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optic neuropathy 1 Flashcards

1
Q

how many retinal ganglion cell axons make up the optic nerve?

A

1-1.5 million

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2
Q

what are the 4 anatomical segments and sizes of the optic nerve?

A 
 4 anatomical segments
 Intraocular: 1 mm
 Intraorbital: 25 mm
 Intracanalicular: 10 mm
 Intracranial: 16 mm
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3
Q

vascular insult

A

intraocular

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4
Q

muscle engorgement/tumors

A

intraorbital

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5
Q

fractures and sinus inflammation

A

intracanalicular

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6
Q

pituitary gland and circle of willis

A

intracranial

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7
Q

where are the cell bodies of retinal ganglion cells?

A

ganglion cell layer

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8
Q

is the optic nerve covered by meninges?

A

yes

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9
Q

what supplies the optic nerve prelaminar?

A

SPCA (peripapillary choroidal vessels); branch of opthalmic artery; branch of internal carotid

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10
Q

blood supply of lamina cribrosa

A

SPCA, circle of zin haller

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11
Q

blood supply of retrolaminar

A

branches from CRA, branches from pial vessels

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12
Q

blood supply of choroid

A

SPCA

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13
Q

what determines papillaedema?

A

bilateral optic nerve head swelling due to raised intracranial pressure

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14
Q

how can we tell difference b/w NV and shunts?

A

angiofluorescence; shuts do not leak and NV does

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15
Q

3 conditions that can cause collaterals/shunts

A

 Optic nerve sheath meningioma
 CRVO
 Chronic glaucoma

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16
Q 
 VA loss
 RAPD
 Dyschromatopsia
 VF defect
 Reduced contrast sensitivity
 +/- normal optic disc appearance 
 Abnormal VEP
A

optic nerve dysfunction

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17
Q

2 types of optic neuritis

A

 Typical: demyelinating optic neuritis

 Atypical: systemic infectious/inflammatory causes

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18
Q

5 hallmarks of typical optic neuritis

A 
 Primary demyelination of the optic nerve
 - Autoimmune: antibodies attack myelin sheath
 Sudden VA loss
 -Progresses over 1 week
 -Improvement begins by 1 month
 Pain on EOMs: 90% of patients
 +/- RAPD
 Dyschromatopsia: usually worse than VA
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19
Q

 Retrobulbar: 2/3
 Age: 18-46; average 32 years
 77% female
 Laboratory testing unnecessary

A

typical optic neuritis characteristics

20
Q

 Diffuse: 48%
 Altitudinal/arcuate/nasal step: 20%  Central/centrocecal: 8%
 Other:16%
Bottom line: predilection for central 30o, but any pattern is possible

A

optic neuritis VF abnormalities

21
Q

 Numbness in hands
 Problems with bladder control
 Pulfrich phenomenon: altered perception of moving objects
 Stereo-illusion of swinging pendulum
 Perceived depth due to relative difference in signal timings
between the two eyes
 Uthoff sign
 Worsening of neurologic symptoms with increased body temperature

A

optic neuritis associated symptoms

22
Q

 Better understanding of relationship between ON and MS
 Sponsored by NEI
 Clinical trial of corticosteroid therapy for ON
 Conducted between 1988-1991

A

optic neuritis treatment trial (ONTT)

23
Q

 Patients presented with typical unilateral acute optic neuritis
 3 treatment arms
 IV methylpredinisolone 250mg QID x 3 days, followed by
oral prednisone 1mg/kg/day x 11 days
 Oral prednisone 1mg/kg/day x 14 days
 Oral placebo x 14 days

24
Q

ONTT RESULTS

A

 High dose IV steroids accelerated visual recovery
 Oral steroid treatment alone increased rate of recurrence of ON
 IV steroids reduced risk for development of MS after initial attack of ON for 2 years – no benefit after 2 years
 Typical ON: no underlying systemic or infectious etiology, therefore no need for bloodwork
 Brain MRI extremely useful in identifying patients who are at higher risk for developing MS

25
Q

 ONTT 15 year follow-up
 294 subjects from original 457 cohort (65%)
-most had good VA
 No significant difference in visual function among 3 treatment arms
 QOL measurements lower in patients with worse vision and associated neurologic deficits from MS

A

longitudinal optic neuritis study (LONS)

26
Q

 15 year overall risk: 50%
 75% in women

 Initial MRI most predictive risk factor
 0 lesions: 25%
 1 lesion: 60%
 3+ lesions: 78%

A

LONS: risk for developing MS after ON

27
Q

 White race
 Family history of MS
 Ill-defined neurologic complaints
 Pervious episode of acute optic neuritis

A

LONS: other risk factors for MS

28
Q

whats typical of optic neuritis?

