Ophthalmology SC012: Neuro-Ophthalmology Flashcards
Neuro-ophthalmic examination
- VA
- Snellen chart - Pupillary exam
- Colour vision
- Ishihara colour plates - VF
- Confrontation test
- Scotoma may be difficult to detect simply by confrontation - Ocular motility
- Ophthalmoscopy
- Direct / Indirect
- Last ∵ need to dilate pupil
***Neuro-ophthalmic problems
- Pupillary disorders
- Afferent
—> RAPD
—> Visual impairment
- Efferent
—> Anisocoria
—> LND
Diseases:
- Adie’s pupil
- Horner’s syndrome
- Argyll Robertson pupils
- Motility disorders
- CN3 palsy
- CN4 palsy
- CN6 palsy
- INO
- MG - Optic nerve disease
- Papilledema (although not optic neuropathy itself)
- Papillitis
—> “Typical” optic neuritis
—> “Atypical” optic neuritis - Ischaemic optic neuropathy (ION)
—> AION (Arteritic / Non-arteritic)
—> PION - Transient monocular visual loss (TMVL) (Amaurosis fugax)
- Optic atrophy
- VF defects
- Pupillary disorders
Classification:
- Afferent vs Efferent disorder
Afferent disorders S/S:
1. **RAPD (if unilateral / asymmetrical)
2. **Visual impairment (VA, colour vision, VF defect)
Causes:
- Optic neuropathies
- Severe retinopathies (less common e.g. Total RD, CRVO, CRAO)
Efferent disorders S/S:
1. **Anisocoria (unequal pupil size) **without RAPD (if unilateral / asymmetrical)
2. **Light near dissociation (LND)
- i.e. no constriction to light but can accommodate to near objects
- dorsal aspect of Edinger-Westphal nucleus affected while ventral aspect spared
- causes: e.g. Adie’s pupil, Argyll Robertson pupil
—> Adie’s pupil: Abnormally **unilateral **large pupil, Near response slow + prolonged
—> Argyll Robertson pupil: Abnormally **bilateral ***small pupil, Near response brisk + immediate
Diseases:
1. Adie’s pupil
2. Horner’s syndrome
3. Argyll Robertson pupil
RAPD
Most patients do not have anisocoria (usually only in severe optic neuropathy e.g. total transection of optic nerve)
- but most patients only have a few optic nerve fibres affected
—> no anisocoria
Use normal side of eye as baseline
—> swinging torch test
—> abnormal side will dilate when light shine on it
Anisocoria
Mostly due to ***Efferent disorders
- Check for obvious causes (History + P/E)
- Trauma (e.g. sphincter tear)
- Iritis (e.g. Posterior synechia)
- Medications (e.g. mydriatics, miotics)
- CN3 palsy
- Severe unilateral ***afferent disorder (e.g. optic atrophy, optic nerve transection leading to total absence of light perception) - Check which eye is abnormal
- Determine degree of anisocoria in **bright + **dim lighting conditions
—> Difference in size greatest in bright light = **Large pupil is abnormal
—> Difference in size greatest in dim light = **Small pupil is abnormal
Abnormally large / Dilated pupil
Commonly due to loss of **parasympathetic tone to pupil
1. **CN3 palsy
2. ***Adie’s / Tonic pupil
3. Trauma to orbital parasympathetics
Other causes:
4. Direct damage to iris sphincter (e.g. surgery)
5. Dorsal midbrain syndrome
6. Pharmacologic mydriasis
- Adie’s / Tonic pupil
- ***Benign idiopathic condition
- Adie’s syndrome: Benign ciliary ganglionopathy: damage to ***ciliary ganglion (CN3)
- Mostly ***unilateral + in young females
- Tonic (i.e. Abnormal) pupil larger under ambient (esp. bright) light
