1. The document provides an overview of approaches to evaluating vision loss, including determining whether it is monocular or binocular and transient or persistent. 2. Examinations should include visual acuity, color vision, visual fields, pupils, and examination of the eyes and optic discs. 3. Causes of transient and acute vision loss are discussed, including optic neuropathies, ischemic events, migraine, and PRES. 4. Progressive vision loss may be due to compressive lesions, glaucoma, or retinal disorders.

1. Approach to vision loss
Dr Vaishal Shah
SR Neurology
GMC, Kota

2. General approach
• Decide whether it is monocular or binocular.
• Transient / persistent
Examination –
Visual acuity with pin hole
Colour vision. Pseudoisometric colour plates. - Early optic nerve
disease may manifest as a reduction in saturation or brightness of
colors

3. General approach
Field testing – Confrontation in both eye separately.
• An abrupt change across the horizontal axis in one eye suggests optic
nerve disease, and an abrupt change across the vertical meridian in
both eyes indicates visual loss of intracranial origin.
• Kinetic ( goldmann) perimetry
• Automated static perimetry.

5. General approach
Pupil – RAPD localise lesion to optic nerve. Exceptions include central
or large-branch retinal artery occlusions and large retinal
detachments.
Local eye examination – Ophthalmologist’ domain. Gross
examination can be done including proptosis, congestion.
• ‘‘If you can’t see in, the patient can’t see out.’’
Fundus – Disc – o –centric. Habit of seeing macula as well.

6. TRANSIENT MONOCULAR VISION LOSS

7. TRANSIENT BINOCULAR VISUAL LOSS
• Other than transient visual obscuration in patient of bilateral papilledema,
it is always due to transient dysfunction of visual cortex.
• Visual migraine aura – M/C cause in age < 40 years
• TIA – old patients. Needs thorough cardiac/ vertebrobasilar workup.
• PRES – a/w headache, altered mental status. Seen in preeclampsia,
Cyclosporine chemotherapeutic agents
• Rarely – Occipital seizure

8. Migraine
• Typically patients see small scotoma surrounded by jagged, luminous,
shimmering edges.
• Scotoma enlarges over several minutes, then gradually disappears
followed by hemicranial throbbing headache.
• Patient might experience visual aura without headache – acephalgic
migraine.

9. SUDDEN MONOCULAR VISUAL LOSS
WITHOUT PROGRESSION
• Localise to eye or optic nerve.
• Classic feature of unilateral optic neuropathy. Central visual loss, clear
view through ocular media, RAPD, swollen or pale optic disc.
• Important to differentiate between lesion of macula vs optic nerve
• Usually Painless, visual distortions, appropriate colour vision
involvement, vision is slow to recover after bright light, absence of
RAPD – Macular disease ( M/C – CSR )

13. SUDDEN BINOCULAR VISUAL LOSS WITHOUT
PROGRESSION
• If trauma history is negative, then most commonly by stroke involving
retrochiasmal visual pathways.
• Simultaneous bilateral ischemic optic neuropathy.
• Chiasmal compression due to pituitary apoplexy – headache, diplopia,
altered mental status, hemodynamic shock. Presentation might not
be severe always.

15. ACUTE ONSET VISUAL LOSS
Sudden onset painful monocular vision loss that subsequently worsens is
commonly due to optic nerve inflammation (optic neuritis). Fundus - normal
• Progresses over hours to days before stabilizing and then improving. MS –
visual recovery good.
• NMO – visual recovery poor.
• Other causes – ADEM, Anti MOG, CRION, post vaccine associated optic
neuritis.
LHON - Produces acute or subacute painless, often permanent, central
visual loss, usually in young adult men. Monocular initially, other eye
becomes affected within 6 months.