A

2/3 are retrobulbar

29
Q 
 Severe disc swelling
 No pain
 Disc or peripapillary hemorrhage  Retinal exudates
 NLP vision
 Male sex
A

LONS: low risk for MS

30
Q

 In typical ON, make clinical diagnosis
 Obtain MRI of brain and orbits with gadolinium
 Treatment: high dose IV steroid x 3 days; oral prednisone taper x 11 days
 Refer high-risk patients to neurologist
 Abnormal brain MRI

A

LONS recommendations

31
Q

 Randomized, double-blind, placebo controlled, multicenter study
 383 subjects enrolled from 1996-1998
 Study group received weekly Avonex injections
 Inclusion criteria
 18-50 year old
 First occurrence of isolated, well-defined demyelinating event
 Abnormal unenhanced brain MRI

A

controlled high risk subjects avonex MS prevention study (champs)

32
Q

 Primary: development of CDMS
-Avonexreducedriskby44%
-35%chanceofdevelopingMSwhileondrug -50%chanceofdevelopingMSonplacebo
 Secondary: effect of treatment on MRI findings (subclinical MS)
- FevernewandenlargingT2lesions
 67%fewerenhancinglesions

A

champs endpoints

33
Q

 Brain MRI (T1, T2, Gadolinium)
 Assess for subclinical disease
 Identify high-risk patients
 Interferon therapy in high-risk patients

A

champs recommendations

34
Q

 Treatment available that alters development and/or course of CDMS after first demyelinating event
 MRI not necessary to diagnose optic neuritis, but required to determine who is at greatest risk for MS
 OD’s must be able to promptly diagnose optic neuritis
 Order MRI
 Refer to neurology for treatment initiation

A

indication of champs

35
Q 
 Avonex (interferon beta-1a)
 Rebif (interferon beta-1a)
 Betaseron (interferon beta-1b) 
 Copaxone (glatiramer acetate) 
 Tysabri (natalizumab)
 Novantrone (miloxantrone) 
 Gilenya: first oral medication
A

types of MS TREATMENT

36
Q

WHAT eye finding can MS lead to?

A

macular edema

37
Q

 Proteins in blood serum
 AKA immunoglobulins
 When present in CSF, indicate inflammation of the CNS
 79-90% of patients with MS have permanently observable oligoclonal bands

A

oligoclonal bands

38
Q

what does optic neuritis atypical require?

39
Q 
 Age: 50 years
 Bilateral
 Lack of pain
 Anterior/posterior uveitis
 Retinal exudates/infiltrates
 Severe optic nerve swelling
 Hemorrhages
 VA continues to worsen past 1 week
 Recurrence within short interval or during steroid taper
A

optic neuritis atypical

40
Q 
 Bloodwork
 CBC with differential
 ESR
 CRP
 ACE
 FTA-Abs
 ANA
 Chest X-Ray
 MRI
 Lumbar Puncture
A

optic neuritis atypical

41
Q

 Connective tissue disease  Lupus
 Sjogren’s  Bechet’s

 Infectious  Viral
 Bacterial: Lyme, syphilis

 Infiltrative
 Sarcoidosis
 Cancer: lymphoma, leukemia

A

other causes of optic neuritis (secondary)

42
Q

 NMO antibodies (NMO IgG) target aquaporin 4
 Channel for water transport across astrocyte cell membrane
 NMO IgG found in astrocytes around blood brain barrier
 Inflammatory demyelination results in necrotic damage of white and grey matter

A

neuromyelitis optica pathophys

43
Q 
 AKA Devic’s Syndrome
 Unilateral or bilateral optic neuritis
 Myelitis: inflammation of the spinal cord
 At least 2 of the following
 Contiguous spinal cord lesion > 3 vertebral segments on
MRI
 Brain MRI non-diagnostic for MS
 Positive NMO IgG serology
A

neuromyelitis optica

44
Q

 Can affect children, but median age of onset is 39
 Relapsing (80-90%) or monophasic
 Treatment: immunosuppressive therapy
 IV steroids  Azathioprine  Rituximab

A

neuromyelitis optica

45
Q

 Focal inflammatory disorder of spinal cord
 80% present with numbness and paresthesias
 1/3 complete recovery, 1/3 moderate disability, 1/3 severe
disability
 May progress to MS

A

transverse myelitis

46
Q

 Postinfectious encephalomyelitis
 Fever, nausea, vomiting, positional vertigo
 Typically children s/p viral infection or immunization
 MRI: extensive lesions (basal ganglia, thalamus)
 Tx: high dose IV steroids for 3-5 days, oral taper for 4-6 weeks

A

acute disseminated encephalomyelitis (ADEM)

47
Q

what makes the nerve head pink?

A

prelaminar vascular supply

ocular disease 3 (10 decks)

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