- ***Light near dissociation of tonic pupil
- If associated with generalised hyporeflexia in limbs —> Holmes-Adie syndrome
Confirmation test (when CN3 palsy ruled out e.g. EOM normal, no diplopia, no ptosis):
Instillation of **weak cholinergic (0.1% Pilocarpine) in both eyes
- Tonic pupil constrict markedly (∵ **denervation hypersensitivity of the iris sphincters)
- Minimal / No effect on normal pupil (∵ pilocarpine concentration too low)
—> End result: “Reversal” of anisocoria after 30-60 mins
Abnormally small / Constricted pupil
Often physiological:
1. ***Physiologic anisocoria
- difference <=1 mm
- normal response to light + accommodation
- eye exam otherwise normal
Need to consider:
2. ***Horner syndrome
3. Argyll Robertson pupil (ARP)
- bilateral but may be asymmetrical
3. Pharmacologic miosis (e.g. Pilocarpine, Carbachol)
- Horner’s syndrome
Loss of ***sympathetic tone to affected eye
Types:
1. Central (1st order neuron)
- **Brainstem CVA / tumour
- **MS
- Pre-ganglionic (2nd order neuron)
- ***Apical lung lesion (e.g. Pancoast)
- Neck / thorax surgery
- Jugular vein cannulation - Post-ganglionic (3rd order neuron (along internal carotid artery))
- ***ICA dissection
- Neck surgery
- Tumours involving sellar / parasellar region
Triad of signs:
1. **Partial UL + “Inverse” LL ptosis (lower lid go upwards) (may have contralateral paradoxical UL retraction)
2. **Miosis + Dilation lag
3. ***Anhydrosis (Hemifacial) (only in Central / Pre-ganglionic, ∵ sympathetic to sweat gland already branched off along external carotid artery)
Other signs:
4. **Iris heterochromia
- in congenital case
- difference in iris colour —> **hypochromic iris in affected eye (∵ delay in development of pupil in affected eye)
Confirmation test for Horner’s
**Apraclonidine 0.5/1% (weak α1 agonist, used to ↓ IOP in glaucoma) in both eyes (Cocaine eye drops obsolete)
- Pupil dilation (30-45 mins) + UL retraction (5 min, ∵ not require absorption into eyeball) in affected eye (∵ **denervation hypersensitivity due to upregulation of α-receptors)
- Minimal / No effect on normal eye
—> End result: “Reversal” of anisocoria + ptosis
—> False negative if acute Horner’s (<1 week, ∵ takes time for denervation hypersensitivity to develop)
Localisation test for Horner’s (Optional)
Conduct >=1-2 days after confirmation test with apraclonidine:
- ***Hydroxyamphetamine 1% in both eyes, after an hour:
- Central + Pre-ganglionic lesions: Both pupils dilate (mydriasis of the pupil, ∵ post-ganglionic neuron is intact and therefore able to release NE)
- Post-ganglionic lesions: Affected pupil fails to dilate (∵ NE not available to be released in affected post-ganglionic nerve endings)
(Hydroxyamphetamine: sympathomimetic which stimulates release of stored endogenous NE from the postganglionic axon terminals into neuromuscular junction at iris dilator muscles)
OR
- ***Phenylephrine 1% (very weak) in both eyes, after an hour:
- Central + Pre-ganglionic lesions: Both pupils remain undilated
- Post-ganglionic lesions: Affected pupil dilates (∵ denervation hypersensitivity)
Imaging investigations for Horner’s
New, recent onset:
- MRI **base of brain to mid-thorax
