Neuro-ophthalmology

Neuro-ophthalmology Dr Russell Watkins

This Lecture
ONH abnormalities
ONH swelling
Chiasmal lesions
Retrochiasmal lesions

ONH Abnormalities
Congenital optic pit
Usually unilateral
Often inferotemporal
Associated with serous macular detachment
Arcuate scotomata & other field defects can occur

ONH Abnormalities
Optic disc coloboma
Deep excavation
May produce various field defects
Vision may be normal or reduced
“ Morning glory” syndrome
Unilateral coloboma with excavation filled with glial tissue & surrounded by pigment
“ Spoke-like” origin of vessels
Poor vision & associated with retinal detachment

ONH Abnormalities
Tilted disc
Usually bilateral
Associated with high myopia, astigmatism, field defects
Optic nerve hypoplasia
Small ONH with pallid halo
Poor vision & various field defects & an RAPD if unilateral
Associated with aniridia & microphthalmos

ONH Abnormalities
Myelinated nerve fibres
Congenital
White flame-shaped patches, usually adjacent to ONH, producing an enlarged blindspot

ONH Abnormalities
Optic disc drusen
Congenital, often familial, usually bilateral
Optic cup absent
May be buried or exposed on ONH, which become more prominent with age
Buried drusen are differential of ONH swelling
Exposed drusen appear as multiple glistening bodies
Autofluorescence

ONH Abnormalities
ONH drusen (cont.)
Associated with
Vitreous haemorrhage
SRNVM
Angioid streaks
Retinitis pigmentosa
Bergmeister’s papilla
Benign glial remnant (hyaloid artery) on ONH

ONH Swelling
Causes
Papilloedema
Papillitis
Anterior ischaemic optic neuropathy
Pseudopapilloedema
Accelerated hypertension
Intraocular inflammation
CRVO
Optic nerve compression

ONH Swelling
Causes (cont.)
ONH infiltration e.g. met, lymphoma
Ocular hypotony
Toxic optic neuropathy
Diabetic papillopathy

ONH Swelling
Papilloedema
Disc swelling in the presence of  ICP
VA usually unaffected until late
Visual obscurations may occur
Staged as
Early
Acute decompensated
Chronic
Terminal

ONH Swelling
Early papilloedema
Absent spontaneous venous pulsation
Nerve fibre swelling at ONH
ONH capillary dilatation ±peripapillary haemorrhage
Retinal folds

ONH Swelling
Acute decompensated papilloedema
Grossly swollen hyperaemic ONH
BV masking
Loss of cup
Haemorrhages
CWS

ONH Swelling
Chronic papilloedema
“ Champagne cork” appearance
Fewer haemorrhages
Macular star
Later, arcuate scotomata
Terminal papilloedema
Flat, pale, atrophied ONH
Arteriolar attenuation
Poor VA

ONH Swelling
Optic neuritis
Acute  VA
Paracentral or central scotoma
Pain with ocular movement
Colour desaturation
RAPD
Uthoff’s phenomenon
Pulfrich’s phenomenon
VER abnormalities in inflammatory disease only

ONH Swelling
Types of optic neuritis
Papillitis
Swollen hyperaemic ONH with haemorrhages
Retrobulbar neuritis
Normal ONH
Neuroretinitis
Papillitis with macular star

ONH Swelling
Causes of optic neuritis
Multiple sclerosis (most commonly)
Devic’s disease (neuromyelitis optica)
Young adults
Rapid, severe, bilateral visual loss
Paraplegia
Viral encephalitis
Infectious mononucleosis
HZO

ONH Swelling
Causes of optic neuritis (cont.)
Inflammation of adjacent structures (orbit, meninges, sinuses)
Granulomatous ONH inflammation e.g. TB, sarcoidosis, syphilis
Intraocular inflammation

ONH Swelling
Anterior ischaemic optic neuropathy (AION)
GCA
Other vasculitides
Arteriosclerosis
Systemic hypertension
Systemic hypotension
Carotid artery disease
Diabetes mellitus

ONH Swelling
General features of AION
 VA (variable)
RAPD
Visual field defect
Colour vision abnormalities
Variable ONH swelling
Other signs dependent on aetiology

