Evaluation of diplopia: What is life threatening?
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Transcript of Evaluation of diplopia: What is life threatening?
Neuro-ophthalmic Disease SymposiumDiagnosis and Management Pearls
Mountain West Council of Op-tometrists
Las Vegas, NevadaApril 24, 2010
• Andrew G. Lee, M.D.
• Danica J. Marrelli, O.D.
• Robert P. Wooldridge, O.D.
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Evaluation of diplopia: What is life threatening?Andrew G. Lee, MDChairman of Ophthalmology, The Methodist Hospital, HoustonProfessor of Ophthalmology, Weill Cornell Medical CollegeAdjunct Professor of Ophthalmology, University of IowaClinical Professor of Ophthalmology, UTMB Galveston
• I have no financial interest in the contents of this talk
• I will not be discussing any off label uses of drugs
• Lee’s P’s
• Pain (severe, worst of life) in elderly
• Perception loss
• Pupil involvement
• Progressive proptosis
• Paresthesias or paralysis
• Overview: Lee’s “A”s: The five chances to save a life
• Arteritis (Giant cell)
• Apoplexy (Pituitary)
• Abscess (Mucor)
• Aneurysm (pupil involved third nerve palsy)
• Arterial (carotid or vertebral) dissection
• *At the end I want to give you an additional important take home message
• The 7 “Must Call” triage list (Give to your techs tomorrow)
• Acute painful ophthalmoplegia
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• Acute painful bitemporal hemianopsia
• Acute painful anisocoria (big or small)
• Acute painful visual loss in elderly
• Acute painful (HA) bilateral optic disc edema (papilledema)
• Acute “no light perception” vision
• Acute painful severe HA (“worst pain of my life)
• Beautiful Sunday….but what if it had been Monday 8 AM instead
• Giant cell arteritis: What everyone knows….
• Elderly patient (often female)
• Acute onset headache, jaw claudication, temporal artery pain, neck or ear pain
• Loss of vision (typically due to ischemic optic neuropathy)
• Elevated erythrocyte sedimentation rate (ESR) & C-reactive protein
• But….You should also know that it can be GCA if
• Transient double vision
• Any ophthalmoplegia in elderly
• Ask about GCA symptoms in diplopia in elderly patient
• Patients do not come in with the diagnosis written on their forehead (but sometimes they do)
• The artery on the side of my head hurts
• Delay in GCA diagnosis common
• Br J Rheumatol. 1997 Feb;36(2):251-4. Clinical features in patients with perma-nent visual loss due to biopsy-proven giant cell arteritis. Font et al.
• 146 biopsy + GCA
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• 23 (16%) lost vision
• GCA Sx for average of 1.3 months
• 35% PMR x 10.8 months
• 65% premonitory visual Sx for 8.5 days
• Clear delay in diagnosis in 65% (15)
• Giant cell arteritis can kill people….
• Aortitis
• Systemic vasculitis
• Crow et al. J Gerontol A Biol Sci Med Sci 2009.
• Mortality in GCA: 5-year survival: 67% for controls vs 35% for GCA cases (p < .001)
• Holiday Headache
• 22 y/o woman
• Severe headache
• New diplopia (partial third)
• 20/50? Effort (blurred vision)
• Fundus normal OU
• HVF: “unreliable”
• Thursday 4:45 PM
• Perform a confrontation field
• Beware acute bitemporal field loss
• “Unreliable HVF” = “I have no visual field on this patient!”
• Life threatening diagnosis?
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• Pituitary tumors common
• Incidence of pituitary tumors = 7 per 100K population per year
• As high as 1 in 500 > 65 years
• “The average ophthalmologist should see about one pituitary tumor per year….are you missing your quota?” ----B. Katz MD
• Pituitary apoplexy
• Acute onset
• Usually severe headache
• Bitemporal hemianopsia
• Apoplexy can kill (8%)
• Hypopituitarism (cortisol)
• Emergent scan
• Pituitary apoplexy
• Semple et al. Neurosurgery. 56(1):65-73, 2005.
• 62 patients (Average age 51.1 years)
• Average time presentation: 14 days after ictus
• 81% no previous history of pituitary tumor
• Headache (87%) with diminished visual acuity in 56% (bitemporal hemianopia 34%)
• 73% hypopituitarism; 8% diabetes insipidus
• Acute ophthalmoplegia in a diabetic
• 35 y/o WM with diabetes
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• History of diabetic ketoacidosis
• Complete left ptosis
• Acute onset almost complete left sided ophthalmoplegia
• What should be the evaluation?