- Urgent angiographic imaging **CTA / MRA for suspected carotid artery dissection esp. if acute onset with pain on neck / face / head
Chronic:
- Most will have normal imaging (considered idiopathic / benign e.g. congenital Horner)
Light Near Dissociation (LND)
- ∵ Lesion affecting midbrain
- Accommodative response preserved (ARP), Pupillary response absent (PRA)
Causes:
Bilateral
1. True Argyll Robertson pupils (AR pupil)
- from **Neurosyphilis
2. Pseudo-AR pupil
- DM
- Parinaud’s syndrome
- Myotonic dystrophy
- Alcoholism
—> Bilateral LND should have **Serologic testing for syphilis + ***MRI brain (including brainstem)
Unilateral
1. Adie’s pupil
2. Aberrant regeneration of CN3 after CN3 palsy
- Motility disorders
S/S:
- Diplopia
Diseases:
1. CN3 palsy
2. CN4 palsy
3. CN6 palsy
4. INO
5. MG
Diplopia
History:
- Binocular (Neuro-ophthalmic disorders) / Monocular (Eye disorders)
- Persistent / Transient (Diurnal? —> MG)
- Sudden (Vascular causes e.g. Ischaemic mononeuropathy) / Gradual + Progressive onset (e.g. Tumour)
- Horizontal (e.g. CN6 palsy) / Vertical / Diagonal (e.g. CN3 palsy) / Rotational separation
- Painless / Painful
- Same / Varying amount of image separation with different gaze positions (Concomitant vs Incomitant squint)
Treatment:
1. ***Fresnel prism
- realignment of visual axis (in vertical and horizontal diplopia but not in torsional)
- orientation described as “base-out” vs “base-in” (eg. base-out prism used in CN6 palsy to deviate light medially)
- Unilateral occlusion (Patching) of poor eye if unsuccessful
Binocular diplopia vs Monocular diplopia
Binocular diplopia
- Image from an object focused on ***non-corresponding retinal location of the 2 eyes
- Disappears when either eye is covered
- Occurs when strabismus (comitant / incomitant) acquired after 7-8 yo (diplopia image suppressed in young children)
Monocular diplopia:
- Image from an object focused on 2 retinal locations of affected eye
- Persists despite covering fellow eye
- Not neurological disorder (e.g. uncorrected refractive error, dry eyes, corneal scar, cataract)
- CN3 palsy
CN3 supply:
- Upper lid (Levator palpebrae)
- EOM (Superior rectus, Medial rectus, Inferior rectus, Inferior oblique)
- Iris (Iris / Pupillary sphincter)
S/S:
1. Ipsilateral ***ptosis
-
**Exotropia, incomitant
- ipsilateral eye abducted (intact LR) + mildly depressed (intact SO)
- worse with contralateral gaze (inability to **adduct) - Ipsilateral ***pupil dilation (+ Anisocoria) with impaired / absent pupillary light reflex
- pupil will constrict with pilocarpine 1% (and not in pharmacologically dilated pupils)
Isolated CN3 palsy causes:
1. **Microvascular disease (risk factor: DM, HT, HL)
- Pupil **spared
—> ***Medical CN3 palsy (Ischaemic mononeuropathy)
-
**Intracranial aneurysm (esp. of **PComA)
- Pupil **involved
—> **Surgical CN3 palsy (require urgent surgical treatment) - Others
- Tumour
- Trauma
NB: Confirm CN4, 6 intact (normal intortion + abduction) to rule out brainstem disorder
(From JC30:
“Surgical” CN3 palsy
—> **Peripheral parasympathetic fibres affected (run peripheral of CN3) —> **Dilated pupils + ***Ptosis
—> Central motor fibres intact (preserved eye movement)
- ***Urgent angiogram before rupture!
