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Ocular Disease 3 - Midterm > Optic Neuropathies > Flashcards

Optic Neuropathies Flashcards

1
Q

what type of injury is most likely to occur in the intraocular section of the optic nerve?

A

vascular insult

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2
Q

what type of injury is most likely to occur in the intraorbital section of the optic nerve?

A

muscle engorgement or tumors

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3
Q

what type of injury is most likely to occur in the intracanalicular section of the optic nerve?

A

trauma/fractures and sinus inflammation

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4
Q

what type of injury is most likely to occur in the intracranial section of the optic nerve?

A

pituitary gland and circle of willis

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5
Q

what is the blood supply to the pre-laminar region?

A

short posterior ciliary artery

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6
Q

what is the blood supply to the lamina cribrosa?

A

short posterior ciliary artery and circle of zinn haller

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7
Q

what is the blood supply to the retro-laminar region?

A

branches of the central retinal artery and pial vessels

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8
Q

what are the three conditions that can cause optic nerve shunt/collateral vessels?

A

optic nerve sheath meningioma, CRVO, and chronic glaucoma

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9
Q

what are the hallmark signs of an optic neuropathy?

A

VA loss, RAPD, dyschromatopsia, VF defect, reduced contrast sensitivity, +/- optic disc appearance, and abnormal VEP

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10
Q

what is typical optic neuritis?

A

autoimmune condition = primary demyelination of the optic nerve myelin sheath

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11
Q

what is the pattern of VA loss in typical optic neuritis?

A

progresses over 1 week and improvement begins by 1 month

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12
Q

what is the typical demographic for typical optic neuritis?

A

young adults (18-46), female > male, and no history of systemic disease

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13
Q

what type of swelling does typical optic neuritis have?

A

2/3 of cases are retrobulbar

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14
Q

what are the VF defects for typical optic neuritis?

A

any pattern is possible (diffuse is most common)

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15
Q

what are 4 associated signs with typical optic neuritis?

A

numbness in hands, problems in bladder control, pulfrich phenomenon, and uthoff sign

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16
Q

what did the optic neuritis treatment trial (ONTT) conclude?

A

high does IV steroids accelerated visual recovery, oral steroids alone increased rate of recurrence and IV steroids reduced risk of MS development for 2 years

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17
Q

why is an MRI useful in patients who have typical optic neuritis?

A

it can identify patients who are at higher risk of developing MS

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18
Q

what did the longitudinal optic neuritis study (LONS) conclude?

A

the initial MRI is the most predictive factor for developing MS after ON, the 15 year overall risk was 50% (females > males)

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19
Q

what did the CHAMPS study conclude?

A

the medication Avonex (interferon therapy) reduced risk of development of MS and T2 lesions

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20
Q

which medication for MS is oral and has CME as a side effect?

A

Gilenya - can cause CME 3-6 months after starting medication (need OCT at the start and after 4 months)

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21
Q

what blood test is used to check for MS?

A

oligoclonal bands (immunoglobulins) present in CSF indicate inflammation in CNS (79-90% of MS patients have bands)

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22
Q

what is atypical optic neuritis?

A

a systemic infection or inflammatory cause

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23
Q

what is the presentation for atypical optic neuritis?

A

ages 50, bilateral, lack of pain, uveitis, retinal exudates/infiltrates, optic nerve swelling, hemorrhages, VA worsens past 1 week

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24
Q

what is the most common symptom in typical optic neuritis?

A

90% has pain with EOM movements

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25
Q

what are the causes of atypical optic neuritis?

A

connective tissue disease (lupus, sjogrens, bechet), infectious (lyme, syphilis), infiltrative (sarcoidosis, cancer)

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26
Q

what is neuromyelitis optica (NMO) - Devic’s syndrome?

A

unilateral or bilateral optic neuritis + inflammation of spinal cord (limb weakness)

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27
Q

what is the typical age for NMO?

A

average age is 39 (can affect children)

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28
Q

what causes NMO?

A

NMO antibodies (NMO IgG) target aquaporin 4 - NMO IgG is found in astrocytes and around the blood brain barrier

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29
Q

how is NMO different from MS?

A

NMO has more severe attacks, includes spinal cord, MRI is normal, no CSF oligoclonal bands, and usually has an autoimmune disease coexisting

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30
Q

what is transverse myelitis?

