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The NeuroThe Neuro--anatomy ofanatomy of

VisionVision

T. R. Mizen M.D.T. R. Mizen M.D.

Associate Professor of Ophthalmology,Associate Professor of Ophthalmology,Neurology, and NeurosurgeryNeurology, and Neurosurgery

NeuroNeuro--ophthalmologyophthalmology

Rush University Medical Center: ChicagoRush University Medical Center: Chicago

Anatomy of the visual pathwayAnatomy of the visual pathway

EyeEye --> Optic> Optic

nervenerve -->>ChiasmChiasm -->>Optic TractOptic Tract -->>LateralLateralGeniculateGeniculate -->>Optic radiationOptic radiation--> Occipital> OccipitalLobeLobe

The Eye: optical component:The Eye: optical component:MediaMedia

The corneaThe cornea

Scarring, irregularityScarring, irregularity

The anterior chamberThe anterior chamber

T e ensT e ens

CataractCataract

The vitreousThe vitreous

hemorrhagehemorrhage

The Eye: RetinaThe Eye: Retina

The film ofThe film ofthe camerathe camera

MacularMaculardegenerationdegeneration

heheretinocorticalretinocorticalpathwaypathway

The visual pathwayThe visual pathway The anterior visual pathwayThe anterior visual pathway


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The Optic Nerve: etiology ofThe Optic Nerve: etiology ofdysfunctiondysfunction

Alterations in blood supplyAlterations in blood supply

InflammationInflammation InfarctionInfarction

CompressionCompression

Optic nerve vasculatureOptic nerve vasculature

Visual field defects: retina and opticVisual field defects: retina and opticnervenerve

NeuroNeuro--anatomy of the NFLanatomy of the NFL

Irregular defects: monocular or binocularIrregular defects: monocular or binocular

Arcuate bundle defectsArcuate bundle defects

Central papillomacular defectsCentral papillomacular defects

Altitudinal defectsAltitudinal defects

Optic nerve lesionsOptic nerve lesions

Retina and Nerve Field DefectsRetina and Nerve Field Defects

Irregular binocular defects: ringIrregular binocular defects: ringscotoma of RPscotoma of RP

Arcuate and papillomacular defectsArcuate and papillomacular defects


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Altitudinal and Nasal fiber defectsAltitudinal and Nasal fiber defects Optic nerve lesionsOptic nerve lesions

The ChiasmThe Chiasm

Decussation of visual fibersDecussation of visual fibers

Decussation of pupil fibersDecussation of pupil fibers

Multiple neighboring influencesMultiple neighboring influences

PituitaryPituitary

VascularVascular

CSFCSF

Skull baseSkull base

The Chiasm and Junction of theThe Chiasm and Junction of theoptic nerveoptic nerve

The optic tractsThe optic tracts

Carry fibers to the LGBCarry fibers to the LGB

Carry pupil fibers to the midbrainCarry pupil fibers to the midbrain enlageenlageofof EdingerEdinger WestphalWestphal via the brachium ofvia the brachium of

Incongruous field defectsIncongruous field defects

The optic tractsThe optic tracts


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The lateral geniculateThe lateral geniculate

PosterolateralPosterolateral

thalamusthalamus RetinotopicRetinotopic

organizationorganization

Layer 1,4,6 fromLayer 1,4,6 fromcontralateral eyecontralateral eye

Layer 2,3,5 fromLayer 2,3,5 fromipsilateral eyeipsilateral eye

The fovea projects toThe fovea projects to50% of the LGB50% of the LGB

Optic radiationsOptic radiations

Meyers loop: temporal lobeMeyers loop: temporal lobe

Parietal lobe path directParietal lobe path direct Majority of fibers from other thalamicMajority of fibers from other thalamic

nuc enuc e

Meyers loop: optic radiationsMeyers loop: optic radiations Posterior radiationsPosterior radiations

Occipital cortexOccipital cortex

Striate cortex V1Striate cortex V1

Caudal 50% encode central 10 degreesCaudal 50% encode central 10 degrees

Middle 40% encodes 10Middle 40% encodes 10--60 degrees60 degrees Rostral 10% encodes 60Rostral 10% encodes 60--90 degrees90 degrees