Medical vs Surgical CN3 palsy
Medical:
- Ophthalmoplegia with Pupillary sparing
Surgical:
- Pupillary involvement with EOM sparing)
- CN4 palsy
CN4 supply:
- Superior oblique (Intortion + Depression of eye)
S/S:
1. ***Vertical squint, incomitant
- ipsilateral eye elevated (+ extorted)
- squint (+ diplopia) worse with down gaze, contralateral gaze, ipsilateral head tilt
- ***Contralateral head tilt
- compensation to minimise torsional diplopia (hard for brain to suppress cyclodeviation / torsional image)
Causes:
- Unilateral: **Microvascular disease
- Bilateral: Congenital, **Closed head trauma —> Characteristic ***chin down position (∵ both eyes elevated)
- CN6 palsy
CN6 supply:
- Lateral rectus
S/S:
1. **Esotropia, incomitant
- ipsilateral eye **adducted (intact MR)
- worse with ipsilateral gaze
- ***Ipsilateral face-turn
- compensation to minimise horizontal diplopia
Causes:
1. Unilateral
- ***Microvascular disease (acute onset, do not worsen)
- Trauma (esp. children)
- Viral infection (in children) (e.g. middle ear infection —> near petrous bone)
- ***↑ ICP (important to rule out esp. if bilateral / associated with papilledema)
—> False-localising sign (∵ stretching of the nerve in its long intracranial course, or compression against petrous ligament or ridge of petrous temporal bone (i.e. 唔係條nerve自己有問題, 係個腦其他地方有問題整到條CN6))
Investigations:
1. ***Cranial / Orbital imaging
—> Urgent / early if papilledema present / progressive condition
—> Young patients (<55), as higher chance of space-occupying lesions (in HK esp. NPC)
—> If no gradual resolution over 3 months (spontaneous recovery can be seen ischaemic mononeuropathy)
- ***Lumbar puncture (once a mass / venous thrombosis excluded —> to evaluate CSF and its pressure)
- Internuclear Ophthalmoplegia (INO)
**MLF (Medial Longitudinal Fasciculus):
- tract of internuclear neurons within brainstem
- carries output from **Contralateral CN6 nucleus to **Ipsilateral CN3 nucleus
- **coordinates horizontal movement of both eyes during **lateral gaze (otherwise one eye move faster than the other)
- **lesion of MLF interrupts this connection —> manifests clinically as INO
Clinical features on **Contralateral gaze:
1. Failed adduction of **Ipsilateral eye
2. Out-beating nystagmus (fast phase laterally) of abducting ***Contralateral eye
3. Retains adduction on convergence
INO:
- may be unilateral / bilateral
- eyes may be straight / exotropic on primary gaze
Causes:
1. Elderly
- ***Microvascular disease commonly (usually unilateral + recover in weeks - months)
- Young adults
- ***Demyelination (Bilateral)
- Trauma - Children
- Pontine glioma
Investigations:
1. MRI brain + brainstem (***All patients)
NB: Consider **MG if **ptosis present / no nystagmus
- Myasthenia Gravis (MG)
Chronic autoimmune disorder that affect ***any age / gender
Pathophysiology:
- AutoAb to ACh receptor (Anti-AChR Ab) —> interfere with NMJ transmission in skeletal muscle
S/S:
1. Ptosis + Diplopia (50%)
- characterised by muscular fatigability (sustained upgaze)
- can mimic nearly any **oculomotor paresis (e.g. CN3, 4, 6 palsy, INO)
- but **NO pupil involvement (i.e. no Anisocoria) / nystagmus (i.e. INO)
Consider MG in any patients with unexplained ptosis / ocular movement problems
Diagnosis:
- Clinical
Investigations (**support diagnosis):
1. **Anti-AChR Ab serology (Seronegative in 10% generalised MG / 60% ocular MG (not uncommon))
2. EMG
3. Tensilon (Edrophonium) / Ice test / Sleep test
4. Thyroid function (associated autoimmune hyper / hypothyroidism e.g. **Graves’)
5. CT thorax (*thymoma)
Optic nerve diseases (Optic neuropathy)
Diseases:
1. Papilledema (although not optic neuropathy itself)
- Papillitis
- “Typical” optic neuritis