A

focal inflammatory disorder of the spinal cord - has numbness and paresthesias (peripheral limbs)
may progress to MS

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31
Q

what is acute disseminated encephalomyelitis (ADEM)?

A

post-infectious encephalomyelitis (fever, nausea, vomiting, vertigo)
typically children status-post viral infection or immunization
MRI = extensive lesions in basal ganglia and thalamus

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32
Q

what is non-arteritic anterior ischemic optic neuropathy (NAION)?

A

ischemic, non-inflammatory vascular insult to the pre-laminar and retro-laminar optic nerve (posterior ciliary artery involved)

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33
Q

what is the typical clinical presentation for NAION?

A

acute, painless VA loss (mild-severe), older patients (>55 and males>females) with cardiovascular risk factors, and a disc at risk (smaller)

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34
Q

what is the optic nerve appearance in NAION?

A

hyperemic edema (acute state), flame hemorrhages, +/- macular star and disc pallor develops 2-3 weeks after initial insult

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35
Q

what is the typical VF defect in NAION?

A

altitudinal

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36
Q

is NAION unilateral or bilateral?

A

starts unilateral - can become bilateral sequentially

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37
Q

what causes NAION?

A

chronic HTN causes an alteration in autoregulatory response - vasodilation fails with decreased BP and ischemia to PCA results in decreased optic nerve perfusion

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38
Q

what is the treatment for NAION?

A

monitor 2-4 weeks, if VA or VF is still worsening then needs additional work-up

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39
Q

what is arteritic ischemic optic neuropathy (AION)?

A

inflammation of elastic tissue in arterial walls in vessel occlusion and causes ischemia (systemic inflammatory condition of the medium sized vessels all over the body)
affects the ophthalmic artery

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40
Q

what is the typical demographic for AION?

A

65+, females > males, bilateral within 1-2 days, 50% have polymyalgia rheumatica

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41
Q

why is AION an ophthalmic emergency?

A

the whole eye looses blood supply and will result in complete blindness

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42
Q

what are some symptoms of AION?

A

severe VA loss, scalp tenderness, jaw claudication, mild fever, weight loss, arthralgias/myalgias

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43
Q

what are the signs for AION?

A

pallid optic nerve swelling, no hemorrhages, extensive cotton wool spots, preceded by episodes of TIA

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44
Q

what is the treatment for AION?

A

needs STAT IV steroids for 3-5 days, temporal artery biopsy, Labs: ESR and CRP

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45
Q

what is giant cell arthritis (CGA)?

A

systemic vasculitis of medium/large arteries, self-limiting but may persist for years, oral steroids protect surviving optic nerve

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46
Q

what do you have to rule out in patients with NAION under age 40?

A

DM, HTN, hyperlipidemia, elevated homocysteine, vasculitides (SLE, Wegener’s), coagulopathy and perform blood work

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47
Q

what causes posterior ischemic optic neuropathy?

A

most commonly = post-surgical (especially long procedures with severe blood loss)
or a spontaneous cause (GCA, athersclerosis, radiation)

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48
Q

what are the symptoms of posterior ischemic optic neuropathy?

A

patient recovers consciousness and discovers poor VA in one or both eyes

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49
Q

what are the signs of posterior ischemic optic neuropathy?

A

initially the optic disc is normal - then pallor develops 4-6 weeks after (if there is - APD then suspect bilateral posterior cerebral artery infarction)

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50
Q

what is diabetic papillopathy?

A

a milder form of NAION in diabetic patients - the vision is typically unaffected

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51
Q

what is a hallmark sign of diabetic papillopathy (more than in NAION)?

A

hyperemic disc swelling with dilated pre-laminar vessels (will also see diabetic retinopathy - dot/blot hemorrhages)

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52
Q

what is papilledema?

A

optic nerve edema caused by raised intracranial pressure - need to confirm with lumbar puncture

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53
Q

what is stage 1 of papilledema?

A

very early = incomplete C-shaped peripapillary halo, no elevation, blurring of superior/inferior and nasal aspects and normal temporal disc

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54
Q

what is stage 2 of papilledema?

A

early = blurring or all borders, complete peripapillary halo (360), elevation of nasal border

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55
Q

what is stage 3 of papilledema?

A

moderate = increased ONH diameter, partial obstruction of vessels at disc margin, peripapillary halo with finger-like projections

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56
Q

what is stage 4 of papilledema?

