STATdx ORBIT > OPTIC NEURITIS > Flashcards

OPTIC NEURITIS Flashcards

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1
Q

What is optic neuritis (ON)?

A

Inflammation of the optic nerve causing acute/subacute vision loss, pain with eye movement, and dyschromatopsia; most commonly demyelinating.

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2
Q

List major clinical subtypes of optic neuritis.

A

Papillitis (optic disc swelling), retrobulbar neuritis (normal disc early), neuroretinitis (disc edema + macular star), and perineuritis (sheath-predominant).

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3
Q

Which systemic diseases most commonly underlie demyelinating ON?

A

Multiple sclerosis (MS), myelin oligodendrocyte glycoprotein antibody disease (MOGAD), neuromyelitis optica spectrum disorder (NMOSD, AQP4-IgG).

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4
Q

Typical age/sex distribution for idiopathic demyelinating ON?

A

Young adults (20–45 years), female predominance.

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5
Q

Cardinal symptoms of ON?

A

Pain with eye movement, decreased visual acuity, color desaturation (red), central scotoma, RAPD if unilateral.

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6
Q

Preferred imaging modality and protocol for suspected ON.

A

MRI of orbits with and without gadolinium using fat-suppressed T1 post-contrast and STIR/T2; include brain MRI with FLAIR to assess MS lesions.

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7
Q

Typical MRI appearance of ON on T2/STIR.

A

T2/STIR hyperintensity and swelling of an optic nerve segment.

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8
Q

Typical MRI appearance of ON on post-contrast T1 fat-sat.

A

Intraneural enhancement of the affected segment; often short-segment in typical demyelinating ON.

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9
Q

Does ON restrict diffusion on DWI?

A

Classically no frank diffusion restriction; may show variable signal—true restriction suggests ischemic optic neuropathy or abscess.

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10
Q

Role of CT in ON.

A

Limited for demyelinating ON; may help exclude calcified lesions (meningioma) or trauma/sinonasal disease if needed.

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11
Q

What optic nerve segments can be involved on MRI?

A

Intraocular (disc), intraorbital, canalicular, intracranial segments; the optic chiasm and tracts may also be involved.

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12
Q

What segment length favors typical MS-related ON?

A

Short-segment (1–2 cm) involvement of intraorbital nerve, unilateral.

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13
Q

What segment pattern favors NMOSD-related ON?

A

Longitudinally extensive involvement (>50% of nerve length), chiasm/tract involvement, often bilateral, severe edema.

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14
Q

What segment pattern favors MOGAD-related ON?

A

Anterior optic nerve with optic disc edema, long-segment intraorbital involvement, frequent bilateral disease; perineural enhancement may occur.

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15
Q

Imaging hallmark of optic perineuritis.

A

Circumferential peri-sheath ‘tram-track’ or ‘doughnut’ enhancement sparing the nerve core; can extend along scleral insertion.

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16
Q

What does pain with eye movement indicate in ON?

A

Stretch of the inflamed optic nerve sheath and intraconal tissues—common in demyelinating ON.

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17
Q

Time course of visual loss in ON.

A

Worsens over several days, typically peaks by 1–2 weeks, then gradually improves.

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18
Q

What is Uhthoff phenomenon?

A

Worsening of visual function with heat/exercise, seen in demyelinating disease.

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19
Q

What is Pulfrich phenomenon?

A

Perception of distorted motion due to inter-ocular latency differences; may occur after ON.

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20
Q

Key finding from the Optic Neuritis Treatment Trial (ONTT) about IV steroids.

A

IV methylprednisolone speeds visual recovery and reduces short-term MS conversion risk; does not change final visual acuity.

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21
Q

ONTT finding on oral prednisone alone.

A

Oral prednisone alone increased the risk of ON recurrence and is not recommended as monotherapy.

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22
Q

Long-term prognosis of typical ON.

A

Most recover to 20/40 or better within months, but subtle color/contrast deficits may persist.

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23
Q

Risk of MS after a first episode of ON.

A

Strongly related to brain MRI: presence and number of white matter lesions predict higher conversion risk.

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24
Q

List ‘atypical ON’ red flags.

A

Severe/progressive vision loss, poor steroid response, bilateral or recurrent ON, longitudinally extensive MRI, perineural enhancement, hemorrhagic disc, or systemic infection/inflammation.