- “Atypical” optic neuritis - Ischaemic optic neuropathy (ION)
- AION (Arteritic / Non-arteritic)
- PION - Transient monocular visual loss (TMVL) (Amaurosis fugax)
- Optic atrophy
(Optic neuropathy causes:
1. **Ischemic optic neuropathy
2. **Optic neuritis
3. ***Compressive optic neuropathy
4. Infiltrative optic neuropathy
5. Traumatic optic neuropathy
6. Mitochondrial optic neuropathies
- Nutritional optic neuropathies
- Toxic optic neuropathies
- Hereditary optic neuropathies)
Optic disc swelling (+ SpC Revision)
Pathophysiology (UpToDate):
Disruption of axoplasmic flow within the nerve
—> Obstipation of intra-axonal fluid
—> Swelling of the axons and leakage of water, protein, and other cellular contents into the extracellular space of the optic disc
—> Optic disc edema
Fundal signs:
1. **Elevation of optic disc (can be **physiological esp. in short eye ball)
2. **Loss of optic cup (can be **physiological esp. in short eye ball)
3. **Blurred disc margin
4. Vascular tortuosity
5. +/- Disc **hyperaemia (dilation of disc capillaries) / pallor
6. +/- Disc haemorrhages (Peripapillary haemorrhage: bleeding in nerve fibre layer / retinal haemorrhage)
7. Dilation + Tortuosity of retinal veins
8. Soft exudates / Cotton wool spots
Once swelling resolved —> End up with pale neuroretinal rim
DDx:
1. Systemic diseases (Bilateral)
- **Malignant hypertension
- **Papilledema (Optic disc swelling secondary to ↑ICP)
—> Hydrocephalus / Meningitis / SAH / Brain abscess / Brain tumour / Dural venous sinus thrombosis / Pseudotumour cerebri
2. Optic neuropathy (Unilateral)
- **Inflammatory
- **Ischaemic
- **Infectious
- **Compressive
Causes (**4 “I”s):
1. **ICP↑ (Papilledema)
2. **Inflammation (e.g. Papillitis (by anterior optic neuritis))
3. **Infarction (e.g. AION)
4. Infiltration (e.g. tumour, sarcoidosis)
5. Compression (i.e. compressive optic neuropathy) (e.g. TED)
6. Toxins (e.g. Ethambutol)
7. Malignant hypertension, Anaemia, Pregnancy
Pseudo-papilledema (Elevated disc **without edema of retinal nerve fibre layer):
- Asymptomatic (mostly) —> Normal people
- Vessels normal
- Unilateral / Bilateral
- occurs in:
—> **Hyperopic discs (crowding of nerve fibres entering disc)
—> ***Tilted optic disc (developmental variant)
—> Optic disc drusen (VF defect, non-progressive)
- Papilledema
- Swelling of optic discs from ***↑ ICP
- Vision initially unaffected but may have **recurrent **transient visual obscurations (TVO) —> lasting seconds of “greyout”, flickering, BOV
- Others symptoms of ↑ ICP:
—> Headache
—> N+V
—> CN6 palsy with diplopia (“false localising sign”)
Causes of ↑ ICP:
1. Intracranial SOL
- Tumour
- Epidural / Subdural haematoma
- Intracerebral edema / haemorrhage
- Trauma
- Meningitis
- Encephalitis
- Dural venous thrombosis - Idiopathic intracranial hypertension
- Pseudotumour cerebri
Management (**Urgent):
1. Immediate **CT / MRI scan
2. ***Lumbar puncture (once a mass / venous thrombosis excluded —> to evaluate CSF and its pressure)
NB:
- Chronic papilledema can cause **permanent optic nerve damage (Optic atrophy) if not relieved
- Bilateral optic disc swelling in **malignant hypertension, **anaemia, **pregnancy are NOT caused by ↑ ICP —> should be differentiated from True papilledema
Idiopathic intracranial hypertension
Symptoms:
- Headache
- Transient visual loss (lasting seconds, often triggered by postural changes)
- Diplopia
- Tinnitus, Dizziness, N+V
Diagnosis:
- ↑ ICP with papilledema
- **Normal brain imaging
- **Normal CSF composition
Associated factors:
- Female
- Obesity
- Medications: OCP, Tetracycline, Nalidixic acid, Vit A / derivatives, Systemic steroid withdrawal
Treatment:
1. Weight loss (if overweight)
2. Discontinue causative medication(s)
3. Acetazolamide +/- Furosemide
