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Neuro-Ophthalmology > Approach to the Patient with Decreased Vision > Flashcards

Approach to the Patient with Decreased Vision Flashcards

1
Q

how many degree of central vision does the Amsler grid test

A

20 degrees (10 degrees radius from fixation)

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2
Q

what do the different roman numerals in a Goldmann perimetry test indicate

A 
Size of stimulus object
0: 1/16 mm^2
I: 1/4 mm^2
II: 1 mm^2
III: 4 mm^2
IV: 16 mm^2
V: 64 mm^2
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3
Q

degrees of visual field tested in Goldmann perimetry

A

60 degrees from fixation in every direction except 90 degrees from fixation temporally

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4
Q

thresholds for reliability in static perimetry

A

25% false positives, 25% false negatives

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5
Q

good office test to distinguish between optic v retinal causes of visual loss

A

photostress testing (will be delayed in macular but not optic nerve dysfunction)

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6
Q

Name the visual field defect:

  1. involves fixation only
  2. extends from fixation to blind spot
  3. involves a region next to but not involving fixation
  4. involves a region symmetrically surrounding but not involving fixation
A
  1. central scotoma
  2. cecocentral scotoma
  3. paracentral scotoma
  4. pericentral scotoma
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7
Q

Ddx for optociliary shunt vessels

A

chronic papilledema, optic sheath meningioma, old CRVO, chronic glaucoma

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8
Q

symptoms in IIH

A

headache that improves with lying down, nausea, TVOs, diplopia (from abducens nerve palsy), pulsatile tinnitus

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9
Q

drugs that can cause elevated ICP

A

tetracyclines, OCPs, steroid use or withdrawal, cyclosporine, vitamin A and its derivatives, lithium

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10
Q

tests to order for all patients with expected increased ICP

A

MRI, MRV, LP

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11
Q

treatment for IIH

A

weight loss, acetazolamide. can use topiramate or furosemide as well. surgery includes ONSF (this helps protect ON from further damage but will not treat headache or affect ICP), and CSF shunting procedure (better for treating headache and lowering ICP but complications include infection, occlusion, need for re-operation)

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12
Q

ICP cutoff to diagnose IIH

A

> /= 25 cm H2O of opening LP pressure in lateral decub, for adults

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13
Q

% female and % obese in adult IIH

A

90% each

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14
Q

differences between adult and pediatric IIH

A

peds: affects boys more. usually not obese. often do not have headache. may have multiple cranial neuropathies

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15
Q

compare/contrast AAION and NAION in age, sex, presenting symptoms, visual acuity, disc appearance, FA findings, natural history, and treatment

A
  • mean age: AAION 70, NAION 60
  • sex: AAION F>M, NAION F=M
  • Sx: AAION- TVOs, headache, jaw claudication, scalp tenderness, weight loss, fatigue, myalgias. NAION- none
  • disc: both swollen, but AAION pale and NAION hyperemic. also, cotton wool spots w/ AAION. C/D 20/200 60% NAION
  • FA: delayed choroidal filling for AAION; disc delay for both
  • progression: fellow eye involvement 54-95% AAION and 12-19% NAION
  • Tx: systemic steroids for AAION. nothing with proven benefit for NAION
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16
Q

what are Foster-Kennedy syndrome and pseudo-Foster Kennedy syndrome

A

Foster-Kennedy syndrome: intracranial mass compressing one optic nerve and causing elevated ICP, leading to an ipsilateral pale nerve and contralateral swollen nerve

pseudo-Foster Kennedy syndrome: NAION occurring in fellow eye, with previous eye pale and affected eye swollen and hyperemic

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17
Q

risk factor for NAION

A

small c/d, HTN, HLD, DM

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18
Q

differentiate NAION and optic neuritis

A
  • age: NAION >50, optic neuritis M
  • VF defect: altitudinal for NAION, central for ON
  • disc edema: 100% NAION and pale, 35% ON and may be hyperemic
  • retinal heme: common NAION, rare ON
  • FA: delayed disc filling NAION, normal ON
  • MRI: optic nerve enhancement with ON but not NAION
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19
Q

70 yo diabetic p/w blurred vision OS. disc is swollen and hyperemic OS with dilated vasculature but no leakage into vitreous on FA. remainder of fundus exam is normal. enlarged blind spot on HVF. diagnosis?

