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Oral boards > Friedman neuro-ophthalmology > Flashcards

Friedman neuro-ophthalmology Flashcards

1
Q

What are optic nerve drusen?

A

superficial or buried hyaline bodies in the prelaminar optic nerve that have become calcified

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2
Q

How do you confirm optic nerve drusen?

A

B-scan (with gain turned down)
CT scan
autofluroescence

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3
Q

complications of optic nerve drusen

A

cause VF defects (typically enlarged blind spot, arcuate scotoma, sectoral scotoma that is stable/nonprogressive)

  • anterior ischmeic optic neuropathy
  • choroidal neovascularization
  • subretinal/vitreous hemorrhage
  • vascular occlusion
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4
Q

NAION associations?

A

HTN, DM, ischemic heart dz, hypercholesterolemia, smoking

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5
Q

GCA questions

A 
headache
scalp tenderness
jaw claudication (pain with chewing)
weight loss
fever
anorexia
neck pain
eye pain
diplopia
joint pain (Sx of polymyalgia rheumatica)
anemia
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6
Q

GCA testing

A

ESR: greater than age/2 for males and (age+10)/2

CRP: > 2.45 mg/dL
CBC (low hematocrit, high platelets)

FA: choroidal nonperfusion in arteritic form

temporal artery Bx w/in 2 weeks, at least 3 cm in length

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7
Q

GCA Rx

A

IV 1 gm qd x 3 days.

Rx does not improve outcome in affected eye but is necessary to prevent visual loss in fellow eye
>follow by an internist/rheumatologist to monitor therapy response and to slowly taper steroids

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8
Q

Other complications of GCA

A

BRAO/CRAO
ophthalmic artery occlusion
anterior segment ischemia
CN palsy (esp CN6) and stroke

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9
Q

Foster Kennedy dz and findings?

A

Foster Kennedy: Front lobe mass (usually meningioma)

Anosmia, ipsilateral ON atrophy 2/2 tumor compression, contralateral ON edema 2/2 elevated ICP

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10
Q

pseudo-Foster Kennedy?

A

bilateral AION

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11
Q

Questions to ask pt if concern of CN3 palsy

A

Headache?
trauma?
cancer?

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12
Q

What do you need to R/O in young pt with CN3 pupil-involvement?

A

PCOM (posterior communicating artery aneurysm) - neurosurgical emergency
Use MRI, MRA/CTA or both

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13
Q

CN3 pupil-SPARING older pt

A

can observe for pupil involvement during the 1st week, but generally such cases 2/2 microvascular dz (80% are pupil sparing) and resolve spontaneously in 3 months

Perform work-up if pupil becomes involved, history of cancer, other neurologic abnml or palsy does not resolve after 3 months.

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14
Q

CN6 etiologies

A

MCC: vasculopathic
Also: trauma, GCA, infection, MS, increased ICP, rarely tumors

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15
Q

CN6 DDx

A 
TED
orbital inflammatory pseudotumor (idiopathic orbital inflammation)
myasthenia gravis
convergence spasm
strabismus
medial orbital wall fracture
orbital myositis
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16
Q

CN6 work-up

A

can monitor for 3 months if 2/2 DM

Other work-up to consider: check BP, lab tests (CBC, ESR, CDRL/RPR, FTA-ABS/MHA-TP, ANA, LP and tensilon)

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17
Q

Multiple CN palsies DDx

A

V: vascular lesions in the brain stem/subarachnoid space, cavernous sinus, orbital apex
I: infection/inflammation, meningitis
T
A: (mimickers: CPEO, myasthenia, MS, Guillian-Barre, PSP)
M
I
N: tumor

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18
Q

Orbital apex syndrome

A

decreased visual acuity (CN2) and color vision + CN palsies

(CN2, 3, 4, V1 and 6) - NOT V2 or sympathetics

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19
Q

A-V fistulas

A 
CN palsies +
proptosis
conjunctival injection
chemosis
increased IOP
bruit
retinopathy
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20
Q

Cavernous sinus thrombosis

A

CN palsies (can see CN3, 4, V1 and V2, and 6 and sympathetic involvement with Horners)+
fever
lid edema
signs of facial infection

Key difference between orbital apex and cavernous sinus thrombosis is cavernous sinus thrombosis involves V2 and sympathetics

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21
Q

Multiple CN palsies testing

A

CT/MRI-MRA

fasting blood glucose, CBC with diff, ESR, VDRL, RPR, FTA-ABS or MHA-TP, ANA, blood cultures
LP, Tensilon test

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22
Q

orbital cellulitis organisms

A

MC 2/2 gram positive bacteria (strep and staph)

also - fungi (phycomycetes), mucor

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23
Q

Mucormycosis

A

aggressive infection from Mucor fungi that causes necrosis, vascular thrombosis, orbital invasion

histology: broad nonseptate fungae hyphae

Can cause retinal vascular occlusions and orbital apex syndrome

may extend intracranially to cause cavernous sinus thrombosis, meningitis, brain abscess, death.