• Life threatening diagnosis?
• Cavernous sinus lives close to other structures
• How could a fungal orbital apex lesion be missed on MRI?
• Need contrast to see enhancement
• Fungi are dark on MRI
• No fat suppression can miss lesion
• Super-dangerous because tempting to give steroids to…
• Presumed retrobulbar optic neuritis
• Presumed Tolosa Hunt syndrome
• Aspergillosis of orbital apex
• Complementary roles for CT & MR in fungal orbital apex disease (T2 dark)
• What’s wrong with this picture?
• 60 y/o diabetic man
• New onset ptosis right
• Right adduction, elevation, & depression deficit
• 45 exotropia (XT)
• Diagnosis: “Ischemic third nerve palsy”
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• Plan: “Return 6 weeks”
• Tell your technicians….
• If the patient’s complaint is diplopia or ptosis or….
• If you have to lift a ptotic lid to put in the dilating drops then….
• STOP, come get the doctor before dilating
• Acute pupil involved third n. palsyLife threatening diagnosis?
• Rule of the pupil
• A pupil involved third nerve palsy
• Aneurysm of posterior communicating artery until proven otherwise
• Endovascular treatment
• Highest stakes encounter an eye doctor will see
• Choice of imaging strategy in third nerve palsy
• CT/CTA first to look for SAH/aneurysm in pupil involved third nerve palsy
• MRI/MRA first to look for non-aneurysmal etiologies or do MRI second if CTA nega-tive first
• Catheter angiography if MRI/MRA and CTA not of sufficient quality or insufficient confidence level to rule out aneurysm
• Vertebral dissection & top of the basilar syndrome
• Acute onset homonymous hemianopsia
• Acute onset bilateral progressive ophthalmoplegia
• Paresthesias or paralysis (top of basilar)
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• Initial structural MRI may be normal but DWI might show evolving acute infarct
• May be spontaneous dissection: no trauma
• Dissection can propagate or embolize
• Vertebral artery dissection
• Top of the basilar syndrome
• Bottom line: Its your job
• Lee’s P’s
• Pain (severe, worst of life) in elderly
• Perception loss
• Pupil involvement
• Progressive proptosis
• Paresthesias or paralysis
• Danica J. Marelli, O.D.
• Case 1: 46yo WF
• CC: headache, droopy RUL x 2 days
• POH: unremarkable
• PMH: unremarkable, last physical exam 6 months ago (rou-tine)
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• Meds: Multivitamin
• All: None
• Exam Findings:
• BVA: 20/20 OD, OS
• CVF: FTFC OD, OS
• External Exam & Pupils: See photo
• Questions:
• What is your working diagnosis?
• What diagnostic tests do you need to perform?
• Discussion:
• Sympathetic innervation to the eye: a review
• Horners Syndrome: clinical picture
• Horners Syndrome: pharmacologic testingo Confirmatory testingo Differentiating pre- from post- ganglionic Hornerso Apraclonidine: benefits & pitfalls
• Post-ganglionic Horners: What’s next?
Andrew G. Lee, M.D.Unexplained visual loss in children & adults:
7 easy steps to finding the cause9
• Insure visual loss = actual chief complaint
• Complete eye exam every time (no shortcuts)
• Special effort to detect subtle causes of visual loss
• Formal visual field if unexplained symptoms
• Special tests (e.g., MERG, OCT, fluorescein angiography, neuroimaging if indicated)
• Rule out optic neuropathy or hemianopsia
• Rule out ORGANIC and prove non-organic BEFORE labeling someone as such
• Step 1: Chief complaint = “blurred vision” is not sufficient!
• What do you mean by blurred?
• One eye or both?
• Central or side vision or both?
• Double vision?
• Jumping eyes? (nystagmus)
• Processing of visual information?
• “Blurred vision” may not mean loss of vision (afferent disease)
• Double vision
• Is it double vision?
• Is it monocular or binocular (cover one eye)
• Nystagmus (oscillopsia)
• Is it jumping or moving?
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• Visual processing
• Agnosias (e.g., prosopagnosia, simultagnosia)
• Visual variant of Alzheimer’s disease
• Step 2: Complete eye exam
• By complete I mean….complete (don’t use short cuts in your neuro-op patients!)
