OD to retina, if those fibres were to die, would cause a VF defect along pathway of that fibre (will follow horizontal midline)
    • Remains stable or very slowly progresses
39
Q

Drusen - Optic Disc

A
  • Appears small in diameter (if drusen pushing things inwards)
  • Anomalous branching vascular patterns
  • Round, whitish, yellow refractile bodies - describe in terms of size (in disc diameters, how many) and location (clock like, or nasal/temporal etc)
  • Disc may be pale/atrophy/RNFL loss
40
Q

Buried Drusen vs Swollen Disc

A
  • Both may elevate the OD and blur its margins
  • OD drusen does not have:
    • Lack of hyperaemia
    • Lack of microvascular changes (telangiectasia etc)
    • Normal/atrophic nerve fibre layer
    • Anomalous retinal vascular patterns
41
Q

Tilted Optic Disc

A
  • 1-2% of the population
  • 80% bilateral
  • Congenital or associated with myopia (as eye grows in myopia, OD can change and its orientation can tilt)
  • Oblique insertion of ON
  • Often the area the disc is tilted away from there is atrophy
  • Normal vision
42
Q

Tilted Optic Disc - Examination

A
  • Visual field - Bitemporal loss (can be associated with area of atrophy), superior arcuate scotoma
43
Q

Myelinated Nerve FIbres

A
  • 1% of population
  • Unilateral in 80%
  • Myelin covers the nerves after they have left the ONH - function of myelin is to speed up the transmission of nerves
  • During development sometimes the myelin doesn’t stop just behind the ONH and can protrude within the ONH
44
Q

Myelinated Nerve Fibres - Signs and Symptoms

A
  • Usually asymptomatic
  • Fundus examination
    • Visible yellow patch of myelin around ONH
  • Visual fields
    • Enlarged blind spot corresponding to the area of myelin (covering photoreceptors so light can’t get to that area)
45
Q

Hypermetropic Crowded Disc

A
  • Hypermetropic eyes are smaller and have smaller discs
  • Small discs can make BV’s look crowded/dilated and can be misdiagnosed for a swollen or unusual looking disc
  • BV’s just look thicker in comparison to the disc, in reality it is normal
46
Q

Intraocular Disease

A
  • CRVO
  • Posterior uveitis
  • Posterior Scleritis
  • Hypotony
47
Q

Other Optic Neuropathies - Excavated OD anomalies

A
  • OD pit
  • Coloboma
  • ON hypoplasia
  • Morning glory disc syndrome
48
Q

Optic Disc Pit

A
  • Congenital
  • Depression of disc surface
  • Associated with VF defect
  • Serous macular detachment (fluid seeping through hole)
    • Communication between optic pit and macula - that area of the disc normally contains the fibres which travel to the macula then you can get some fluid in a tunnel where the fibres should have been
    • Can be liquified vitreous or subarachnoid fluid
    • That detached area of the retina would have a greyish appearance, normally temporal/inferior to the disc
  • Associated central vision loss when situated on maculopapular bundle (bit of fibres that takes information back from the macula to the brain)
49
Q

Optic Disc Pit - Management

A
  • Difficult (higher risk as affects macula)
  • Observe (25% spontaneously resolve, some develop macular involvement)
  • Argon laser along temporal aspect of disc
  • Pars plana vitrectomy (take out vitreous if it is the vitreous that is leaking into the pit)
50
Q

Coloboma

A
  • A focal glistening white, bowl-shaped excavation, decentred inferiorly
  • Congenital defect from incomplete closure of the embryonic fissure (gap left at bottom)
  • Unilateral or bilateral
  • Usually occur inferiorly
51
Q

Coloboma - Examination

A
  • Visual acuity
    • Reduced
  • Visual Fields
    • Superior field defect (as is an inferior disc problem)
    • Can mimic glaucomatous loss (as affecting ONH)
  • Fundus
    • Larger than normal OD
    • Can involve uvea and retina if large
52
Q

Colobomas - Associations

A
  • Microphthalmos (small eye)
  • Colobomas of iris, choroid and retina
53
Q

Optic Nerve Hypoplasia

A
  • Reduced number of nerve fibres
  • In isolation (by chance), part of bigger problem with development or associated with:
    • Midline structures of the brain
    • Endocrine abnormalities – growth hormone and other pituitary hormones (eye won’t grow during development and causes reduced number of nerve fibres and other pituitary hormones)
    • Suprasellar tumours
54
Q

Optic Nerve Hypoplasia - Predisposing Factors

A
  • Maternal diabetes
  • Agents ingested by mother during pregnancy including alcohol, LSD, quinine, steroids, diuretics, anticonvulsants, cold remedies etc
  • Spectrum of severity from asymptomatic to no perception of light depending on how many nerve fibres haven’t developed
  • Unilateral or bilateral
55
Q

Optic Nerve Hypoplasia - Bilateral Cases

A
  • Roving eye movements (not enough nerve fibres - macula not developed properly - poor vision - can’t fixate on something - eye will rove side to side looking for clear vision)
  • Sluggish pupil responses - not many fibres working there and taking info about how much light there is
  • Less severe bilateral cases:
    • Squint in one eye
    • Minor VF defects
56
Q

Optic Nerve Hypoplasia - Unilateral Cases

A
  • Squint in affected eye
  • RAPD
  • Unsteady fixation in affected eye
57
Q

Optic Nerve Hypoplasia - Examination

A
  • Visual Fields
    • Peripheral and arcuate defects (as affects ONH)
  • Disc appearance
    • Small diameter of disc (comparison of 2 eyes useful if unilateral)
    • Grey disc colour and surrounding hypopigmentation
    • Relatively large retinal BV diameter
    • Double ring sing is characteristic - white ring of visible sclera

If ratio of, disc diameter: disc-fovea distance > 3:1, likely they have this

58
Q

Optic Nerve Hypoplasia - Management

A
  • Referral for endocrine opinion
  • MRI in all cases
59
Q

Morning Glory Disc Anomaly

A
  • Rare congenital malformation, embryonic origin unclear
  • Funnel-shaped staphylomatous excavation of the ON
  • Usually unilateral
  • More common in females
60
Q

Morning Glory Disc Anomaly - Examination

A
  • Visual acuity <6/60
  • RAPD
  • Visual field loss
  • Fundus
  • Enlarged disc
    • Disc pink or orange colour
    • Chorioretinal pigmentation around excavation (blue/grey pigment coming from the choroid)
    • White glial tissue on central disc surface
    • Retinal vessels appear at periphery of disc
    • Serous retinal detachment

Clinical Ophthalmology (10 decks)

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