A

marked = elevation of entire nerve head, near total obstruction of major blood vessels at the disc

57
Q

what is stage 5 of papilledema?

A

severe = dome-shaped protrusion, obliteration of cup, total obscuration of blood vessels on the disc

58
Q

why is papilledema a medical emergency?

A

need to rule out any intracranial masses with neuroimaging

59
Q

what are the clinical features of papilledema?

A

bilateral, VF enlarged blind spot or arcuate, initial edema is on ONH periphery, and absent SVP

60
Q

what are some symptoms of papilledema?

A

headache, transient visual obstructions, pulsatile tinnitus, diplopia (CN6 palsy)

61
Q

what is the order of the diagnostic work-up for papilledema?

A

MRI first to rule out structural lesion - then lumbar puncture
lab tests for inflammation/infection

62
Q

what are the two most common mechanisms of increased ICP in papilledema?

A

increased brain volume (tumor, hemorrhage, trauma) and decreased CSF drainage (hydrocephalus, meningitis, venous sinus thrombosis)

63
Q

what are the two least common mechanisms of increased ICP in papilledema?

A

increased CSF production and decreased skull volume

64
Q

what are the medical causes for pseudotumor cerebri?

A

COPD, malignant HTN, sleep apnea, and renal failure

65
Q

what are the medication causes for pseudotumor cerebri?

A

tetracyclines, excessive vitamin A, steroids, and birth control pills

66
Q

how does a venous obstruction cause psuedotumor cerebri?

A

either with a central venous sinus thrombosis or jugular venous thrombosis

67
Q

what are the signs and symptoms for idiopathic intracranial hypertension (pseudotumor cerebri - unknown cause)?

A

headache, nausea, vomiting, transient visual obstructions, and papilledema
all lab work and MRI results must be normal

68
Q

what is the LP opening pressure in idiopathic intracranial hypertension (IIH)?

A

greater than 25 cmH20 with normal CSF composition

69
Q

who typically gets IIH?

A

triple F = fat, fertile, females

70
Q

what are the treatments for IIH?

A

weight loss = 6% reduction results in papilledema resolution

Acetazolamide = first line of medical treatment

71
Q

what are the causes of unilateral optic nerve edema - papillitis?

A

papillophlebitis, diabetic papillopathy, CRVO, NAION, AION, infiltrative and infectious

72
Q

what is papillophlebitis?

A

very similar to CRVO - patients are typically young and healthy, etiology is unknown but suspected inflammation of the retinal vessels, resolves in 3-6 months

73
Q

what can cause infiltrative optic neuropathy?

A

(one or both nerves) = leukemia, lymphoma, breast/lung/bowel metastases, and sarcoid
patients usually have a known malignancy

74
Q

what are the 2 types of compressive optic neuropathies that are non-neoplastic?

A

thyroid eye disease (EOMs choke off optic nerve) and aneurysm (ICA)

75
Q

what are the 3 neoplastic intracranial causes of compressive optic neuropathies?

A

sphenoid wing meningioma, pituitary adenoma, and metastases

76
Q

what are the 2 neoplastic optic nerve causes of compressive optic neuropathies?

A

optic nerve sheath meningioma and optic nerve glioma

77
Q

who typically gets a pituitary adenoma?

A

females > males, 40-50 years old

78
Q

what are the hyperpituitarism symptoms caused by a pituitary adenoma?

A

cushing syndrome (excessive cortisone - moon face, obesity, hirsutism), acromegaly, and prolactinoma (amenorrhea, infertility, gynecomastia)

79
Q

what is the typical VF defect in a patient with a pituitary adenoma?

A

bitemporal hemianopsia

80
Q

who typically gets an optic nerve sheath meningioma?

A

females > males, usually in 4th decade

metastasis is rare

81
Q

who typically gets an optic nerve glioma?

A

children (75% before age 20) and 50% have NF1

benign course in children (low mortality) and causes significant VA loss

82
Q

what type of traumatic optic neuropathy can occur at the optic disc/laminar zone?

A

optic nerve avulsion - forceful backward dislocation of optic nerve from the scleral canal

83
Q

what type of traumatic optic neuropathy can occur at the intraorbital zone?

A

penetrating FB, displaced fracture or bone fragment, compression by hematoma
usually see CRAO and disc edema

84
Q

what type of traumatic optic neuropathy can occur at the intracanalicular zone?

