optic neuropathy 2 Flashcards by Christie Wong

 Ischemic, non-inflammatory condition
 Vascular insult to pre-laminar and retro-laminar optic
nerve
 Clinical presentation
 Acute painless vision loss: mild to severe
 Typically older patient with cardiovascular risk
factors
 Disc at risk

optic neuropathy (naion)

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Opticnerveappearance
 Hyperemicedema
 Flamehemorrhages
 +/-macularstar

NAOIN CHARACTERISTICS

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naion vf defects

Altitudinal:62%
 Inferior:47%
 Centralscotoma:21%

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 HTN
 DM
 Age>55years
 Atheroscleroticdisease
 Glaucoma
 Smallopticnerves:mechanical 
 Viagra?
 M>F
 Bilateral (sequential)

risk factors for naion

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 Some visual recovery possible

 May have mild improvement/deterioration

naion prognosis

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va outcomes of naion

 50%: VA > 20/60

 40%: VA

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 Chronic HTN causes alteration in autoregulatory response
 Vasodilation fails to occur in decreased BP
 Nocturnal hypotension occurs in morning hours
 Ischemia to PCA results decreased optic nerve perfusion

naion pathogenesis

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 Age:40+
 1+vasculopathicriskfactors:HTN,DM,elevated
cholesterol, smoking
 Oneeyeinvolved
 VerysuddenVA/VFloss,typicallyuponwaking
 Noeyepain,diplopia,orneurologicsymptoms
 NormalEOMs
 +RAPD
 Mild-severehyperemicONHswelling
 FellowONH:“discatrisk”

naion clinical diagonistic criteria

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 Monitor in 2-4 weeks
 If VA or VF still worsening, diagnosis is suspect and
patient needs workup
 If stable, re-examine in 3-4 months
 Prognosis
 Sameeyerecurrence:3-5%
 Felloweyeinvolvement:25%
 40%recoversomeVA,butVFremainspoor

naion follow up

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pathogenesis of AION

inflammationofelastictissueinarterial walls results in vessel occlusion

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epidemiology of aion

 Age: 65+
 F>M
 75% bilateral: fellow eye involved in 1-2 days
 Decreased likelihood of fellow eye involvement after 6-8 weeks of initial insult
 50% have polymyalgia rheumatica: pain and stiffness of shoulders, pelvic girdle, and torso

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 Severe VA loss preceded by episodes of transient vision loss
 Scalp tenderness
 Jaw claudication
 Mild fever
 Weight loss
 Arthralgias/myalgias

symptoms of aion

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opthalmic emergency pathy

aion

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 Pallid optic nerve swelling
 No hemorrhages
 Extensive cotton wool spots
 Preceded by episodes of TIA

signs of aion

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 Management
 STAT hospital admission and IV steroids for 3-5 days, then
oral taper (on final day of IV treatment) x 1+ year
 Temporal artery biopsy
 Laboratory: ESR, CRP
 GCA: systemic vasculitis of medium and large arteries
 Self limiting, but may persist for years
 Oral steroids protect surviving ON as disease burns itself out
 Steroids may be discontinued after 12-18 months unless symptoms or blood inflammatory markers persist
 Use ESR and CRP levels to guide steroid taper

management of aion

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 Rule out early onset DM, HTN, and hyperlipidemia
 r/o elevated homocysteine
 r/o vasculitides: SLE, Wegener’s
 r/o coagulopathy
 Bloodwork: ESC, CRP, ACE, ANA, RPR-VDRL, RBC Folate, B12, Bartonella, Lyme

naion in pts

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 Cardiac
 Spinal
 Thoracic
 Abdominal

POSTSURGICAL pion

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 Vasculitis(GCA)

 Atherosclerosis  Radiation

spontaneous pion

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PatientrecoversconsciousnesstodiscoverpoorVA

in one/both eyes

symptom of pion

 Initiallyopticdiscisnormal
 Pallordevelopsin4-6weeks  RAPD
 IfRAPDabsentandbothpupilsbrisklyreactive
 Suspectbilateralposteriorcerebralarteryinfarction  Akacorticalblindness

signs of pion

 Diagnosis of exclusion
 Unilateral or bilateral
 Vision typically unaffected
 May be a mild form of NAION
 Diabetic retinopathy usually present
 Hyperemic disc swelling with dilated pre-laminar vessels
 VF: enlarged blind spot
 Disc swelling resolves within
2-10 months
 May have mild residual pallor

diabetic papillopathy

papillopathy vs. papilitis

papilitis: swelling of nerve
papillopathy: disease of optic nerve

Optic nerve edema caused by raised intracranial pressure

PAPILLEDEMA

 Clear fluid that surrounds the CNS
 Gives support, protection, and nourishment
 Present in ventricles, central canal of spinal cord, and subarachnoid space
 Produced in choroid plexus of third, fourth, and lateral ventricles
 Enters into dural venous sinuses via arachnoid granulations
 Drains via internal jugular veins