4. Surgery (if above measures ineffective for papilledema / intractable headache)
- Optic nerve sheath fenestration
- Lumboperitoneal shunt
- Papillitis (by Anterior optic neuritis)
- Optic nerve inflammation —> **Inflammatory edema of disc (but majority of optic neuritis do NOT have papillitis (i.e. **Retrobulbar neuritis))
-
**Similar appearance to papilledema, BUT
—> Papilledema: **Bilateral, vision initially unaffected
—> Papillitis: ***Unilateral / Asymmetrical (commonly), vision impaired
Causes:
1. Demyelination (MS)
2. GCA
3. Infection
4. Nutritional
5. Toxicity
6. Trauma
Optic neuritis
“Typical” (**Demyelinating) optic neuritis
- commonly young females (18-45 yo)
- unilateral, with periorbital discomfort / pain with **eye movement
- features of optic neuropathy in affected eye
—> **RAPD
—> **Impaired VA, **colour vision, VF
- acute (hours) - subacute (days) onset which progresses to peak severity at 1-2 weeks, followed by spontaneous gradual recovery over 1-2 months
- frequently associated with **Multiple sclerosis (higher risk of developing MS later in life), but can occur in isolation
—> further ***MRI imaging to stratify risk of developing MS
Management:
1. ***MRI brain
- white matter lesions related to risk of MS development
- Acute treatment
- Observation (∵ spontaneous recovery)
- Steroid
—> IV (3 days) —> Oral (11 days) to hasten recovery within first 4-6 weeks (no difference with long-term outcome) (Oral steroid alone ***CI as may ↑ recurrences) - Long-term treatment (MS progression modifying treatment)
- Ocrelizumab, Beta-IFN, Glatiramer etc.
“Atypical” optic neuritis (NOT follow all of above features)
- occurs with:
—> **Neuromyelitis optica (NMO) (brain + spine imaging)
—> **Syphilis
—> **HIV
—> **SLE
—> ***RA
—> Post-viral infection (children)
Management:
- Workup for causes of “Atypical” optic neuritis e.g. brain + spine imaging for NMO, blood tests for syphilis, HIV, SLE, RA
- Ischaemic optic neuropathy (ION)
**Acute, **painless visual loss in adults, from ***microvascular infarction of optic nerve
2 types:
1. Anterior (AION)
- more common
- usually unilateral
- **chalky white **swollen optic disc swollen, **altitudinal VF defects, **peripapillary haemorrhage
- Impaired flow from posterior ciliary arteries (PCA)
- 2 variants: **Arteritic / **Non-arteritic
- common signs for ALL AION:
—> RAPD
—> Altitudinal VF loss
—> Swollen optic disc
- Posterior (PION)
- location: Retrobulbar
- less common
- usually bilateral
- optic disc normal (∴ do NOT rule out ION even if optic disc normal), variable VF defects
- ***systemic hypotension (e.g. during cardiac bypass / prolonged spinal surgeries / shock)
- sometimes seen with systemic vasculitis
Arteritic AION
- Initially **unilateral, but may **rapidly become bilateral
- Elderly (>60 yo)
- Associated with **Giant cell arteritis (GCA) (i.e. **Temporal arteritis)
- Suspect Arteritic AION when:
—> **Elderly
—> **Severe visual loss
—> Optic disc ***very pale
Other symptoms:
- Headache
- **Scalp tenderness (e.g. hair combing)
- **Jaw claudication (pain with chewing)
- ***Polymyalgia rheumatica: Proximal muscle pain + stiffness
- Constitutional (fever, malaise, anorexia, weight loss)
Investigations:
- ESR, CRP, Plt (all ↑)
- ***Temporal artery biopsy (within 2 weeks of starting steroid if possible)
Treatment:
- Immediately start ***high dose steroids (do NOT wait for biopsy result, ∵ can prevent other eye involvement)
- Transient monocular visual loss (TMVL) (Amaurosis fugax)
- Commonly ∵ ***Emboli in adults
—> last seconds - mins
—> may affect entire / only upper / lower half of VF - Check for
1. **Ipsilateral carotid artery stenosis (carotid bruit)
2. **Cardiac source of emboli (check pulse, ECG)
3. ***GCA - Check for other causes e.g.