A

*most common location
usually due to frontal/maxillary blunt trauma (occurs with or without fracture)
can be direct (damage from bone fragments) or indirect (tearing of pial vessels and shearing of axons)

85
Q

what will the optic nerve look like in an intracanalicular zone trauma?

A

appears normal initially - pallor develops 4-6 weeks later

86
Q

what imaging do you order and what is the treatment for traumatic optic neuropathies?

A

CT of orbits

mega dose corticosteroids or optic nerve decompression (if poor VA)

87
Q

what are the 3 great masqueraders?

A

syphilis, lyme, and sarcoid

88
Q

what is the most common cause of infectious optic neuropathy?

A

bacteria is most common cause
syphilis, lyme, TB and bartonella are most common
(can also be treponema pallidum)

89
Q

how does bartonella heneselae (cat scratch disease) usually present?

A

fever, malaise, adenopathy
VA symptoms start 2-3 weeks after systemic symptoms resolve
mild disc edema + macular edema

90
Q

what are some viral causes of infectious optic neuropathy?

A

HZV (more common), measles, mumps, chickenpox

91
Q

what are some fungi causes of infectious optic neuropathy?

A

typically in immunocompromised patients

mucormycosis or cryptococcal meningitis

92
Q

what are some parasite causes of infectious optic neuropathy?

A

toxoplasma and toxocara

93
Q

what are the two conditions that present with macular edema (aka stellate neuroretinitis)?

A

infectious optic neuropathy and malignant hypertension

94
Q

what are some signs and symptoms of developmental anomalies of the optic nerve?

A

reduced VA, VF loss, color vision deficiency, less likely to have RAPD because it will probably affect both nerves
all anomalies are stable or non-progressive

95
Q

what are some associated findings with developmental anomalies of the ONH?

A

CNS abnormalities, endocrine dysfunction, developmental delays, strabismus, amblyopia, ocular colobomas, hyperelorism, microphthalmos and aniridia

96
Q

what is optic nerve hypoplasia?

A

a subnormal number of axons in the optic nerve

characterized by a small optic nerve with a double ring sign

97
Q

what causes optic nerve hypoplasia?

A

insult to visual pathways before completion of development = toxic, infectious, ischemia, hereditary, fetal alcohol syndrome, De-Morsier syndrome

98
Q

what can optic nerve hypoplasia be associated with?

A

developmental abnormalities of anterior midline brain structures (mental retardation and endocrine deficits)

99
Q

what is De-Morsier syndrome (aka septo-optic dysplasia)?

A

disorder of early brain development (3 parts)
optic nerve hypoplasia
abnormal formation of midline brain structures (corpus collosum and septum pellucidum)
pituitary hypoplasia
**typically cause by sporadic mutation

100
Q

what causes an optic nerve coloboma?

A

incomplete closure of the fetal fissure during prenatal development (defect is always inferior - may include retina, choroid, iris or lens)
commonly bilateral

101
Q

what is the VF defect seen with optic nerve colobomas?

A

arcuate defect

102
Q

what is an optic nerve pit?

A

small, partial coloboma
usually inferior-temporal aspect of ONH
they have a larger optic disc
may lead to macular edema in 4th decade

103
Q

what is megalopapilla?

A

enlarged optic disc and large physiologic cup - same number of axons but they are spread out

104
Q

what is morning glory syndrome?

A

a dysplastic disc (disorganized axons)

excavated funnel shape, surrounded by elevated ring of chorioretinal pigmentation

105
Q

who typically gets morning glory syndrome?

A

females > males
unilateral and OD is more common
no hereditary pattern

106
Q

what is morning glory syndrome associated with?

A

basal encephalocele - deficit in skull floor, allowing brain tissue to protrude outside the cranial cavity, CSF leaks

107
Q

what are the 3 cardinal signs of morning glory syndrome?

A
  1. cup is enlarged with deep depression and white tissue at base
  2. raised annulus surrounds disc with variable amount of pigmentation
  3. retinal blood vessels emerge from disc in radial fashion (like spokes on a wheel)
108
Q

what is tilted disc syndrome?

A 
due to oblique insertion of the optic nerve into the globe - nerve typically looks oval shaped 
a scleral crescent is usually present 
situs inversus (blood vessels go nasal before going temporal)
109
Q

what does the VF look like in tilted disc syndrome?

A

bitemporal appearance

110
Q

what is pseudopapilledema?