A

diabetic papillopathy

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20
Q

70 yo diabetic p/w blurred vision OS. disc is swollen and hyperemic OS with dilated vasculature but no leakage on FA. remainder of fundus exam is normal. diagnosis?

A

diabetic papillopathy

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21
Q

28 yo otherwise healthy female p/w blurred vision OD. vision 20/30, no RAPD, color normal. VF shows blind spot enlargement. disc is swollen with dilated, tortuous veins and scattered flame heme. FA shows circulatory slowing without regions of occlusion. diagnosis and work up?

A

papillophlebitis (basically a mild CRVO in young healthy patient that should resolve with little or no sequelae in 6-12 months). Can consider hypercoaguability work up

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22
Q

T or F regarding optic disc drusen:

  1. rarely affect nonwhites
  2. equal sex prevalence
  3. bilateral in 50%
  4. secondary neovascularization can occur in rare cases
  5. RAPD may be present
  6. visual acuity often is affected
  7. can cause vessel obscuration at the disc margin
  8. hyperemia and dilation of surface microvasculature can occur
  9. can produce visual field defects
  10. can be detected on B-scan and OCT
  11. autofluoresce on FA
  12. can cause disc leakage on FA
  13. usually become more visible over the years
A
  1. true
  2. true
  3. false; b/l 75-86%
  4. true
  5. true
  6. false; acuity rarely affected
  7. false; vessel obscuration suggests disc edema and not drusen
  8. false; these findings can occur with certain causes of disc edema but not drusen
  9. true (example: nasal step)
  10. true
  11. true
  12. false; disc leakage suggests disc edema
  13. true
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23
Q

differentiate disc drusen from astrocytic hamartomas involving the disc

A

astrocytic hamartomas begin at disc margin and extend into peripapillary retina, they arise in deeper layer of retina and thus typically obscure disc vessels, they may have a fleshy/pink color, they do not autofluoresce, and they may show tumor-like vascularity on FA

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24
Q

acute, severe, painless monocular vision loss in 20 yo male. disc appears hyperemic and elevated but does not leak on FA. peripapillary telangiectasias are present and there is tortuosity of the medium sized retinal arterioles. diagnosis, inheritance, workup, and treatment

A

Leber hereditary optic neuropathy. mitochondrial inheritance but only affects males (possible protective effect of estrogen). If no family history, should order MRI to eval for optic neuritis or mass. no treatment has been proven beneficial

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25
Q

most common position for point mutation in LHON? worst prognosis? highest rate of spontaneous improvement?

A

11778 most common and worst prognosis. 14484 best chance of spontaneous recovery. 3460 is other location

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26
Q

most common hereditary optic neuropathy? gene and chromosome? when does it present? classic disc finding?

A

autosomal dominant optic neuropathy. OPA gene, chromosome 3, involved in mitochondrial membrane integrity. 1st decade of life. cookie-cutter temporal atrophy

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27
Q

bilateral small and grayish appearing optic discs. MRI reveals absence of septum pellucidum: diagnosis, other findings, and management

A

septo-optic dysplasia (aka de Morsier syndrome). may have pituitary hypoplasia, with dwarfism from decreased growth hormone most common. requires endocrine consult

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28
Q

bilateral optic nerve hypoplasia with symmetrical inferior altitudinal VF defect: diagnosis and etiology

A

superior segment hypoplasia, caused by maternal diabetes

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29
Q

visual field defects in congenital tilted disc syndrome? how can this defect be improved?

A

bilateral (80%) superotemporal defects that do not respect the midline (correspond to infranasal colobomatous excavation); can get partial improvement from myopic refractive correction

30
Q

large orange staphylomatous disc with vessels emanating from the periphery of the disc: diagnosis, demographics, workup

A

morning glory disc anomaly. females, unilateral. MRI to eval for basal encephalocele

31
Q

% of optic neuritis that presents with edema? with pain?