16. ACUTE ONSET VISUAL LOSS
LHON continued…
• Visual recovery is variable and infrequent, and depends on the
mitochondrial DNA mutation.
• In the acute phase, the classic triad of ophthalmic findings includes
Telangiectatic vessels around the optic disc
Nonedematous elevation of the optic disc
Absence of leakage from the disc on fluorescein angiography.

18. CHRONIC PROGRESSIVE VISUAL LOSS

19. CHRONIC PROGRESSIVE VISUAL LOSS
• Visual field defects of patients with chiasmal or retrochiasmal lesions
may go unnoticed as long as central visual acuity is spared.
• Bitemporal visual field defects that respect the vertical meridian are
diagnostic of lesions, almost always compressive in etiology, at the
optic chiasm – Pituitary adenoma, meningioma, craniopharyngioma,
aneurysm. – MRI is mandatory.

20. CHRONIC PROGRESSIVE VISUAL LOSS
• Retinal disorders like vitamin A deficiency retinopathies, toxic
retinopathies, carcinoma associated and melanoma associated
paraneoplastic retinopathies needs to be differentiated from bilateral
optic neuropathies - Optic nerve pallor may be present in all.
Elecroretinogram is helpful.
• Primary open angle glaucoma.
• To rule these disorders – Ophalmologist opinion is required.

22. Bilateral optic nerve drusen

23. 37/F, 5 week prior to presentation,
she had decreased vision in the
inferior visual field in the right eye,
which worsened over 4 to 5 days. She
had no eye pain, pain with eye
movement, or headaches. She had a
brain MRI that showed no optic nerve
enhancement. Her vision failed to
improve during the following 4 weeks.
Visual acuity was 6/24. Colour vision
was normal but mild red desaturation
was present in right eye. RAPD was
present in right eye. Visual fields
showed an inferior arcuate defect in
the right eye.
Diagnosis?
Right NAION

24. A 33-year-old woman was referred
for an 8-day history of progressive
decreased vision in her left eye.
One day prior to the onset of visual
loss, she had experienced pain
over her left forehead that
worsened with eye movements.
Her past medical history was
unremarkable, and she was on no
medication. visual acuity was
20/400 with no color perception
and a dense relative afferent
pupillary defect. Visual field testing
showed a large dense central
scotoma. Motility was full.
Diagnosis?...Next investigation?? Optic neuritis
MRI brain with orbital cuts

25. Temporal pallor after 2
months

26. A 55-year-old woman presented with
progressive 6 months of painless
visual loss in the left eye. She had
been evaluated by an ophthalmologist
1 month prior to this presentation, at
which time she had visual acuity of
6/12 in the left eye with decreased
colour vision, left RAPD, an enlarged
blind spot in the left eye. Funduscopic
examination showed temporal pallor
of the left optic disc. MRI of the brain
showed nonspecific white matter
changes, and a diagnosis of optic
neuritis, possibly related to multiple
sclerosis, was made by
ophthalmologist. Patient came to
neurologist for second opinion. MRI
repeated.
Diagnosis? Optic nerve sheath meningioma

27. • Optic disc edema with
macular star
Neuroretinitis

28. • A 65-year-old woman had episodic visual loss. In her twenties and
thirties, she had experienced episodic headaches with nausea,
photophobia, and phonophobia, but with no associated visual
phenomena. 2 years before the present examination she had begun
to experience episodes of bilateral visual disturbances, which she
described as the appearance of gold line just off the center of vision
in both eyes. The line enlarged over approximately 5 to 10 minutes,
enclosing a central area. After 20 minutes, the process gradually
broke up like a puzzle and normal vision was restored. She denied
associated headache or eye pain. Diagnosis??
Acephalgic migraine with visual aura

29. An 82-year-old man reported acute binocular visual
loss. His past medical history was notable for coronary
artery disease with previous myocardial infarction and
heavy cigarette use. On examination, visual acuity was
6/30 in both eyes and color vision was impaired in
both eyes. Pupils, motility, and fundi were normal.
Next investigation?

30. Thank you