The temporal crescentThe temporal crescent

Occipital cortexOccipital cortex


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Occipital cortexOccipital cortex The integrative componentThe integrative component

Occipitoparietal pathwayOccipitoparietal pathway

The where pathwayThe where pathway Occipitotemporal pathwayOccipitotemporal pathway

T e w at pat wayT e w at pat way

Visual integrationVisual integration Visual integration: where pathVisual integration: where path

Occipitoparietal where pathwayOccipitoparietal where pathwayOccipitotemporalOccipitotemporal function: whatfunction: what

pathwaypathway


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Occipitotemporal what pathwayOccipitotemporal what pathway

Testing techniquesTesting techniques

ConfrontationConfrontation

Patient drawingPatient drawing

Bowl perimetryBowl perimetry

Kinetic: Goldman perimeterKinetic: Goldman perimeter

Static: Humphrey perimeterStatic: Humphrey perimeter

Testing techniquesTesting techniques

ConfrontationConfrontation

Patient drawingPatient drawing

Bowl perimetryBowl perimetry

Kinetic: Goldman perimeterKinetic: Goldman perimeter

Static: Humphrey perimeterStatic: Humphrey perimeter

Testing methods: The AmslerTesting methods: The Amslergridgrid

Finger confrontationFinger confrontation


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Finger confrontation:Finger confrontation:SimultaneousSimultaneous

Kinetic perimetryKinetic perimetry

Involves a hemispheric bowlInvolves a hemispheric bowl

Target is moved from noneTarget is moved from none--seeing toseeing toseeing point, the kinetic thresholdseeing point, the kinetic threshold

eve ops sopters: areas o equa ret naeve ops sopters: areas o equa ret nasensitivitysensitivity

Target size is varied, velocity constantTarget size is varied, velocity constant

Examiner dependentExaminer dependent

Bowl perimeterBowl perimeter The Kinetic visual fieldThe Kinetic visual field

The normal kinetic fieldThe normal kinetic field An abnormal kinetic fieldAn abnormal kinetic field


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Static perimetryStatic perimetry

Tests each point for a visual thresholdTests each point for a visual threshold

Develops a three dimensional map of theDevelops a three dimensional map of thevisual fieldvisual field

ompar son to age matc e normaompar son to age matc e normadatabasedatabase

A statistical box plotA statistical box plot

Computer driven, technician monitoredComputer driven, technician monitored

Static perimeterStatic perimeter

Static perimetryStatic perimetry

Samples smaller area than kineticSamples smaller area than kineticperimetryperimetry 90% of significant deficits occur within the90% of significant deficits occur within the

central 30 degreescentral 30 degrees

More sensitive and quantitative resultsMore sensitive and quantitative results

Not technician dependentNot technician dependent

Multiple testing machines availableMultiple testing machines available Can compare a test from another locationCan compare a test from another location

A normalA normalstatic fieldstatic field

Interpretation: 4 stepsInterpretation: 4 steps

Is the field normal or abnormal?Is the field normal or abnormal?

Is the abnormal field the result of poorIs the abnormal field the result of poorcooperation?cooperation?

s t e a norma e t e resu t o ans t e a norma e t e resu t o anoptical or retinocortical abnormality?optical or retinocortical abnormality?

Can the abnormality be localized?Can the abnormality be localized?

Localizing field defectsLocalizing field defects


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Monocular: nerve fiber bundleMonocular: nerve fiber bundledefectsdefects

Papillomacular bundlePapillomacular bundle

Arcuate bundleArcuate bundle Nasal radial bundlesNasal radial bundles

Irregular binocular defects:Irregular binocular defects:ring scotoma of RPring scotoma of RP

Optic nerve lesionsOptic nerve lesions Anterior junction lesionAnterior junction lesion

Posterior junction lesionPosterior junction lesion Chiasmal lesionsChiasmal lesions


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Retrochiasmal lesionsRetrochiasmal lesions

The defects become homonymous, on theThe defects become homonymous, on the

same side as the visual spacesame side as the visual space A complete homonymous hemianopsiaA complete homonymous hemianopsialocalizes only to the retrochiasmal arealocalizes only to the retrochiasmal area