—> Migraine
—> Hyperviscosity, Hypercoagulability
—> MS
—> Papilledema
—> Ocular pathologies - Longer duration (20-40 mins) + Associated photopsia / headache: suggestive of vasospasm cause (Migraine) rather than embolic causes
- Optic atrophy
***End result of all optic neuropathy —> extensive retinal ganglion cell loss
Clinical features:
- Impaired VA, VF, colour vision
- RAPD (if unilateral / asymmetrical)
- ***Pale optic disc
Causes:
1. **ALL types of optic neuropathies (e.g. ischaemic, traumatic, toxic, compressive, glaucoma, Leber hereditary optic neuropathy (LHON))
2. **Papilledema (long-standing)
3. Secondary to extensive ***Retinopathy (e.g. CRAO, CRVO, Retinitis pigmentosa)
Investigations (if no obvious cause from History):
1. Intracranial / Orbital imaging (e.g. CT / MRI)
2. Selected serologies (e.g. Syphilis, Autoimmune markers, B12)
Visual field loss terminology
Terms to describe VF loss:
1. Scotoma
- area of abnormal / decreased / absent vision within an otherwise ***intact VF (i.e. focal localised VF defects)
- Hemianopia
- loss of **half of VF
- usually refers to **right / left VF loss in **either eye
- **altitudinal hemianopia: loss of superior / inferior VF - Homonymous hemianopia
- loss of either right / left VF in both eyes (stroke most common cause) - Bitemporal (Heteronymous) hemianopia
- loss of temporal VF in ***both eyes
(5. Binasal hemianopia
- exceedingly rare, with only case reports / small case series reporting various causes e.g. hydrocephalus, neurosyphilis, intracranial tumour)
Common causes of VF defects
- Central scotoma
- **Optic nerve lesions (e.g. Optic neuritis, Toxic optic neuropathy)
(- Can also be due to **Retinal lesions e.g. AMD, Macular hole, Central serous retinopathy) - Altitudinal defects
- ***Optic nerve lesions (e.g. AION, Glaucoma) - Bitemporal defects
- Chiasmal lesions (e.g. Pituitary adenoma, Craniopharyngioma) - Homonymous hemianopic defects
- Retrochiasmal (optic tract / radiation, occipital cortex) lesions (e.g. vascular, tumour, demyelination)
Summary
- Testing of ***both VA + VF critical in evaluation of the abnormal optic disc
- A patient with a unilateral optic neuropathy may have equal + reactive pupils in ambient light, but a positive swinging-flashlight test (RAPD+)
- A blurred disc margin is NOT specific for papilledema, check for other S/S (e.g. ↑ ICP)
- Chiasmal lesions are the most likely cause of Bitemporal field defect
- If one of following abnormal:
- Pupil
- Lid position
- Ocular motility
—> check for involvement of one another to aid in diagnosis - If ocular motility impaired —> check CN5 (corneal sensation) + CN7 (facial muscles) for possible brainstem lesions
- Slowly progressive visual loss / CN palsy —> suggest compression from **expanding lesion (e.g. intracranial / orbital tumour / aneurysm)
- Acute visual loss / diplopia —> suggest ***vasculopathies (acute onset but does not progress)
DDx of Pale neuroretinal rim (i.e. Optic neuropathy / Optic disc atrophy) (SpC Revision)
Rmb: Glaucoma early stage: neuroretinal rim is still pink (differentiate from other non-glaucomatous optic neuropathy where neuroretinal rim is pale)
- Inflammatory optic neuropathy (e.g. optic neuritis (e.g. Multiple sclerosis))
- Ischaemic optic neuropathy (e.g. NAION, AION)
- Compressive optic neuropathy (e.g. pituitary tumor, dysthyroid optic neuropathy)
- Infiltrative optic neuropathy (e.g. leukemia, lymphoma)
- Traumatic optic neuropathy (e.g. blunt/penetrating ocular injury)
- Radiation optic neuropathy (e.g. radiation therapy)
- Infectious optic neuropathy (bacteria, viruses, fungi, parasites)
- Nutritional deficiency optic neuropathy (e.g. B12, folate deficiency)
- Toxic optic neuropathy (e.g. ethambutol, methanol)
- Hereditary optic neuropathy (e.g. Leber’s hereditary optic neuropathy)