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24
Q

Lid Retraction DDx

A 
Thyroid eye disease
Post surgery
Contralateral ptosis (Hering’s Law)
Congenital (rare)
Progressive supranuclear palsy
Parinaud’s syndrome
Aberrant regeneration of CN3
Proptosis
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25
Q

Wener Classification of eye findings in TRO mnemonic

A 
NO SPECS
No signs or symptoms
Only signs
Sof tissue involvement
Proptosis
EOM involvement
Cornea involvement
Sight loss (optic nerve compression)
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26
Q

TED findings

A 
proptosis
lid signs: lid retraction/lag on downgaze, lagophthalmos
restricted EOM (strabismus)
exposure (Conj hyperemia, keratopathy)
ON compression (optic neuropathy)
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27
Q

How long to wait for strabismus and TED

A

wait until strabismus stable for at least 6 months

28
Q

Other Rx for TED

A

punctal occulsion tarsorraphy
orbital decompression (if causing keratopathy or optic nerve decompression)
diplopia (prism glasses)

steroids, XRT

29
Q

steps for TED for surgery

A

1) orbital decompression
2) strabismus
3) lid surgery

30
Q

DDx proptosis

A

V: orbital vasculitis, cavernous sinus thrombosis, AV fistula
I: cellulitis, idiopathic orbital inflammation
T: trauma
A
M
I
N: orbital/lacrimal gland tumors

31
Q

Leber’s Hereditary Optic Neuropathy demographic and VF deficit

A

Males, 10-30y/o
VF deficit?
Central or cecocentral

32
Q

Leber’s Hereditary Optic Neuropathy Fundus and FA appearance?

A 
Hyperemia and elevation of optic disc
Peripapillary telangiectasia
Tortuosity of medium arterioles
Findings may precede visual loss (visual loss can lead to vision 20/200)
May also appear normal

FA shows?
No leakage or staining of disc
2nd eye affected weeks - months later

33
Q

Leber’s Hereditary Optic Neuropathy Inheritance and Rx?

A 
Inheritance?
Mitochondrial DNA (therefore maternal inheritance - ~50% sons affected)
Most common = mt 11778

Treatment?
Coenzyme Q
Prognosis:
Based on mutation type

Associated conditions?
Cardiac conduction abnormalities (WPW)

34
Q

drugs that can cause toxic neuropathy

A 
Ethambutol
isoniazid
chloramphenicol
streptomycin
methanol
digitalis
chloroquine
quinine
35
Q

What tests to order if concern of optic nerve pathology

A

HVF or Goldman and color vision testing

36
Q

Junctional scotoma

A

lesion of optic nerve near the chiasm

Central VA loss in ipsi/L eye and superotemporal field defect in the contralateral eye

37
Q

DDx for chiasmal syndrome

A

MCC: mass lesion but possibly due to hemorrhage

V: aneurysm, pituitary apoplexy
I: chiasmal neuritis
T: trauma
A: sarcoidosis
M
I
N: tumors (i.e. meningioma)
38
Q

Optic neuritis findings:

A

Central visual loss, APD, dyschromatopsia
Pain with eye movement (90%)

Uhthoff’s Phenomenon?
VA decrease with exercise / increased body temp

Pulfrich phenomenon?
Lateral motion of pendulum appear to have depth
Average time to nadir = 4.5 days

39
Q

Workup if atypical optic neuritis (lasting > 1 month)?