Congruous lesions are identical in size,Congruous lesions are identical in size,shape, and depth: applies only toshape, and depth: applies only toincomplete hemianopsiaincomplete hemianopsia Imply a more posterior lesion: CorticalImply a more posterior lesion: Cortical

anatomyanatomy

CompleteCompleteretrochiasmal lesionretrochiasmal lesion

A completeA complete

homonymoushomonymoushemianopsia is nonhemianopsia is non--

Homonymous hemianopsiaHomonymous hemianopsia IncongruousIncongruoushomonymoushomonymous

hemianopsia:hemianopsia: optic tractoptic tract CongruousCongruous homonymoushomonymous

hemianopsia:hemianopsia: optic radiationoptic radiation

Retrochiasmal field defectsRetrochiasmal field defects

Homonymous sectoranopiaHomonymous sectoranopia

Lateral geniculateLateral geniculate

Homonymous pie in the skyHomonymous pie in the sky

Tempora o eTempora o e

Homonymous quadrant: occipital lobeHomonymous quadrant: occipital lobe

Temporal crescent: occipital lobeTemporal crescent: occipital lobe

Macular sparing: occipital lobeMacular sparing: occipital lobe

LGB lesionLGB lesion

posterior choroidalposterior choroidalartery occlusionartery occlusion

anterior choroidalanterior choroidalartery occlusionartery occlusion

Temporal lobeTemporal lobe

Meyers loop lesionMeyers loop lesion


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Occipital cortex lesionOccipital cortex lesion

Superior lesionSuperior lesion

Inferior lesionInferior lesion

Occipital cortex anatomyOccipital cortex anatomy

Occipital cortex lesion:Occipital cortex lesion:posterior right halfposterior right half

Cortex lesion: anterior half leftCortex lesion: anterior half leftcortexcortex

Location,Location,not size,not size,mattersmatters

Monocular temporal crescentMonocular temporal crescent

The only example of a monocular fieldThe only example of a monocular fielddefect from a retrochiasmal lesiondefect from a retrochiasmal lesion

The only cortical representation of aThe only cortical representation of a

monocular visual fieldmonocular visual field Most likely infarction of the anterior 10%Most likely infarction of the anterior 10%

of the cortexof the cortex

Measured by kinetic perimetry out at 60 toMeasured by kinetic perimetry out at 60 to90 degrees90 degrees


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Temporal crescentTemporal crescent Temporal crescent preservedTemporal crescent preserved

Bilateral hononymousBilateral hononymoushemianopsiahemianopsia

A larger lesionA larger lesion

Involves both sides of the visual cortexInvolves both sides of the visual cortex

Usually vascularUsually vascular

May be watershed from hypotensionMay be watershed from hypotension

Should not be confused with malingeringShould not be confused with malingering

Bilateral homonymousBilateral homonymoushemianopsiahemianopsia

Which patient is more aware ofWhich patient is more aware oftheir loss of visual field?their loss of visual field?

??


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Neuro-ophthalmology:O tic Nerve

T. R. Mizen M.D.

Associate Professor of Ophthalmology, Neurology, andNeurosurgery

Neuro-ophthalmology

Rush University Medical Center: Chicago, IL

Optic nerve review -1

Optic disc hypoplasia

Optic nerve drusen Lebers hereditary optic neuropathy

normal vision (usually)

Vision loss

with a normal nerve: optic neuritis

with a swollen optic nerve :Ischemic optic neuropathy

Peri-operative ION: a special circumstance

Optic nerve review -2

Optic nerve tumors

sheath meningioma

optic nerve glioma

ox c op c neuropa y

Traumatic optic neuropathy

Radiation optic neuropathy

Optic nerve hypoplasia

May occur unilateral or bilateral

Variable appearance: marked or minimal

Variable vision: poor vision with small

May occur in isolation or with ocular orforebrain abnormalities

When bilateral and accompanied by poorvision and nystagmus, usually otherdevelopmental abnormalities observed