• Check relative afferent pupillary defect yourself
• Check color vision & visual field
• Ophthalmoscopy
• High magnification & high clinical suspicion
• Don’t take the shortcut
• M ain Causes For No APD In Unilateral Visual Loss
• M acular disease (e.g. macular hole)
• M edia (cataract, refractive)
• M aking it up (non-organic)
• M issed it (look again!)
• *Bilateral optic neuropathy & retrogeniculate etiologies = normal pupil
• Complete eye exam
• Slit lamp biomicroscopy
• Look after dilation
• Beware oil droplet cataract
• Look for posterior subcapsular cataract
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• Match lens opacity to visual acuity
• Retroillumination
• Look at lens & grade opacities (“NSC/PSC = 20/30” or ≠ “20/30”)
• Step 3: Rule out things you don’t want to end up sending to your neuro-ophthalmologist
• Oil droplet cataract or subtle posterior subcapsular cataract
• Refractive error, keratoconus
• Epiretinal membrane, cystoid macular edema, macular hole, geographic atrophy of retinal pigment epithelium
• Most common etiologies Unexplained anterior segment visual loss in adults
• Mild PSC
• Keratoconus
• Irregular astigmatism
• Use retinoscope & direct (view “in = out”)
• Use the pinhole (also best corrected vision)
• Consider keratometry or topography
• Most common etiologies for unexplained visual loss in a kid
• Uncorrected refractive error
• Unrecognized amblyopia
• Nonorganic overlay
• Poor cooperation
• Incomplete examination
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• Special toys
• Step 4: Formal visual field
• “Unreliable” visual field is the same information as NO visual field per-formed
• Confrontation visual field = minimum
• Media & refractive etiologies rarely produce field defects
• Any respect of vertical meridian significant
• Common errors in evaluation children
• Failure to perform a visual field
• Settling for an “unreliable” automated perimetry as your only visual field
• Failure to complete the exam because of “poor cooperation”
• Assuming that sullen is evidence for non-organic etiology (sullen is nor-mal teen behavior)
• Full Eight Point Exam
• Formal visual field (even if 20/20)
• Homonymous & bitemporal hemianopsia may have 20/20 acuity
• Retrochiasmal disease will have NORMAL structural eye exam (no RAPD, no optic atrophy)
• Normal eye exam does not r/o pathology
• Look At The Macula
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• Subtle macular lesions can be missed without high magnification and high suspicion (e.g. macular hole, cystoid macular edema)
• “WNL” should mean “within normal limits” NOT “WE NEVER LOOKED’
• Most Commonly Missed Posterior Segment Etiologies For Visual Loss
• Epiretinal membrane
• Cystoid macular edema
• Samll macular hole
• Subtle serous retinal detachment
• Retrobulbar optic neuropathy
• Diagnosis and Plan From The Retina Service
• IMPRESSION ‘NOT RETINA’
• PLAN
• “REFER TO NEURO-OPHTHALMOLOGY
• OCT in unexplained visual loss
• Measurement of retinal nerve fiber layer (RNFL)
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• Measurement of retinal thickness
• Detection of subtle macular pathology
• Old relationship with medical retina in organic appearing unexplained visual loss
• Look really hard at macula
• Hallucinate macular pathology
• Do macular photostress test
• Scratch head
• Do a fluorescein angiogram
• Call in medical retina specialist
• Scratch heads together
• OCT in Unexplained visual lossIs it retina or optic nerve?
