Vaphiades 3-31-08 Ophthalmol Review

Front 1

Criteria most suggestive of GCA(odds for positive biopsy)

Back 1

Jaw claudication (odds 9X greater)
Neck pain (3.4X greater)
CRP > 2.45 mg/dL (3.2X greater)
ESR 47-107 mm/hr (2X greater)
Age 75 or older (2X greater)
CRP + ESR 97% specific for GCA

Front 2

Giant cell arteritis symptoms

Back 2

Headache (50-90%) boring pain, temporal artery tenderness, worse at night
Anemia, thrombocytosis
Anorexia, weight loss, myalgias, fever, scalp tenderness, tongue pain
Fluorescein: posterior ciliary a. occlusion with filling defect choroid

Front 3

Tx of GCA

Back 3

High dose IV (1.2-2.0 mg/kg/day) or oral steroids (never alternate day)

Front 4

What if GCA is not treated?

Back 4

2nd eye involvement 25-50% in weeks to months if no therapy

Front 5

Is there RAPD in the affected eye during GCA?

Back 5

yes

Front 6

Do cataracts cause RAPD?

Back 6

no

Front 7

3 causes of RAPD

Back 7

Optic nerve lesion
Large macular lesion
Retinal detachment

Front 8

Without swinging flashlight, is there anisocoria with RAPD?

Back 8

no

Front 9

What's the problem?

Acute unilateral visual loss
Ipsilateral RAPD
Periocular pain (92%)
Normal (65%) or swollen (35%) optic nerve
Visual improvement over time in most

Back 9

Optic Neuritis

Front 10

What is the Modified ONTT protocol

(optic neuritis treatment trial)

Back 10

1 gm IV methylprednisolone QDx3D
Prednisone taper

Front 11

If you think a pt has optic neuritis, what details about the pt's condition are "protective against MS"?

Back 11

Negative MRI
Painless visual loss
Severe disc edema
Disc or peripapillary heme
Macular exudates

Front 12

If optic neuritis will correct itself without treatment, why give the steroid treatment?

Back 12

reduced the rate of developing CDMS during the first 2 years

Front 13

What's the problem?

From intraorbital optic nerve sheath
Slowly unilateral progressive visual loss
Usually middle aged women
On MRI enlarged optic nerve which enhances diffusely
MRI can detail intracanalicular optic nerve

Back 13

Optic nerve sheath meningioma

Front 14

What's the problem?

16-23% of intracranial tumors from arachnoid cell clusters
2:1 female:male
Papilledema from increased ICP
Isointense on T1
Marked enhancement with gad

Back 14

Meningiomas

Front 15

The following defines what condition?

Signs and symptoms of elevated ICP
Elevated OP with normal CSF formula
Normal neuro-ophth exam (except 6th)
Papilledema
No mass, sinus thrombosis or ventriculomegaly

Back 15

Pseudotumor Cerebri Definition

Front 16

Pseudotumor Cerebri Associations

(pt characteristics)

Back 16

Obesity
Young age
Female
Endocrinologic
Exogenous agents

Front 17

Tests, Work-up necessary from Pseudotumor cerebri diagnosis

Back 17

Gadolinium enhanced MRI and MRV
Lumbar puncture

Front 18

Therapy for pseudotumor cerebri

Back 18

Weight loss, low salt diet
Acetazolamide, furosemide
Lumboperitoneal shunting
Optic nerve sheath decompression

Front 19

Transient Monocular Blindness (TMB) AKA

Back 19

Amaurosis Fugax

Front 20

TMB is caused by Abrupt onset due to transient ischemia of which artery

Back 20

ophthalmic or central retinal artery

Front 21

What are pt complaints during TMB?

Back 21

Field deficit may be shade (usually from above)
Develops over seconds
Usually the entire field, may be partial
Phosphenes are rare (*test question*)

Front 22

What do phosphenes usually signify?

Back 22

Zig zag lines and lights = migraines or tear or break in the retina.

Front 23

What are the causes of TMB

Back 23

Thromboembolism from ICA
Cardiac embolism
Aortic embolism
Giant cell arteritis
ICA dissection

Front 24

Rare causes of TMB

Back 24

Hypoperfusion of the retinal vasculature if = or > 90% ICA stenosis
Vasospastic monocular visual loss

Front 25

Work-up and Tx for TMB

Back 25

Neuroimaging of the brain, intracranial vessels and carotid arteries
Serum blood studies, echocardiogram and electrocardiogram
Antiplatelet therapy

Front 26

What type of tumor causes the following?

9.5% of intracranial tumors
Slow growing, insidious visual loss
Bitemporal hemianopia
Oculomotor nerve involvement (1-14%)

Back 26

pituitary tumor

Front 27

Most common nonglaucomatous optic neuropathy of the middle-aged and elderly

Back 27

Anterior ischemic optic neuropathty (AION)

Front 28

Most cases (94.7%) of AION are
arteritic or nonarteritic ?

Back 28

nonarteritic

Front 29

What are pt complaints with AION?