Optic nerve

hypoplasia

Possible association

with increased abuse

of alcohol and drugs

Phenytoin, quinine,alcohol, LSD, cocaine

Maternal diabetes

Perimetry: irregular

borders, stable over

time

Septo-optic dysplasia: deMorsiers

syndrome Bilateral ONH: MRI imaging and endocrine evaluation

Growth hormone and DI may be treated resulting in normalgrowth

Unilateral ONH: periodic eye and Peds exam ? Imaging: glioma or craniopharyngioma associated with

irregular optic nerves


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Optic disc drusen

3.4 - 24 / 1,000population

Bilateral in 75% Disturbance of axonal

metabolism in the

scleral canal

Increase in size with time,more visible with time dueto calcium deposition

Associated visual fielddefects: at times notnoticed by patients

Disc drusen:ophthalmoscopic criteria

Central cup absent,smaller nerve

Anomalous vascularbranching, vessels arisingfrom the apex of thenerve, retention ofvascular detail

Transillumination of discdrusen

Irregular disc margins,peripapillary RPEchanges

No hemorrhage or cottonwool spots

Optic disc drusenAppear on CT: calcified

Abnormal appearance

with RPE atrophy

DDx: Drusen and papilledema

Dominant Optic Atrophy (DOA)

Dominant autosomalinheritance

Onset age 4 8 years

Vision: 20/30-20/70, rare

20/200 Wedge temporal pallor,

temporal sectoralexcavation

Centocecal enlargementof blind spot, mid-zonaltemporal depression, fullperipheral fields

DOA


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LHON: Lebers Hereditary Optic

Neuropathy Described by Leber in 1871

Sudden and severe loss of

visual acuity Large dense central

scotoma

Inherited strictly in the maternalline with incomplete penetrance

Affected males do not transmitthe trait

Defective cytoplasmicmitochondrial DNA

equen a an a era

Second and third decades oflife

Predominantly young males:80%

Usually healthy: cardiacconduction, some withneurologic symptoms

Substitutes A for G

Affects capacity tomanufacture ATP

LHON

Acute phase mild optic

disc hyperemia

Peripapillary

microangiopathy also

presymptomatic phase

Slowly marked disc pallor

evolves

The acutely hyperemic

disc does not leak on

fluorescein angiography

LHON

11778: Wallace mutation:

50 76%

3460: 7-30%

14484: 10-31%

No treatment

Succinate and co-enzyme

Q: mitochondrial function

Trigger factors: tobacco

82% of patients with

11778 were males

British study: 2.5:1

male:female 11778

14484 mutation may

recover vision more often

The swollen optic nerve Causes are protean

Differentiate disc edemafrom papilledema, whichis disc edema fromelevated ICP

Papilledema, papillitis,

Papilledema: elevated ICPand disc edema

Multiple causes (see table)

Space-occupying lesion

Supratentorial orinfratentorial

and Ischemic opticneuropathy (ION) arecommon and can beconfused

The medical history isparamount

Disruption of axoplasmicflow at the level of thelamina cribrosa: fast andslow

Subsequent hypoxia andvascular changes on thedisc

May take hours to evolveand weeks to resolve

Optic nerve: blood supply,

subarachnoid space Elevated ICP without mass lesion


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Idiopathic Intracranial

Hypertension: IIH Intracranial hypertension

without a discernable

origin

A diagnosis of exclusion

1-2/100,000 general

population

19-21/100,000 obese

women reproductive age

from teens through 5th

decade, the hormonally

active child bearing years

In children no gender

preference nor a

tendency toward obesity

-

Associated medications:

Steroids Lithium

Nalidixic acid Danazol

Tetracycl ines Amiodarone

Vit A toxicity Chlordecone

IIH: Symptoms and the modified

Dandy criteria Daily diffuse headache

Transient obscurations of

vision Pulsatile tinnitus

Neck stiffness

Dandy criteria:

Signs and symptoms

of elevated ICP:headache, nausea,TOV, tinnitus

ou er, eg, or arm pa n

Diplopia: CN VI palsy

exam

Elevated CSFpressure with normalparameters

Normal imaging toexclude mass lesion ordural sinus thrombosis

IIH: Imaging and CSF profile Papilledema: early to moderate

early moderate

Papilledema advanced atrophic

IIH: Treatment: Medical

Lower CSF pressure

Acetazolamide (Diamox)