A

ANA, anti-DNA, VDRL, FTA, CXR, ACE, ESR

Prognosis for typical optic neuritis - Good (VA >20/40 in 95% untreated)

40
Q

ONTT

A

15-year risk of MS with MRI?
0 lesions: 16%
1 or more lesions: 72%
overall risk: 50%
PO prednisone increased recurrence
IV methylprednisolone (250 mg IV q6h x 3 days followed by pred 1 mg/kg day for 11 days then rapid taper) recovered vision faster if treated in first 2 weeks (BUT NO difference in final VA)
IV methylprednisolone in patients with CNS plaques had fewer recurrences within first 2 years, but equivocal at 3 years

41
Q

CHAMPS

A

IM Interferon beta (Avonex) showed 44% decreased risk of progression to MS with first demyelinating event (includes optic neuritis)
Patients treated with steroids also

42
Q

How to uncover functional visual loss

A

check distance and near vision
monocular and binocular vision

vary test distance
fog
red-green glasses with duochrome test or W4D test
prism dissociation
stereopsis
startle reflex
propioception
name signing
mirror tracking
OKHN
visual fields
43
Q

Causes of ipsi/L Horner’s

A

Anisocoria greater in DARK (due to impaired sympathetic input to side of lesion)

DDx:
Central causes (rarely causes isolated Horner's): Wallenberg syndrome (PICA stroke), neck trauma/tumor, cervical disc dz, demyelinating dz

Preganglionic: tumors (mediastinal, apical, thyroid), trauma, pneumothorax, cervical infection, brachial plexus syndrome, aneurysm, trauma

Postganglionic:
neck lesion, headache, migraine/cluster headache,
carotid dissection (3rd order), c-c fistula, internal carotid artery aneurysm, infection

44
Q

Horner’s testing - apraclonidine

A

Anisocoria greater in dark. REVERSAL of anisocoria with apraclonidine.

Apraclonidine 1% (must give OU)

Alpha adrenergic receptor agonist ACTS MORE ON ALPHA 2 receptors (than alpha 1 receptors). @ ~ 36 hrs, upregulation of alpha-1 receptors 2/2 synaptic denervation.

Normal: mild constriction
Horner: dilates more

Normal pupil response to iopidine - mild constriction 2/2 action on alpha2 receptors (decreased norepi)
Horner pupil - upregulated alpha1 receptors –> dilation

45
Q

Horner’s testing - cocaine 10%

A

Cocaine 10%: Blocks NE reuptake
at presynaptic cleft… therefore more NorEpi stimulates the pupillary dilator muscle

Normal pupil - DILATES

Horner pupil - poor (or none) dilation
2/2 decreased sympathetic tone (so no change with cocaine 2/2 already low NorEpi in synaptic cleft)

Physiologic anisocoria - both pupils dilate nearly equally leading to

46
Q

MCC of transient diplopia

A 
decompensated phoria, convergence, divergence insufficiency
myasthenia gravis
spasm of accommodation
GCA (EOM ischemia)
vertibrobasilar insufficiency
superior oblique myokymia
cyclic esotropia
skew deviation
47
Q

Questions to ask patient with ptosis and diplopia

A

Is ptosis worse on one side, does it vary (throughout the day, from day to day, when pt is tired)?
Prior diplopia?
Happen with other activities - reading, watching TV?
Associated with HA or other neuro Sx?
h/o eye or head trauma?
Any other medical problems, specifically autoimmune disorders?
Any weakness, difficulty in breathing, swallowing, hoarseness?

48
Q

Characteristic ocular findings of MG and tests to confirm

A

Si/Sx:
asymmetric ptosis and variable strabismus
gaze-evoked nystagmus

NO pupil/ciliary muscle involvement
variability/fatiguability - worsening of ptosis with extended upgaze and improvement with rest/cold

Rest test: improvement in ptosis s/p closing eye for 30 min or ice test (improvement in ptosis s/p application of ice pack for 2 min)

NEGATIVE forced ductions
Tensilon can be administered but a negative test does not R/O MG

Dx lab test: ACh receptor antibodies

If tests are negative: definitive Dx by single fiber EMG of peripheral or orbicularis muscle

49
Q

Work-up and Rx for MG

A

R/O thyroid dz, thymoma, other autoimmune disorders.

thyroid function tests, ANA, RF
Chest CT or MRI scan

Refer to neurologist/internist for systemic Rx

Manage strabismus with prism and potentially surgery when stable for at least 6 months

50
Q

swollen optic nerve DDx

A

Meaty - pseudotumor, diabetic papillitis
Mass or Mass shift - tumor, intracranial infection/hemorrhage (DURAL VENOUS SINUS THROMBOSIS)
Medications - tetracyclines, accutane, OCP, vitamin A, lithium
Malignant HTN