Back 29

Abrupt-onset visual loss, frequently upon waking

Typically painless

Visual acuity range from 20/20 to no light perception

Visual fields usually show an inferior altitudinal defect

Front 30

What does the fundus look like with AION?

Back 30

By definition, the optic nerve is swollen acutely in NAION

Peripapillary retinal hemorrhages are common (72%) off the disc

Retinal and macular exudates that form a partial star mimicking neuroretinitis are less common

Front 31

Causes of NAION

Back 31

Hypertension, diabetes mellitus, elevated cholesterol and triglyceride levels, cigarette use, and hyperhomocysteinemia

Nocturnal hypotension and disc autoregulatory abnormalities

Front 32

Meds assoc with NAION

Back 32

Taking blood-pressure lowering medications in the evening or at bedtime may exacerbate nocturnal hypotension

Interferon alpha and amiodarone implicated

erectile dysfunction drugs such as Sildenafil (Viagra) and tadalafil (Cialis) with preexisting risk factors for NAION like arterial hypertension, diabetes mellitus, and hyperlipidemia

Front 33

Another fundoscopic finding in NAION

Back 33

Optic disc drusen are also associated with NAION

Front 34

Tx for NAION

Back 34

No proven treatment, avoid risk factors

Front 35

Inability to recognize a visual target despite preservation of mental and visual function

Back 35

Visual agnosia

Front 36

Inability to recognize familiar faces
Recognize faces by utilizing visual and auditory characteristics (stature, gait, voice, facial hair, clothing and glasses)

Back 36

Prosopagnosia

Front 37

Visual fields of Prosopagnosia

Back 37

Homonymous hemianopia

Front 38

What part of the brain is messed up to cause prosopagnosia

Back 38

Bilateral or right occipital lobe
Stroke, glioma, trauma

Front 39

Can recognize letters but not words
Cannot read the words they have written

Back 39

Alexia without Agraphia (Pure Alexia)

Front 40

Part of the brain affected to cause pure alexia

Back 40

damage to left occipital lobe and splenium of the corpus callosum
Disconnection left hemis language areas
Usually from infarction
Glioma, hematoma (ruptured aneurysm)

Front 41

What's the problem?

Temporal field is larger than corresponding nasal field (unpaired nasal fibers)
Represented at the rostral end of the striate cortex (<10%)
60-110 degrees in the horizontal meridian
May not detect on automated perimetry

Back 41

Temporal Crescent

Front 42

Visual hallucinations in sane patients with visual loss from any lesion of the central nervous system interrupting the flow of visual information to the visual cortex
Non-epileptic visual deprivation

Back 42

Charles Bonnet Syndrome

Front 43

unstructured flashes of light

Back 43

Phosphenes

Front 44

structured geometric figures

Back 44

Photopsias

Front 45

recurrent appearance of of an image after it has disappeared

Back 45

Palinopsia

Front 46

Complex hallucinations ?

Back 46

people, animals etc.

Front 47

What's hemianopic anosognosia?

Back 47

patients with homonymous visual field defects who are unaware of their visual loss in the blind hemifield

Front 48

Vaphiades research (probably good to know about)
Vaphiades et al. (1996) prospectively studied 32 patients with ischemic infarction of the retrochiasmal visual pathways
Negative EEG’s, no auditory component
13 (41%) had PSVP averaging 3 days
Some complex hallucinations lasted 3.5 months
None of the PSVP were localized to any part of the retrochiasmal visual system, except for agitated delirium with hemianopia
Agitation, confusion, and aggressiveness with visual or auditory hallucinations
Mesial occipital, parahippocampal gyrus and hippocampus
In this same group of 32 patients with homonymous visual field defects, 20 (62%) were unaware of their visual loss in the blind hemifield (hemianopic anosognosia)

Back 48

Positive Spontaneous Visual Phenomena

Front 49

Patients with a homonymous hemianopia will often ascribe the visual defect to the eye with the defective _________ visual field (larger than the defective _____ field in the fellow eye)

Back 49

Patients with a homonymous hemianopia will often ascribe the visual defect to the eye with the defective temporal visual field (larger than the defective nasal field in the fellow eye)

Front 50

PSVP may result from ______________ visual deprivation associated with a homonymous hemifield defect or from epileptic irritative discharges

Back 50

PSVP may result from non-epileptic visual deprivation associated with a homonymous hemifield defect or from epileptic irritative discharges

Front 51

Name some Epileptic Irritative Discharges

Back 51

Rapid eye blinking or eyelid flutter
Eye deviation either ipsi or contra to sz focus
Phosphenes or ictal amaurosis (fading of vision OU)

Front 52

Type of migraine:

Usually presents with monocular visual dimming
During an attack, retinal arteries in vasospasm
This is a diagnosis of exclusion

Back 52

Retinal Migraine

Front 53

Migraine work-up

Back 53

Cranial neuroimaging (controversial)
Slow wean off the caffeine often decreases the frequency of events
Migraine therapy

Front 54

What syndrome?

Visual anosognosia (maybe only indifference)
Excuses offered for difficulties (confabulation)
Bi-occipital lobe lesions

Back 54

Anton’s Syndrome