Up to 500 mg QID

e e ects: per ora an an parest es as,

anorexia, metallic taste

Rare renal stones, aplastic anemia

Lasix or other diuretics: less effective

Digoxin in sulfa allergic patients


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IIH: treatment: Surgical

Shunting:

To lower CSF pressure

More effective to reduceheadache

Lumbo-peritoneal

ONSF

Optic nerve sheath

fenestration to directlyreduce the ICP at thelamina cribrosa

g ra e o rev s ons Siphoning effect with low

pressure headache

Ventriculo-peritoneal Less maintainence:

adjustable through the skin

fenestration may close,but the disease processmay be over

Does not successfullyreduce headache

Some patients mayrequire both a cranialshunt and ONSF

IIH: treatment: surgical: ONSF

Optic nerve sheathfenestration to directly

reduce the ICP at thelamina cribrosa

Effective: over time thefenestration may close,but the disease processmay be over

Does not successfullyreduce headache

Some patients mayrequire both a cranialshunt and ONSF

IIH: Management

The major morbidity of IIH is visual loss and

blindness

A medico-legal issue

Meticulous o hthalmolo ic survei l lance

perimetry

Need to image and perform LP

WEIGHT LOSS: losing 6 10% of body weight

can demonstrate reduction in disc edema: ?

Gastric bypass

Optic Neuritis: ON

Acquired optic nerve

disease (usually) without

disc edema

Relatively painless

ro ressive loss of vision

over first week

Predominantly monocular

History important:

preceeding viral illness,

sinus symptoms

Optic neuritis: clinical profile

Loss of acuity

36% 20/40 or better

28% 20/40 to 20/100

36% 20/200 or worse

Abnormal visual field

Fellow eye abnormal

in 67% if patients

Fundus normal to Abnormal color vision

Afferent pupil defect

mild edema in 35 %

Routine blood tests,

CXR, LP of little use

Perimetry: ON


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ONTT: treatment profile

Three groups Oral prednisone

High dose pulsed IVsteroids

MRI: Powerful predictor of

developing MS

5 and 10 year datanow available

Higher recurrencewith oral prednisone

Reduced incidence ofrecurrent neurologicsymptoms with IVsteroids

Optic Neuritis: CHAMPS Controlled High-risk

Subjects Avonex MultipleSclerosis PreventionStudy

Looked at patients age18-50 with first isolated

NEJM 2000 Sept 28;343:898-904

Initiating treatment withinterferon beta-1a at thetime of a firstdemyelinating event is

well defined neurologicevent consistent withdemyelination andinvolving the optic nerve,spinal cord, brain stem orcerebellum

Weekly injections ofinterferon beta-1a(Avonex)

beneficial for patients withbrain lesions on MRI thatindicate a high risk ofclinically definite multiplesclerosis.

CDMS over time by MRI Optic Neuritis: Clinical Course

Visual symptoms

84% recover to baseline in 6 to 12 weeks

Regardless of treatment with steroids

-

5% never recover

Ischemic Optic Neuropathy: ION

The most commoncause for discswelling over the ageof 50

non-arteritic fromarteritic ION Clinical presentation

Associated signs

Clinical exam andtesting

ION

Differentiated into

Non-arteritic AION

(NAION) versus

arteritic AION

Asymptomatic other

than for loss of vision

Pale disc edema

associated with GCA

Clinical study: of all

ION

90% non-arteritic

10% with GCA

u en onset, usua y

noted upon

awakening


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Optic nerve vasculatureION: the optic nerve

The disc at risk:

A smaller optic nerve

Crowded nerve fiber

layer

branching

A small cup/disc ratio

ION: Clinical facts

Most attacks occursuddenly and painlesslyand the deficit is basicallyfixed

Infarction is a one time

Vision loss uponawakening Nocturnal dips

Slow rise in daytime BP

With systemiceven n eac eye

Fellow eye vulnerable:disc anatomy

Arteriosclerotic riskfactors prominent Risk of MI and CVA slightly

increased

hypotension similarpicture evolves

ION: pathophysiology

Associated with anemia

Chronic disease

Acute GI hemorrhage

Especially with anesthesia controlled intentional

hypotension

Hypotension

Associated with MI or CABG

ION: IONDT

Surgical decompression

did not offer any

improvement, and in fact

vision slightly worse in

treatment group

AJO 2002 134:317-28

New NAION diagnosed in

14.7 % of IONDT patients

over 5 years

Natural history suggested

improvement in 3 lines of

vision in 42.7% of

patients at 6 months

ONSD contraindicated

JAMA 1995: 273:625-632

associated with poor

baseline visual acuity in

the study eye and

diabetes, but NOT age,

sex, smoking history, or

aspirin use

Arteritic ION: GCA

ION may beassociated with GCAand the clinicaldistinction is critical

Of all patients withION in large studies90% are non-arteriticand 10% arteritic

opposite eye iftherapy delayed

Medicolegalconcerns: blindness isthe major morbidity

GCA only 10-20 %may experience ION More may experience

diplopia, amaurosisfugax, non-embolicCRAO


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ION: GCA

The clinical suspiciondepends on thesystemic symptoms of

jaw claudication,

The presentation of apatient with ION fromGCA can be difficultto differentiate from

-, ,weight loss, myalgias

In one paradigmvisual symptoms wereexcluded in symptomclusters in thediagnosis of GCA

Visual loss tends tobe more catastrophic Remember that 20%

of NAION can be20/200 or less

ION: GCA

If clinical diagnosissuspect order Westergren

ESR, C-reactive protein,and start oral prednisone 60 to 100 mg daily, 1

mg/kg

Hayreh: ESR positive in95 to 98% of patients with

GCA; C-reactive protein(CRP) positive in 100% Difficulty in defining normal

range of ESR

Consult patientsinternist/PMD: This is a systemic disease

Treatment is long term

Multiple systems may beinvolved

(age +10)/2 for women,Age/2 for men

Arbitrary value of greateror less than 50

C-reactive protein Elevated in other

conditions

? Decreased with statindrugs

ION: GCA

If there is a strong clinical

suspicion for GCA with

visual loss with ION

within 24-48 hours, may

consider high dose

Involvement of the

medical team to treat the

patient

Side effects from steroid

pulsed IV steroids

1000 mg solumedrol IV for

3 days

Place on oral prednisone

With early treatment

involvement of opposite

eye reduced

, ,

gastric ulcers,

osteoporosis

Effects of not treating

GCA: blindness, CVA, MI,

death

ION GCA Temporal Artery Biopsy

If one side negative,

biopsy opposite side if

clinically suspicious

May treat patient with

clinical symptoms

even if biopsy

negative

Search for alternative

diagnosis:

Undetected cancer

Management: arteritic ION

If GCA suspect stat ESR

If acute visual loss iswithin 48 hours admit forhigh dose pulsed IVsteroids, 1000 mg of

solumedrol daily in

Both the disease and thetherapy can be fatal

Monitor ESR to lowerdose

Methotrexate if steroid

divided doses for 3 to 5doses, then oralprednisone at 1 mg/kg

Taper slowly: treatmentfor 1 to 3 years

Consultation with Internistor Rheumatologist forsteroid side effects

Usually after six months of

prednisone

Peri-operative ION

Reported after spinal surgery and radical neckdissection

Visual loss typically upon awakening fromanesthesia

ay occur over severa ays

Visual loss profound: counting fingers

Fundus exam initially normal

Hemodynamic perioperative derangements

No effective therapy; prognosis poor


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Peri-operative ION: reference SURVEY OF OPHTHALMOLOGY VOLUME 50 NUMBER 1 JANUARY

FEBRUARY 2005

MAJOR REVIEW Perioperative Posterior Ischemic Optic Neuropathy:

Lawrence M. Buono, MD, and Rod Foroozan, MD

Peri-operative ION

May need to watch head position:

watershed zone Keep the head higher than the chest

Transfuse if needed

May need to watch for hemodilution

Colloids

Toxic optic neuropathy

Bilateral and

simultaneous

Slow progressive loss

of vision

Ethambutol Chloroquine

Chloramphenicol Vigabatrin

History critical

Toxins implicated

Bilateral central

scotoma on perimetry

rep omyc n su ram

Isoniazid Heavy metals

Chlorpropamide Yohimbine

Digitalis

Perimetry: Ethambutol ON

Tobacco alcohol amblyopia

Chronic alcoholconsumption: years, daily

Chronic tobacco use:years, daily

Poor diet: Dietary

Evaluation:

CBC, B-12, folate,ESR, ANA, VDRL

Urine for heavydeficiency is the commondenominator

Depletion of B vitaminswith toxins fromcigarettes

Treatment: changehabits, daily vitamins

me a screenng

MRI: excludedemyelinatingdisease

Hematologyconsult: B12 testing

Nutritional

optic neuropathy:

Perimetry


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ONSM

Progress insidiously

May progress to completeblindness

Intracranial extension

Rarely biopsy needed

Radiation: identify visionand field, observe, and

with progression, radiate

radiate but when to radiate

Conformal radiation

Surgical excision for

vision not recommended

Debulking and

decompressing ?

Traumatic optic neuropathy:

posterior indirect Without external or initial

ophthalmoscopic

evidence of injury to the

eye or the nerve

Loss of vision, loss of

color vision, APD, visual

field defect

Fundus initially normal

men

Estimated that 2 to 5% of

patients with head injury

have TON

4-5 cases of

TON/100,000/year

acuity with altitudinal

defect

TON

Deceleration injurywith injury to the pialperforators byshearing within the

nerve is fixed to thebone

Contusion to thenerve without fractureto the bone No room to swell

TON: treatment

Surgical decompression:extracranial viatransethmoid ortranssphenoidal

Initial 70% improvement

IV steroids for 48-96hours ? New data to suggest that

steroids in head traumamay be detrimental tosurvival

canal

Comparative analysis: Vision improved 57%

untreated

Vision improved in 32%surgery group

Vision improved in 52% ofthe steroid group

no improvement

Surgery for bone fracture

No treatment may workjust as well

Prognosis guarded


Total radiation dose andfractionation dose

Maximum total dose of5,000 cGy in fractionsunder 200 cGy provide an

acceptable low risk

Typically followingtreatment of paranasalsinus carcinoma or skullbase lesions Also with pituitary,

parasellar, Risk increases in patients

with diabetes

Risk increases in patientson chemotherapy

cranop aryng oma, ron aand temporal glioma, andocular tumors

A retrobulbar opticneuropathy occurringmonths to years followingtreatment 3 months to 8 years

Peak at 1.5 years


Painless acute visual loss

in one or both eyes

Transient obscurations of

vision may precede visual

Steroids: to reduce tissue

edema

Only 2/16 patients had any

recovery

Anticoa ulants: of little

Final vision of NLP in

45%

85% 20/200 or worse

value

Hyperbaric oxygen

Treat early: 24 72 hours

of onset of visual loss

Results not uniform

Treat two weeks to one

month


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4minuteVisualfieldquiz

16 visual fields16 visual fields

15 seconds per field15 seconds per field

One

Righthomonymous,incongruous,denserabove;lefttemporallobeextendingtoparietallobe

Two

Righthomonymous,congruous,splitsfixation:Occipitaltip

Three

Lefthomonymous,incongruous,denserabove,Eitherrightoptictractorrighttemporallobe,withthetemporal

lobemore

likely

statistically

Four

Rightcentralscotoma,lefttemporalhemianopsia:junctional scotoma ofrightopticnerveatjunctionofnerveandchiasm

Five

Lefthomonymousinferiorcongruousquadrantopsia;rightoccipital,possiblerightparietallobelesion


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Six

Blindrighteye,temporalhemianopsia lefteye;rightopticnervelesionextendingintochiasm,orlargechiasmlesion

Seven

Righteyenasalstep,lefteyeringscotoma:glaucoma

Eight

Leftinferiorcongruousquadrantic depression;right

occipital

,

upper

bank

Nine

Completelefthomonymoushemianopsia:rightoptictract,pareital,oroccipital;nonlocalizing; checkOKNfor

parietallesion

Ten

Bilateralcecocentralscotoma:bilateralopticneuropathy

Eleven

centralandperipheral:nonphysiologic


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