• Macular edema or macular hole
• Epiretinal membrane
• Cystoid macular edema or subretinal fluid
• Vitreous traction on macula or optic nerve
• OCT can see better than me
• Visual field defect
• OCT: Macula fast scan
• New paradigm
• Macular OCT
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• If OCT sees no pathology then I don’t bother with medical retina consult
• If OCT is normal but seems retinal then still consider fluorescein an-giogram (OCT can not see perfusion)
• OCT has reduced # of fluorescein angiograms that we perform for unex-plained visual loss by 75% or more
• OCT vs. FFA
• Boston VA acquired OCT system in September 2004
• Retrospective review (n =1102)
• Macular edema or age-related macular degeneration (AMD)
• OCT vs. FFA
• Before OCT, 411 FAs (n=314): $297,498
• After OCT: $325,695 (336 FAs at $243,210, 356 OCTs at $82,485)
• 3 adverse events occurred with FAs (0.73), at a cost of $688 per 100 pa-tients
• Purchase price recovered after 4 months
• Bottom line
• OCT shows macula at micron level
• OCT sees better than me even with a contact lens or high magnification with high suspicion
• OCT has replaced fluorescein as my first ancillary test of choice for structural macular pathology
• Fluorescein still useful for perfusion (OCT can not see macular ischemia or show leakage)
• Step 5: Special techniques: OCT
• OCT helpful in unexplained visual loss16
• “Poor man’s neuro-ophthalmology consult”
• “? Mild temporal pallor” if normal visual field, normal OCT, normal acuity then likely physiologic pallor
• “Poor man’s” medical retina consult
• “Poor man’s” glaucoma consult
• Is this nerve pale? Mild pallor? Temporal pallor? Optic atrophy?
• OCT can see better than me
• Am I pale?
• Consider Ancillary Testing
• Fluorescein angiography/OCT
• If I see something funny in the macula
• Electrophysiology if it “smells like retina”
• Big blind spot with normal peripapillary retina
• Ring scotomas
• Photopsias
• Diffuse retinal arteriolar narrowing
• Unexplained visual loss
• 60 y/o WF with painless progressive loss of vision bilaterally for 3 weeks
• “Swirling and flashing lights”, night blind
• Exam 20/40 OD and 20/50 OS
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• Mild vitritis OU
• Retinal vascular attenuation
• Optic atrophy OU
• Cancer associated retinopathy
• Small cell carcinoma of the lung (90%)
• Breast CA, GYN CA, non small cell lung CA, lymphoma
• Retinal antibodies (e.g., 23 kD recoverin)
• Multifocal Electroretinogram(MERG )
• Focal electrical response of photorecepters and bipolar cells
• Does not detect ganglion cell or axonal response (at present)
• Step 6: Rule out optic neuropathy
• Look for subtle signs of optic neuropathy
• Decreased color vision
• Relative afferent pupillary defect
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• OCT abnormal
• Mild disc pallor or disc edema
• Abnormal visual field
• If you miss a non-optic nerve cause for visual loss (PSC, ERM, refrac-tive) it is no big deal
• If you miss an optic neuropathy it could be a big deal (compressive optic neuropathy)
• Step 7: Prove non-organic before labeling patient non-organic
• Non-organic = preferred term
• Outdated terms or terms which imply psychologic motivation (hysterical, malingerer)
• Do you really know they are faking?
• Do you know their motivation?
• They might be organic with overlay!
• Cases
• 75 y/o WF from the “Psych” ward x 2 wks
• Acute onset visual loss OU
• HM acuity OU
• Pupils reactive and no RAPD
• Ophthalmology found a normal eye exam
• Fundus WNL OU
• Visual field “unreliable”
• Sometimes she says she can see: “You are wearing a white coat, doc-tor.”
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• She denied she was blind: “I can see, of course I can see”
• Visual Loss OU
• MRI: Bilateral occipital infarcts
• Pupil & fundus normal in cortical loss
• Bilateral and symmetric visual loss
• “Unreliable” visual field is not same thing as a NORMAL visual field
• Anton syndrome: Cortically blind patients may confabulate or deny they are blind!
• WE ONLY SEE WHAT WE LOOK FOR. WE LOOK FOR ONLY WHAT WE KNOW
• GOETHE
• A warning….
• You find a cataract (good)
• You take out cataract (great)
• Perfect case & you tell patient so (awesome)…They think you are a great doctor
• Vision does not improve post op (bad)
• Now you notice optic atrophy (worse)…& RAPD, & VF defect….(Hmmm was that there before?)
• Now you have to explain to patient why they need an MRI & neuro-op consult (very bad)…We find a tumor..they think you are really bad doc-tor
• Versus exact same scenario but….
