David M Katz, MD Assistant Clinical Professor Ophthalmology, Georgetown U Associate Clinical Professor Ophthalmology and Neurology, Howard U

1. Transient visual loss
localization and visual field
interpretation
David M Katz, MD
Assistant Clinical Professor Ophthalmology, Georgetown U
Associate Clinical Professor Ophthalmology and Neurology, Howard U
September 8, 2019

2. Transient Visual Loss
• Questions for patients:
– Was vision loss monocular vs. binocular (ex. amaurosis
fugax=one eye vs. occipital lobe lesion= both)?
– Duration of vision loss (ex. seconds usually papilledema,
minutes usually transient ischemic attack (TIA) or migraine)?
– Age of patient (age<45 may be optic neuritis or migraine
aura, >50 may be occipital stroke, ischemic optic
neuropathy or retinal artery occlusion)?
– Pattern of vision loss and recovery (“window shade coming
down/up”= classic amaurosis fugax, bitemporal loss=
chiasm)?
– Other associated symptoms (ataxia, numbness or weakness
think TIA), new onset headache age>50 think giant cell
arteritis (GCA)?

3. Monocular Vision Loss
• Monocular loss is due to an issue with retinal or optic
nerve circulation: amaurosis fugax (carotid or cardiac
emboli or giant cell arteritis) vs. retinal vasospasm
(retinal migraine) vs. unilateral papilledema (very rare)
• If age<45, consider migraine vasospasm or Uhthoff’s
phenomenon (blur induced by increased body
temperature due to optic neuritis/MS)
• If >50, consider amaurosis fugax, especially if they
describe a transient window shade
• If age >60, also consider GCA, especially if new
headache, or jaw claudication, scalp tenderness,
polymyalgia rheumatica (proximal muscle pain and
weakness), fever, weight loss, malaise, anorexia. Check
STAT ESR/non-cardiac CRP/CBC and start prednisone
>60 mg/d or send to ER for IV steroids.

4. Monocular Vision Loss
• If lasts only seconds, especially if triggered by bending over
or Valsalva, consider papilledema, central retinal vein
occlusion or optic disc drusen
• If lasts minutes, consider amaurosis fugax, or if associated
with scintillating lights, migraine vasospasm
• If associated with excessive eye blinking, consider hemifacial
spasm (if bilateral, blepharospasm)
• If gaze evoked amaurosis, usually retrobulbar mass causing
ophthalmic artery compression worse in one direction
• If light induced amaurosis, consider ocular ischemic
syndrome due to severe bilateral internal carotid artery
stenosis/occlusion. With so little blood flow to retinas
prevents cone/rod function.
• If exercise or hot bath induced blur, consider optic
neuritis/MS (Uhthoff’s phenomenon)

5. Amaurosis fugax or retinal artery
occlusion fundus findings
• Yellow-orange refractile plaque: usually at major
vessel branch point. Caused by cholesterol
embolus, usually carotid disease
• Gray-white dull plaque: usually involving two
branch vessels. Caused by platelet-fibrin
embolus, usually cardiac valves or atrial
fibrillation
• Bright white-chalky plaque: usually seen at first
or second vessel bifurcation. Caused by calcium
embolus from calcified aortic or mitral valve,
rheumatic heart disease

8. Amaurosis Fugax Evaluation and
Treatment• Screen patient for HTN, carotid stenosis, atrial fibrillation (holter monitor),
echocardiogram, stat ESR/non-cardiac-CRP/CBC to rule out GCA
• The lack of a cervical bruit does NOT exclude carotid stenosis, in fact
severe carotid stenosis is often silent because too little blood is flowing to
cause a bruit
• If carotid stenosis >60-70%, consider endarterectomy. Carotid stents carry
a higher short term stroke risk
• If acute carotid dissection (look for ipsilateral Horner’s and facial pain),
send to ER for IV heparin, then coumadin for 3-6 months
• If atrial fibrillation, cardiac valvular disease or left ventricular dysfunction
start heparin emergently, then switch to coumadin
• If endocarditis start antibiotics and consider valve replacement surgery
• If patent foramen ovale with R-to-L blood shunt, start heparin emergently
and transfer to coumadin and consider endovascular closure if <65 years
• If cardiac myxoma resect if possible
• If GCA, start high dose steroids (>100 mg/d) vs. 1 g/d IV
methylprednisolone IMMEDIATELY and schedule a >2 cm unilateral
temporal artery biopsy within 7-10 days
• Also consider hypercoaguable states, sickle cell disease, vasculitis,
neurosyphilis, smoking, cocaine, dyslipidemia, diabetes, sleep apnea