A

35%

92%

32
Q

most common visual field defect in optic neuritis?

A

generalized decreased sensitivity (but any defect is possible)

33
Q

color vision affected in optic neuritis?

A

yes; dyschromatopsia, particularly for red, is almost universal and is often out of proportion to decrease in visual acuity

34
Q

atypical findings in suspected optic neuritis that warrant additional workup?

A

lack of pain, significant disc swelling, inflammatory ocular features, bilaterality, involvement of other cranial nerves, lack of recovery by one month

35
Q

Rates of developing MS for first episode of optic neuritis?

A 
10/20/40/60 rule:
At 10 years, the chance of getting MS is:
- 20% if no lesions on MRI
- 40% if MRI not obtained
- 60% if at least one lesion on MRI

**However, this rule may be outdated as the 15-year follow-up on the study revealed 25% if no lesions and 72% if 1 or more lesions

36
Q

optic neuritis features associated with lower risk of developing MS?

A

male sex, optic nerve swelling, absence of pain, NLP vision, retinal hemorrhages and exudates

37
Q

overall visual prognosis for acute unilateral optic neuritis?

A

92% 20/40 or better

38
Q

T or F regarding optic neuritis treatment recommendations:

  1. oral steroid monotherapy is effective at improving visual outcome
  2. oral steroid monotherapy is effective at decreasing recurrence rates
  3. IV steroids followed by oral steroids is effective at improving long-term visual outcome
  4. IV steroids followed by oral steroids can speed recovery by 1-2 weeks
  5. IV steroids decreases lifelong risk of developing MS
  6. IMT has been proven to improve morbidity in the relapsing remitting form of MS
  7. IMT can delay the conversion of patients with acute optic neuritis to definite MS
A
  1. false; no improvement
  2. FALSE! Actually doubled recurrence rates!
  3. false; speeds recovery but no effect on final visual outcome
  4. true; this is why we treat some patients
  5. false; they decrease recurrence rates during the first 2 years, but this protective effect wears off after 2 years
  6. true
  7. true
39
Q

diagnostic criteria for neuromyelitis optica

A

(Provides 99% sensitivity and 90% specificity)

  1. optic neuritis
  2. myelitis
  3. At least 2 of the following:
    - - continuous spinal cord lesion on MRI involving 3 or more vertebral segments
    - - brain MRI nondiagnostic of MS
    - - positive NMO-IgG
40
Q

what does the NMO antibody bind to?

A

aquaporin-4

41
Q

treatment of NMO

A

high dose IV steroids; IVIG or plasmapharesis for refractory cases

42
Q

acute painful vision loss in 50 yo F that has persisted for 2 weeks. MRI shows enhancement of optic nerve sheath. diagnosis, treatment, and prognosis

A

optic perineuritis; pain distinguishes this from nerve sheath meningioma. responds well to steroids but progresses without treatment. not associated with increased risk of demyelinating disease

43
Q

classic diagnostic triad of optic nerve sheath meningioma

A
  1. painless, slowly progressive monocular vision loss
  2. optic atrophy
  3. optociliary shunt vessels
44
Q

management of optic nerve sheath meningioma

A

can observe if visual function and size are stable; treatment is with fractionated radiation therapy. surgery is reserved only for intracranial or trans-sphenoidal extension

45
Q

most common primary tumor of optic nerve?

A

glioma (pilocytic astrocytoma); meningioma 2nd most common

46
Q

classic MRI findings of optic glioma and optic nerve sheath meningioma?

A
  • glioma: globular enlargement and kinking of nerve

- meningioma: thickening and contrast enhancement of nerve sheath that spares optic nerve (“tram track sign”)

47
Q

syndrome associated with optic nerve gliomas?

A

NF1 (7.8-21% depending on source)

48
Q

age of presentation for optic nerve glioma?

A

70% by first decade, 90% by second decade

49
Q

treatment of optic nerve glioma?

A

no universally-accepted method, but chemo is probably first line. 1 study showed radiation to be effective. can observe if vision and size are stable

50
Q

which drugs can cause a rapid onset of toxic optic neuropathy?