CSF

HOW DO WE GRADE PAPILLEDMA

``` FRISEN SCALE  Stage 0: normal optic nerve  Stage 1: very early  Blurring of superior, inferior, and nasal aspects  No elevation  Normal temporal disc  Incomplete peripapillary halo  Stage 2: early  Blurring of all borders  Elevation of nasal border  Complete peripapillary halo  Stage 3: moderate  Increased diameter of ONH  Partial obscuration of vessel at disc margin  Peripapillary halo with finger-like extensions ```  Stage 4: marked  Elevation of entire nerve head  Near total obscuration of major blood vessels on the disc  Stage 5: severe  Dome-shaped protrusion of disc  Obliteration of cup  Total obscuration of blood vessels on the disc

stage 1 frisen scale

``` very early  Blurring of superior, inferior, and nasal aspects  No elevation  Normal temporal disc  Incomplete peripapillary halo ```

stage 2 frisen scale

early  Blurring of all borders  Elevation of nasal border  Complete peripapillary halo

stage 3 frisen scale

moderate  Increased diameter of ONH  Partial obscuration of vessel at disc margin  Peripapillary halo with finger-like extensions

stage 4 frisen scale

marked  Elevation of entire nerve head  Near total obscuration of major blood vessels on the disc

stage 5 frisen scale

severe􏰁 Dome-shaped protrusion of disc 􏰁 Obliteration of cup 􏰁 Total obscuration of blood vessels on the disc

Medical emergency |  Immediate neuro-imaging to r/o intracranial mass

papilledema

 Bilateral  Optic nerve function preserved early in its course  VA can be compromised from macular edema  Visual fields: typically enlarged blind spots  Absent spontaneous venous pulsation  20%ofnormalsdonothaveSVP

clinical features of papillee

```  Headache  Nonspecific characteristics  Worsens with valsalva manouver  Transient visual obscurations  Mild blurring to complete blindness  Lasts for few seconds  Precipitated by postural changes  Pulsatile tinnitus: whooshing sound in ear(s) in time with pulse  Diplopia  Abducens palsy ```

symptoms of papilledema

 MRI to r/o structural lesion  Lumbar puncture to confirm increased ICP and analyze CSF constituents  MRV to r/o venous sinus thrombosis  Laboratory: r/o inflammatory/infectious etiology

diagnostic workup for papilledema

4 mechanisms of increased icp

 Increased brain volume: common  Space-occupying lesion: tumor, hemorrhage, abscess  Cerebral edema: trauma, metabolic disease  Decreased CSF drainage: common  Hydrocephalus  Meningitis  Subarachnoid hemorrhage  Venous sinus thrombosis  Extracranial venous outflow obstruction  Increased CSF production: rare  Decreased skull volume: rare

 COPD  Malignant HTN  Sleep apnea  Renal failure

medical disorders causing pseudotumor cerebri

medications causing pseudotumor cerebri

 Tetracycline antibiotics  Excessive vitamin A  Steroids  Birth control pills

venous obstruction causing pseudotumor cerebri

 Cerebral venous sinus thrombosis |  Jugular venous thrombosis

 Aka idiopathic intracranial hypertension  Modified Dandy Criteria  Signs and symptoms of increased ICP  No localizing neurological signs (except VI palsy)  Patient is awake and alert  No evidence of intracranial mass on MRI/CT  Normal MRV  LP opening pressure of >25 cmH2O with normal CSF composition

pseudotumor cerebri: unknown causes

 MRI of brain and orbits with contrast  MRV: r/o venous sinus thrombosis  CSF microbiology, biochemistry, and cytology  Blood pressure, temperature, chest x-ray  CBC, electrolytes, glucose, liver function, ESR, CRP, ACE, ANA, RPR-VDRL

 All of the following must be performed and found to be negative: IIH investigations

```  Weight loss: 6% reduction results in papilledema resolution  Acetazolamide (Diamox)  Oral diuretics  Steroids  Surgical intervention  Lumbo-peritoneal shunt  Optic nerve sheath fenestration  Repeated LP ```

IIH treatment

```  Papillophlebitis  Diabetic papillopathy  CRVO  NAION  AION  Infiltrative  Infectious ```

unilateral optic nerve edema aka papillitis

 Leukemia  Lymphoma  Breast, lung, bowel metastases  Sarcoid granuloma

infiltration of one or both optic nerves

symptoms of infiltrative optic neuropathy

 Patients usually have known malignancy |  Acute, subacute, or slowly progressive VA and VF loss

 Normal, swollen, or pale ONH  MRI: enlargement of optic nerve  LP: increased protein, malignant cells

signs of infiltrative optic neuropathy

treatment for infiltrative optic neuropathy

urgent referral to oncology