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• Pre-Op: “I think that you have a cataract but if it doesn’t improve your vi-sion there are other things we have to consider including a specialist consult but it is reasonable to start here.” (10 seconds extra time)
• Post-op: “Your vision didn’t improve as much as I would like after surgery remember when we talked about possibly needing to look harder. I am referring you to Dr. X and ordering an MRI”
• A tumor is found…Patient: “Thanks a lot doc, you saved me, you are a great doctor
• Most Common Errors In Unexplained Visual Loss
• Failure to check for RAPD
• Failure to perform a formal visual field
• Failure to perform a confrontation field in an unreliable formal field pa-tient
• Failure to get best corrected vision (contact lens, over-refraction, retinoscopy)
• Jumping to conclusions = non-organic
• Seven steps in unexplained visual loss
• Insure visual loss = actual chief complaint
• Complete eye exam every time (no shortcuts)
• Special effort to detect subtle causes of visual loss
• Formal visual field if unexplained symptoms
• Special tests (e.g., MERG, OCT, fluorescein angiography, neuroimaging if indicated)
• Rule out optic neuropathy or hemianopsia
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• Rule out ORGANIC and prove non-organic BEFORE labeling someone as such
Hysteria and MalingeringRobert P. Wooldridge, O.D.
• Hysteria
• Mental disorder that impairs physical functions with no physiological ba-sis; sensory motor symptoms include seizures, paralysis, temporary blindness; increase in stress or avoidance of unpleasant responsibilities may precipitate
• Subconscious response
• Patient believes he/she has a real problem
• But may have something to gain
• Malingering
• Conscious attempt to deceive for personal gain
• Functional Overlay
• Patient has a true organic disease/problem
• But also has a functional component
• The Usual Suspects
• Hysteria:
• Young: 9-13yo most common
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• Adults possible
• Female>>>>>>Male
• Malingering
• Late teens to adults
• Common Complaints
• Loss of Vision
• Monocular or binocular
• Central or peripheral
• Usually sudden in onset
• Can be dated/connected to an event
• Sometimes vague, uncertain
• Hints of Hysteria
• Reads every line at same slooooow speed, letter by letter
• Ambulates well despite C/O severe LOV
• Severely constricted CVF
• NO APD despite severe unilateral LOV
• Diagnostic Steps
• Careful history
• Refraction
• Full examination
• Stereo
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• CT
• PUPILS!
• Visual Field-Never make a diagnosis without it!
• DFE
• Loss of vision
• 1. Refractive error
• 2. Media opacity
• 3. Macula
• 4. Optic nerve
• 5. Amblyopia-there has to be a cause!
• 6. Hysteria/malingering
• Amblyopia v. Hysteria
• History of poor VA?
• Prior eye exams? (get records)
• Have you ever been 20/20?
• Must have a reason to have amblyopia
• Strabismus
• Refractive
• Obscuration
• NLP Loss of Vision Tricks
• Optokinetic drum
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• Measuring tape, ruler
• Mirror: eye tracking
• 20/50 to 20/400
• Refraction with slow, patient VA
• Telescopic lens suggestion
• Polaroid slide with OU open
• Telescopic lens
• Cyclopleged
• Close OU
• Spin every dial while saying:
• I am putting in a very strong telescopic lens
• *If there is anything wrong, this lens will make you see well*
• Isolated lines; Start at 20/10
• Move up chart slowly
• Lots of positive encouragement be patient for each letter
• Confrontation VF
• Perform at normal two feet
• Again across room
• If cylindrical (tubular), not physiologic
• Mimic finger motions in areas of “blindness”
• Goldmann VF/ Tangent Screen
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• Spiraling isopters
• Inversion of isopters
• Management
• Discuss with parent alone
• Some attempt to determine reason for childs response
• Assure child of healthy eyes
• Give child a way to get better
• Drops
• Glasses
• Voodoo magic
• Parent to reinforce positive feedback
• Billing Coding
• 300.11 Conversion disorder
• Hysterical blindness, deafness, paralysis
• Def.: Mental disorder that impairs physical functions with no physiologi-cal basis; sensory motor symptoms include seizures, paralysis, tempo-rary blindness; increase in stress or avoidance of unpleasant responsi-bilities may precipitate
• Marrelli:
• Case 2: 21 yo WM
• CC: Horizontal diplopia x 3 days
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• HPI: no pain, no headache, no pupil problems
• POH: unremarkable
• PMH: unremarkable
• FH: unknown
• Meds: None
• Exam Findings: See EOMS
• Questions:
• What is the problem with motility?
• Where is the lesion?
• What is the most likely etiology given the patient’s age & health status
• Discussion:
• What is the Clinically Isolated Syndrome?
• What should we do about patients with CIS?
• What is the current thought on treatment of CIS?