A

methanol and ethylene glycol

51
Q

what drug can cause subacute toxic optic neuropathy with disc edema? How do you differentiate this from NAION?

A

amiodarone; subacute onset, bilaterality, diffuse rather than altitudinal visual field loss, slow resolution of disc edema

52
Q

what are the most common prescription drugs implicated in toxic optic neuropathy?

A

ethambutol, linezolid, isoniazid, chloramphenicol, hydroxyquinolones, penicillamine, cisplatin, vincristine

53
Q

treatment for traumatic optic neuropathy?

A

nothing has been shown efficacious

54
Q

three causes of posterior ischemic optic neuropathy

A
  1. postoperative (especially spine, heart, head and neck surgeries with blood loss, prolonged anesthesia, and hypotension)
  2. 2/2 GCA
  3. non-arteritic (NAION-like)
55
Q

33M feeling ill recently, now with acute onset profound vision loss. + RAPD, swollen nerve with vitreous cell and peripheral retinal arterial sheathing.

A

infiltrative optic neuropathy; leukemia, lymphoma, or granulomatous (sarcoid, Wegener’s, syphilis, TB, fungal).

56
Q

right central scotoma and left supratemporal defect?

A

junctional lesion at right optic nerve and chiasm

57
Q

most common cause of chiasmal compression

A

pituitary adenoma

58
Q

difference in visual field defect from pituitary adenoma v craniopharyngioma?

A

Both with bitemporal hemianopsia, but:

  • pituitary adenoma: more superior field loss (compresses from below)
  • craniopharyngioma: more inferior field loss (compresses from above)
59
Q

medical therapy for prolactinoma?

A

bromocriptine or cabergoline (dopamin agonists)

60
Q

in general (although this has been disputed), more congruous visual field defects are generally located ______

A

more posterior in the visual pathway

61
Q

a right optic tract lesion will produce a _____ RAPD

A

left (55% of fibers decussate)

62
Q

optic disc appearance in an optic tract lesion?

A

bow-tie atrophy (nasal radiating fibers and papillomacular bundle, which both contribute to nasal crossing fibers)

63
Q

two types of visual field defects cause by damage to the lateral geniculate body, and the respective arteries that can lead to these defects upon vascular insult

A

LGN lesions produce highly congruous hemianoptic defects.

  • horizontal sectoranopia (like a sideways W pointing to the uninvolved field), from posterior choroidal artery occlusion
  • quadruple sectoranopia (homonymous hemianopia involving the superior and inferior thirds of the affected visual hemifield but sparing a central wedge), from anterior choroidal artery occlusion
64
Q

visual field defect associated with injury to Meyer’s loop?

A

Meyer’s loop is an anterior bowing of inferior fibers as they leave the LGN; defects here cause a superior, incongruous, homonymous wedge defect (“pie in the sky”)

65
Q

patient with homonymous hemianopia more dense inferiorly. what clinical test can you perform to locate the lesion to the parietal lobe?

A

OKN drum; may be abnormal for parietal lobe lesions (generates pursuit), and normal for optic tract or occipital lobe lesions

66
Q

locate the lesion: right homonymous hemianopia, macular sparing, with preserved right temporal crescent

A

anteromedial occipital cortes, sparing the anterior temporal fibers. likely from posterior cerebral artery stroke

67
Q

why is macula often spread in occipital strokes? what vascular insult produces a bilateral paracentral hemianopic scotoma?

A

macula often spared because macular fibers prject to the occipital tip, which receives dual blood supply from PCA and MCA. however, as a watershed area, it is at risk for hypoperfusion during hypotensive and hemorrhagic etiologies (surgery, trauma) and damage can be bilateral

68
Q

what distinguishes cortical blindness form bilateral blindness from prechiasmal or chiasmal lesions?

A

the former will not have an APD, and optic nerves will appear normal

69
Q

denial of blindness in cortically blind patient?

A

Anton’s syndrome

70
Q

perception of motion but no vision of static images in a hemifield?

A

Riddoch phenomenon

Neuro-Ophthalmology (8 decks)

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