ONH Swelling
Features of non-arteritic AION
Infarction of prelaminar ONH due to vascular insufficiency of PCA
Age of onset 45-80 yrs
Painless VA loss maximal at onset, with little recovery (seen in ~5% of cases)
Recurrences in same eye are rare
Fellow eye involved subsequently in 30 to 40%

ONH Swelling
Features of arteritic AION
Infarction of prelaminar ONH due to vascular insufficiency of PCA 2° to vasculitis
Age of onset older than 60yrs; Peak 70-80
F:M = 3:1; more common in Caucasians
Painless VA loss; can be preceding transient obscurations or profound VA  (HM-NLP); VA loss is maximal at onset
Recurrences in same eye can occur
Fellow eye involved subsequently within 10 days in 70% of cases if not treated

ONH Swelling
Other causes of ONH swelling…….

Chiasmal Lesions
Clinical features of chiasmal lesions
Headache
±Visual loss
RAPD
Colour vision abnormalities
Visual field defects
Diplopia
Endocrine dysfunction
ONH may appear normal or pale

Chiasmal Lesions
Visual field defects
Bitemporal hemianopia
Junctional scotomata
Central scotoma accompanied by contralateral superotemporal VF defect

Chiasmal Lesions
Pituitary tumours
Middle aged adults (M=F) present with visual problems or hormonal imbalance
30% of tumours non-functioning
Chromophobe adenoma (often prolactinoma) most common
Bitemporal hemianopia & optic atrophy

Chiasmal Lesions
Meningioma
Adults (esp. middle aged women)
Present with visual loss
In region of chiasm, situated at sphenoidal ridge, tuberculum sellae, olfactory groove
Often asymmetrical field loss e.g. junctional syndrome
Optic atrophy
Hyperostosis on SXR

Chiasmal Lesions
Craniopharyngioma
Children & young adults (M=F)
Slow-growing, often cystic
Present with features of  ICP, hormonal imbalance or visual loss
Various patterns of VF defect
Papilloedema or optic atrophy

Chiasmal Lesions
Aneurysms
Middle aged adults (M=F)
Present with visual loss or ophthalmoplegia
Internal carotid, anterior communicating or ophthalmic arteries
VF defect depends on site of lesion
Variable prognosis

Chiasmal Lesions
Glioma of optic nerve or chiasma
Children (75% are under 10); 60% have NF1
Very slow-growing tumour
Present with visual loss
VF defect depends on site of lesion
Optic atrophy (occasional papilloedema)

Chiasmal Lesions
Other chaismal lesions
Multiple sclerosis
Trauma
Basal meningitis
Sphenoidal sinus mucocele
Sphenoidal sinus carcinoma

Retrochiasmal Lesions
General features
All have homonymous VF defects
The further posterior the lesion, the more congruent the defect
Visual acuity is usually unaffected

Optic tract lesions
Rare
Vague visual complaints
APD on contralateral side
Normal ONH; possibly temporal pallor of ipsilateral ONH & bowtie pallor of contralateral disc
Incongruous hemianopia
Caused by posteriorly extending chiasmal lesions or vascular lesions

LGN lesions
Normal visual acuity
No APD
Normal ONH; possibly temporal pallor of ipsilateral ONH & bowtie pallor of contralateral ONH
Incongruous homonymous hemianopia
Relatively congruous homonymous quadrantanopia

Temporal lobe lesions
Normal visual acuity, no APD, normal ONH
Affect Meyer’s loop  upper homonymous quadrantanopia; only large lesions cause inferior extension of defects
Causes
Gliomas
Vascular lesions
Surgical trauma
Neuropsychiatric symptoms incl. epilepsy

Parietal lobe lesions
Normal VA, no APD, normal ONH
Complete homonymous hemianopia; occasionally lower quadrantanopia
Decreased OKN towards side of lesion
Associated with apraxia
Causes
Metastases
Glioma
Meningioma
MCA thrombosis (the artery of stroke)

Occipital lobe lesions
Congruous homonymous hemianopia
May have macular sparing
Vascular aetiology in 90% of cases
Remainder due to
Trauma (contre-coup)
Tumours

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Neuro-ophthalmology

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