9. Prognosis for Amaurosis Fugax
• The risk of stroke is lower following
amaurosis fugax (2%/yr) than cerebral
TIAs (8%/yr)
• Fewer than 50% of patients with carotid
stenosis present with amaurosis fugax and
>50% of patients with amaurosis fugax
have carotid stenosis

10. Binocular Vision Loss
• Bilateral simultaneous vision loss usually indicates a
cerebral disorder: vertebrobasilar TIA (embolic vs.
thrombotic vs. GCA), occipital lobe vascular
malformation or mass, occipital seizures (unformed
positive visual disturbance), migraine aura, bilateral
papilledema, cerebral hypoperfusion (orthostatic
hypotension), hypoglycemia, malignant hypertension,
or preeclampsia in pregnancy

11. Binocular Vision Loss
• If lasts seconds and is recurrent, bilateral
papilledema likely
• If lasts minutes, TIA or migraine aura
• If scintillating scotoma, migraine or seizure
(rare)
• If associated with vertigo, diplopia, ataxia,
paresthesias, consider TIA
• Transient vision loss is RARELY psychogenic,
always a diagnosis of exclusion

12. Hallucinations
• Cerebral cortical lesions: anterior optic radiation lesions in the
temporal lobes often cause formed hallucinations while posterior
lesions (occipital lobes) cause unformed hallucinations
• Palinopsia is a hallucination in the blind field of a previously seen
image in patients with nondominant occipital lobe lesions
• Polyopia is a hallucination in the blind field of multiple copies of an
object in the intact field
• Migraine auras are almost always binocular but may be homonymous
and include: heat waves, fortification scotoma, cracked glass,
kaleidoscopic images, fragmented vision
• Hypnogogic (going to sleep) and hypnopompic (upon awakening)
hallucinations are common in demented patients
• Anton syndrome: Denied blindness, patients hallucinate and
confabulate visual images. Usually due to bilateral occipital lobe
lesions (pre-eclampsia, strokes)
• Riddoch phenomenon: patients correctly perceive movement in a
complete hemianopic field defect
• Psychiatric: schizophrenia, conversion disorder, drug intoxication or
withdrawal

13. Hallucinations: Toxic-Metabolic
Causes
• Withdrawal (ex. delerium tremens from alcohol)
• Dopaminergics: carbidopa/levodopa (Sinemet),
dopamine agonists (Mirapex, Requip)
• Anticholinergics: Artane, Atropine, Benadryl
• Tricyclic antidepressants: amitriptyline, nortriptyline
• Beta blockers: propranalol, atenolol
• Adrenergics: Sudafed, theophylline, Albuterol
• Narcotics: opioid withdrawal
• Ca channel blockers: verapamil
• Antiarrhymics: lidocaine, digitalis
• Benzodiazepines: Valium, Xanax, Ativan, Klonopin
• Anticonvulsants: phenytoin (Dilantin), phenobarbitol
• Illegal drugs: amphetamine, cocaine, LSD, peyote,
psilocybin mushrooms, mescaline, ecstasy.

14. Abnormal Perception
• Simultanagnosia: inability to see an entire picture
• Prosopagnosia: inability to recognize familiar faces
(recent Wash Post writer wrote about herself, also Oliver
Sacks, MD the neurologist)
• Object agnosia: inability to recognize objects, can by
touch
• Alexia without agraphia: cannot read but can write. In
left brain dominant patients (90%), damage to the left
occipital lobe and splenium of corpus callosum. Visual
input arrives in the right occipital lobe but can’t connect
with the left parietal lobe (language center). They can
write the word “banana” but when you show them what
they wrote, they can’t read the word “banana”

15. Part II
Visual Field Interpretation
• Occipital tip anatomy

16. Reverse cloverleaf
(pt didn’t start
until after a few
stimuli had
passed)
Cloverleaf artifact

18. Inferior arcuate defects OU

24. Progressive superior arcuate
(ex. glaucoma)

25. Thank you
David M Katz, MD
3202 Tower Oaks Blvd, Suite 330
N Bethesda, MD 20852
301-540-2700

26. Ongoing Clinical Trials
REGENERA: placebo controlled trial using sq
gum mastic 2/wk to improve vision >1 year after
NAION (non-arteritic anterior ischemic optic
neuropathy) with 20/50-20/250 acuity
Quark trial: treating acute NAION with intravitreal injection, closed 6/19
SIGHT: surgical IIH/papilledema trial, closed 8/19
LEROS: Leber’s Hereditary Optic Neuropathy treatment using oral idebenone,
closed 7/19