A

small scleral opening - axons must squeeze through, slight elevation of nerve, anomalous blood vessels and indistinct margins (but no obstruction of vessels)

111
Q

what is optic nerve head drusen?

A

hyaline bodies anterior to the lamina cribrosa -can cause pseudopapilledema
lumpy/scalloped appearance

112
Q

what causes optic nerve head drusen?

A

AD inheritance

70% bilateral

113
Q

what are the VF defects seen in optic nerve head drusen?

A

arcuate - can be progressive

114
Q

what are myelinated nerve fibers?

A

extended proliferation of normal tissue - benign
feathery appearance obscures underlying tissue
1% of population

115
Q

what type of vision loss is seen with nutritional or toxic optic neuropathy?

A

painless, slowly progressive, bilateral, symmetric and ranges from 20/50-20/200 (never worse than 20/200)

116
Q

what are the exam findings for nutritional or toxic optic neuropathy?

A

temporal ONH pallor, centro-cecal VF, no RAPD (bilateral) and dyschromatopsia

117
Q

why are the B vitamins essential?

A

they are required for normal RBC formation, repair of tissues and cells and synthesis of DNA

118
Q

what does vitamin B1 (thiamine) do? what causes a deficiency?

A

converts carbohydrates into glucose

deficiency = chronic alcoholics, poor diet, liver disease

119
Q

what does vitamin B6 do?

A

helps with serotonin, NE, myelin formation

120
Q

what does vitamin B9 (folate) do?

A

critical for cell growth and metabolism, works with B6 and B12 to control homocysteine levels

121
Q

what does vitamin B12 do? what causes a deficiency?

A

critical for RBC formation and nerve function

deficiency = pernicious anemia

122
Q

what medications can cause toxic optic neuropathy?

A

anti-TB medications (ethambutol and isoniazid) and some cancer chemotherapies

123
Q

what substances can cause toxic optic neuropathy?

A

lead, methanol, tobacco, alcohol (not directly)

124
Q

what is Leber’s hereditary optic neuropathy?

A

caused by a mutation in the mitochondrial genome (maternally inherited) - there is a decrease in ATP production in the optic nerve and results in degeneration of retinal ganglion cells

125
Q

when does Leber’s hereditary optic neuropathy occur?

A

mutation is present at birth - manifests in early adulthood (25-35)
males > females

126
Q

what type of VA loss is seen with Leber’s hereditary optic neuropathy?

A

acute VA loss in one eye (severe) - fellow eye is involved 2-4 weeks after
may be triggered by alcohol/tobacco or nutritional deficiencies

127
Q

what is the VF defect seen with Leber’s hereditary optic neuropathy?

A

central or central-cecal scotoma

128
Q

what does the optic nerve look like with Leber’s hereditary optic neuropathy?

A

initially hyperemic and pallor develops a few weeks later

dilation of peripapillary retinal vessels (makes nerve appear swollen - but does not leak on FA)

129
Q

what is the management for Leber’s hereditary optic neuropathy?

A

genetic counseling, electrocardiogram, limit tobacco and alcohol
No FDA approved treatment - may try oral idebenone (stimulates ATP in brain)

130
Q

what is autosomal dominant optic atrophy (aka Kjer’s DOA)?

A

most common inherited optic neuropathy
bilateral, symmetric, slowly progressive central VF loss (central-cecal)
VA loss begins in childhood (4-10) then stable at 20/200
females = males

131
Q

which neuropathies have acute onset? which have sub-acute?

A 
acute = optic neuritis, ischemic optic neuropathy, CRVO, trauma 
sub-acute = compressive, nutritional/toxic
132
Q

which neuropathies are unilateral? bilateral?

A 
unilateral = typical optic neuritis, NAION, compressive, trauma
bilateral = toxic/nutritional, hereditary, atypical optic neuritis, AION
133
Q

which neuropathies have altitudinal VF defects?

A

NAION

134
Q

which neuropathies have bitemporal VF defects?

A

parasellar lesions

135
Q

which neuropathies have hemianopic VF defects?

A

ischemic or compressive

136
Q

which neuropathies have central-cecal VF defects?

A

toxic, nutritional, DOA

137
Q

which neuropathies have temporal pallor?

A

DOA, toxic, nutritional

138
Q

which neuropathies have bow-tie pallor?

A

optic tract lesions

Ocular Disease 3 - Midterm (7 decks)

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