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25
When to test for AQP4-IgG and MOG-IgG?
If atypical features present, bilateral/long-segment ON, poor steroid response, or pediatric/recurrent ON.
26
Fundus sign suggesting neuroretinitis rather than typical ON.
Macular star exudates with optic disc edema (often infectious—Bartonella).
27
MRI clues favoring NMOSD ON.
Long-segment optic nerve/chiasm/tract involvement, marked swelling, severe enhancement; often associated with area postrema or cord lesions.
28
Clinical course of NMOSD ON.
Often severe with poor recovery; high risk of bilateral involvement and relapse.
29
MRI clues favoring MOGAD ON.
Anterior nerve + disc edema, longitudinally extensive intraorbital involvement, perineural enhancement; better recovery than NMOSD.
30
Clinical course of MOGAD ON.
Often bilateral, recurrent, steroid-responsive but relapse-prone; visual recovery generally good with treatment.
31
MRI clues favoring MS-related ON.
Short-segment unilateral intraneural enhancement with typical periventricular/juxtacortical brain lesions (Dawson’s fingers).
32
Imaging feature distinguishing optic nerve sheath meningioma from ON.
‘Tram-track’ enhancement around a normal-caliber nerve with calcification/hyperostosis on CT and lack of acute inflammatory edema.
33
How to differentiate ischemic optic neuropathy from ON clinically?
Painless acute vision loss in older vasculopathic patients with altitudinal field defect; MRI usually lacks intraneural enhancement.
34
Sarcoid optic neuropathy imaging clue.
Nodular or leptomeningeal/perineural enhancement, dural-based lesions; may involve chiasm and tracts.
35
Infectious causes of ON to consider.
Syphilis, Lyme, tuberculosis, viral (HSV/VZV/CMV), toxoplasmosis—look for systemic signs and CSF serology.
36
Toxic/nutritional optic neuropathies—key clues.
Bilateral, insidious, central/cecocentral scotomas; no enhancement; etiologies include ethambutol, methanol, B12 deficiency.
37
First-line acute treatment for moderate–severe demyelinating ON.
IV methylprednisolone (e.g., 1 g/day for 3–5 days) followed by an oral taper.
38
When to use plasma exchange (PLEX) in ON?
Steroid-refractory severe ON (especially NMOSD) within days of attack to improve visual outcomes.
39
Role of IVIG in ON.
Considered in MOGAD or refractory cases when PLEX is contraindicated; evidence evolving.
40
Long-term therapy for NMOSD to prevent relapses.
AQP4-IgG–targeted immunotherapies (e.g., eculizumab, inebilizumab, satralizumab) or rituximab/azathioprine/mycophenolate.
41
Long-term therapy for relapsing MOGAD.
Immunosuppression (e.g., rituximab, mycophenolate, azathioprine) or maintenance IVIG; individualized.
42
MS disease-modifying therapy after ON.
Initiate DMT in high-risk patients (typical MS lesions on brain MRI) to reduce relapse risk and disability accrual.
43
Pediatric ON—common etiologies.
MOGAD, ADEM-related demyelination, viral/post-infectious; more often bilateral than adults.
44
Imaging approach in pediatric ON.
MRI orbits + brain + spine if indicated; screen for longitudinally extensive lesions suggestive of NMOSD/MOGAD.
45
Optic perineuritis—typical causes.
Idiopathic, sarcoid, IgG4-related disease, syphilis, TB, granulomatosis with polyangiitis.
46
Optic perineuritis—treatment response.
Often brisk response to steroids but relapses if underlying systemic disease not addressed.
47
Essential elements to include in an ON imaging report.
Laterality, involved segments and length, enhancement pattern, perineural involvement, chiasm/tract involvement, associated brain lesions, and differentials.
48
Why use fat suppression on post-contrast orbital MRI?
To increase conspicuity of subtle intraneural enhancement against orbital fat.
49
Common pitfall: mistaking perineuritis for meningioma.
Both show ‘tram-track’ appearance; meningioma has a solid sheath mass, calcification, dural tail, slow course; perineuritis is inflammatory and steroid-responsive.
50
Common pitfall: calling ON on a motion-degraded MRI.
Motion/poor fat suppression can mimic T2 hyperintensity—correlate with clinical exam and consider repeat imaging.
51
How do corticosteroids alter MRI in ON?
They can reduce enhancement within days—image before treatment when feasible.
52
Case: STIR hyperintensity of right intraorbital optic nerve with short-segment gadolinium enhancement; normal chiasm. Diagnosis?
Typical MS-related retrobulbar optic neuritis.
53
Case: Bilateral long-segment optic nerve enhancement to the chiasm with marked edema. Most likely etiology?
NMOSD-related optic neuritis.
54
Case: Anterior optic nerve T2 hyperintensity with swollen optic disc and perineural enhancement. Most likely etiology?
MOGAD-related optic neuritis.
55
Case: Circumferential optic nerve sheath ‘doughnut’ enhancement at the globe with sparing of the nerve core. Diagnosis?
Optic perineuritis.
56
Case: Tram-track enhancing tubular sheath mass with calcified canalicular segment on CT. Diagnosis?
Optic nerve sheath meningioma (not ON).
57
RAPD meaning in unilateral ON.
Relative afferent pupillary defect indicates asymmetric optic nerve function loss.
58
Visual field pattern in ON.
Central or cecocentral scotoma is typical; altitudinal defects favor ischemic optic neuropathy.
59
Color vision finding in ON.
Red desaturation disproportionate to Snellen acuity loss.
60
OCT findings after ON.
RNFL and ganglion cell layer thinning over weeks to months indicating axonal loss.
61
When to pursue lumbar puncture in ON?
Atypical cases, suspected infection/inflammation, or when MS diagnosis is uncertain; look for oligoclonal bands.
62
Serologic tests to obtain in atypical ON.
AQP4-IgG, MOG-IgG, syphilis serology, Lyme, ACE, ANA/ANCA as indicated.
63
Expected timeline of MRI changes in ON.
Enhancement peaks in the first 2 weeks and diminishes over 4–6 weeks; T2 signal may persist longer.
64
How brain MRI influences counseling after ON.
Presence of MS-typical lesions markedly increases risk of future MS; guides DMT initiation.
65
Indications to repeat orbital MRI in ON.
Worsening symptoms, atypical course, or to document resolution/response in clinical trials.
66
Single best MRI clue for typical ON.
Short-segment intraneural enhancement of the intraorbital optic nerve with corresponding STIR hyperintensity.
67
Single best MRI clue for NMOSD ON.
Longitudinally extensive optic nerve/chiasm involvement with severe enhancement and edema.
68
Single best MRI clue for MOGAD ON.
Anterior nerve with optic disc edema and frequent perineural enhancement.
69
Key management pearl from ONTT.
Avoid oral prednisone monotherapy; use IV steroids for acute attacks when treatment is indicated.
70
High-yield differential when you see ‘tram-track’ appearance.
Optic perineuritis vs optic nerve sheath meningioma—distinguish by clinical acuity, calcification, mass effect, steroid response.
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