51
Q

Testing swollen optic nerve in office

A 
RAPD
color vision
visual field
EOM (consider forced ductions)
lid position and presence of proptosis and resitance of globes to retropulsion

Check BP to R/O HTN
check serum blood glucose level

52
Q

Work-up for swollen optic nerve (and IIH criteria)

A

MRI/MRV
LP with opening pressure

IIH criteria:

1) Normal neuro-imaging
2) Normal neuro exam except possible CN6 palsies
3) high CSF pressure (> 250 mm H2O) with normal composition
4) si/sx of increased ICP (i.e. HA, vomitting, papilledema)

53
Q

IIH associations

A 
Medications - tetracyclines, accutane, OCP, vitamin A, lithium
COPD
dural sinus thrombosis
radical neck surgery
recent weight gain
pregnancy
54
Q

IIH Rx

A

weigh loss, d/c medications that can cause swollen optic nerves
Vision loss, VF, intractable headache - Rx with diamox or LASIX

If progressive vision loss: ON sheath fenestration, LP shunt

55
Q

Orbital floor fracture w/entrapment - MC involves which bones?

A

maxillary bone and posterior medial floor (weakest point of the orbit)

56
Q

Other signs of blow-out fracture

A 
limited supraduction (limited elevation and depression)
subconj hemorrahge
AC cell and flare
globe ptosis
infraorbital nerve hypesthesia
lid emphysema
57
Q

Rx for blow-out fracture

A

ice compress
nasal decongestant
avoid blowing nose

PO antibiotics and steroids for 10 days
re-eval for surgery in 7-10 days to allow for reduction of swelling

58
Q

Indications for surgery - with entrapment or without entrapment

A

Any entrapment is an emergent reason for surgical intervention because of the chance for muscle necrosis, but without entrapment, we look at:

  1. Diplopia within 25 degrees of primary gaze
    This is the softest of the 3 indications- there often is diplopia that meets this criteria due to bruising of the extraocular muscles. But if it is improving, we often will watch it for a bit to see if it resolves.
  2. Enophthalmos > 2mm
    Enophthalmos tends to worsen over time both because swelling decreases and because there is a phenomenon known as late fat atrophy that occurs within the orbit. Enophthalmos >2mm is both cosmetically noticeable and likely to cause diplopia because the eyes are too disparate in position to allow fusion of images
  3. Greater than 50% of floor involved in fracture (assessed by eyeballing scan)
    If greater than 50% of floor is involved in fracture, then there is a very large chance that pt will develop significant enophthalmos
59
Q

Pediatric vs. adult floor fracture

A

pediatric floor fractures are different b/c bones are pliable and trapdoor situation may occur in which inferior rectus or surrounding tissue can become entrapped
>nausea and bradycardia occur owing to the oculocardiac reflex
>referred to “white-eyed blow-out fracture” b/c eye is usually quiet but requires emergent surgery to prevent premanent damage to entrapped tissue

60
Q

Globe displacement/dystopia DDx

A 
Adult orbital tumros:
cavernous hemangioma
meningioma
neurilemmoma (spingle cells in Antoni A pattern)
fibrous histocytoma
lymphoid lesion
lacrimal gland
sinus tumor
mtz

Use pt age, direction of globe displacement, presence/absence of pain to narrow DDx

Most lesions are intraconal masses that cause proptosis

Lacrimal/sinus tumors tend to displace globe DOWN

Down and out - consider sinus mucocele* - MC from frontoethmoid sinus

*CT: opacification of ethmoid sinus with erosion into orbit

61
Q

horizontal gaze palsy with inability to ADDuct one eye DDx

A

INO
MR palsy
Myasthenia gravis

62
Q

Where is the INO lesion?

A

MLF - medial longitudinal fasiculus

63
Q

Etiology of INO

A

50 yo - usually vascular

Other: trauma, infection, compression

64
Q

bilateral INO signs

A

inability to ADDuct either eye
impaired convergence
appearance of exotropia in primary gaze

65
Q

INO vs. one-and-a-half syndrome

A

one-and-a-half syndrome: lesion of PPRF (paramedian pontine reticular formation) or CN6 nucleus and ipsi/L MLF = ipsi/L gaze palsy AND INO (only eye movement = ABduction of contra/L eye with nystagmus)
Etiology: stroke, MS, basilar artery occlusion, pontine tumors.

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