Robert P. Wooldridge,O.D.Transient Monocular Loss of Vision
• Carol W
• 68 yo WF
• H/O blow out Fx OS 1992
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• Repaired; asymptomatic
• S/P Phaco/IOL OU 2007
• MH: HTN, dyslipidemia, S/P PFO closure, pacemaker, acid reflux, osteopenia
• Allergies: sulfa,cipro, hydrocodone, Percocet, Lortab, Tramadol, Flagyl, Morphine
• 12/13/07
• Routine postop visit
• Notes two episodes of dinner plate-sized blurry area with jagged edges OS
• Pain OS a few times a week
• VA 20/20 OU
• Ant seg, DFE normal
• Dx: Migraine with aura
• 2/08/08
• Routine po visit
• C/o irritation/mild pain OS
• VA 20/20 OU
• Pupils/motility NL
• SLE, DFE normal
• VF as seen
• 2/28/08 RPW exam
• C/o pain OS-dull ache since phaco 4 mos. ago
• Never had pain prior to surgery
• Nothing makes pain better or worse
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• No pain on movement
• 4 episodes of transient LOV x 20 mins.- believes OS only
• central scotoma increases in size with jagged edges
• No subsequent HA, nausea, or other symptoms
• No H/O migraines in past
• Exam
• VA 20/15 OU
• SLE: Ant. Seg normal
• IOP 13 OU
• DFE: Normal OU
• VF: Repeat necessary?
• What is Your Impression?
• 1. Ophthalmic migraine
• 2. Pain related to old orbital Fx
• 3. Retrobulbar optic neuritis
• 4. Temporal arteritis
• What is Your Plan?
• 1. Refer to PCP or neurologist for migraine Rx
• 2. CT scan orbits
• 3. CBC/ESR/CRP
• 4. MRI brain
• Impression/Plan
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• 1. Pain OS- no apparent cause
• 2. Transient LOV OS
• Plan:
• 1. PF qid, Xibrom bid OS
• 2. CBC, ESR, CRP, CMP
• 3. Doppler U/s carotids
• 4. Cardiovascular exam by cardiologist
• With echo with bubble
• 5. Already on ASA
• 6. Cover each eye during episode to confirm laterality
• Follow-up
• 1. CBC, ESR, CRP, CMP normal
• 2. Echocardiogram reveals ASD-atrial septal defect
• 3. Doppler U/S carotids: + plauque
• 4. Reports plaque “behind eye”
• Cardiologist rx’es Plavix, ACE inhibitor, statin, Coreg
• No additional episodes
• Transient Monocular Blindness
• Acute, transient LOV in one eye
• Ascending or descending curtain or total LOV
• Lasts seconds to minutes
• Complete recovery
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• Possible Causes
• Transient retinal ischemia
• Embolus, arteritis
• Impaired retinal perfusion
• Carotid artery stenosis
• Onset over 5 minutes
• Lasts minutes to hours
• Slow to recover
• Temporary vasospasm
• Constriction of retinal vessels
• Diagnosis of exclusion!
• Plan
• 1. Rx: one ASA qd
• 2. CBC, ESR, CRP, stat
• CMP, lipid profile, fasting glucose
• PT (prothrombin time), PTT (partial thromboplastin time),
• Protein C, Protein S
• 3. Doppler US of carotids
• 4. Echocardiogram
• R/O source of emboli
• R/O PFO (patent foramen ovale)
• 5.+/- MRI/MRA
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• Steps in Determination
• Onset
• Sudden
• Laterality
• Monocular v. Binocular
• Unilateral v Bilateral
• Difficult to determine
• Did patient cover one eye to check?
• Hemianoptic VF loss
• Characteristics Indicating True Transient LOV
• Inability to read
• Vision loss restricted to hemisphere
• Presence of slowly expanding scotoma or scintillation
• Accompanying neurologic symptoms suggesting hemispheric brain dysfunction
• Etiology
• Ischemic
• Usually embolus from carotid artery
• Aortic arch or heart secondary possible sources
• Ocular vasospasm
• Systemic hypotension
• Arteritis pailledema (rare)
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• Hyperviscous/hypercoagulable state (rare)
•• Binocular Transient LOV Causes
• Migraine (most common)
• Ischemia
• Seizure
• Migraine
• Scintillations (80%)
• Fortifications (20%0
• March(20%)
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