The optic nerve begins anatomically at the optic disc but
physiologically and functionally within the ganglion cell layer that
covers the entire retina.
ON comprise of approximately of 1.0-1.2 million ganglion cell axons.
ON is the second cranial nerve is 5 cm in length.
ON has four portions, they are:
- (i) intraocular portion
- (ii) intraorbital
- (iii) intracanalicular
- (iv) intracranial
• It is an outgrowth of the brain
• Its fibers possess no neurolemmal cells
• It is surrounded by the meninges, unlike any peripheral nerve
• Both the primary and secondary neurons are in the retina.
Intraocular segment (optic nerve head) is the shortest, The size of the
optic disc varies widely, averaging 1.76 mm horizontally and 1.92 mm
vertically.. The ophthalmoscopically visible portion is called the optic
disc. Main branches of CRA and CRV passing through the cup.
Intraorbital segment is 25–30 mm long and extends from the globe to
the optic foramen at the orbital apex. Its diameter is 3–4 mm because
of the addition of the myelin sheaths to the nerve fibres. At the orbital
apex the nerve is surrounded by the tough fibrous annulus of Zinn, from
which originate the four rectus muscles.
Intracanalicular segment traverses the optic canal and measures
about 6 mm. Unlike the intraorbital portion, it is fixed to the canal,
since the dura mater fuses with the periosteum.
Intracranial segment joins the chiasm and varies in length from 5 to 16
mm (average 10 mm). Long intracranial segments are particularly
vulnerable to damage by adjacent lesions such as pituitary adenomas
The arterial supply of the optic nerve head is as follows: the retrolaminar nerve is supplied
chiefly by pial vessels and short posterior ciliary vessels, with some help from the CRA
and recurrent choroidal arteries.
The lamina is supplied by short posterior ciliary arteries or by branches of the arterial
circle of Haller and Zinn (circle of Zinn-Haller).
The prelaminar nerve is supplied by the short posterior ciliary arteries (cilioretinal
arteries, if present) and recurrent choroidal arteries.
The nerve fiber layer is supplied by the CRA.
Proximally by the pial vascular network and by neighboring branches of the ophthalmic
Distally, it is also supplied by intraneural branches of the CRA.
Anteriorly, it is supplied by short posterior ciliary arteries and occasional peripapillary
It is supplied almost exclusively by the ophthalmic artery.
It is supplied primarily by branches of both the Internal Carotid A. and the ophthalmic artery.
Optic neuropathy is a frequent cause of vision loss encountered by
The diagnosis is made on clinical grounds.
The history often points to the possible etiology of the optic
Inflammatory. Optic neuritis, including demyelinating, parainfectious,
infectious and non-infectious, and neuroretinitis.
Ischaemic. Anterior non-arteritic, anterior arteritic, posterior ischaemic
and diabetic papillopathy.
Hereditary. Leber hereditary optic neuropathy, other hereditary optic
Nutritional and toxic
Papilloedematous. Secondary to raised intracranial pressure.
Compressive. Including secondary to an orbital lesion.
Infiltrative. Inflammatory conditions (e.g. sarcoidosis), tumours and
ETIOLOGICAL CLASSIFICATION OF ON
1. The MODE OF ONSET of visual loss is an important clue to the
etiology of the optic neuropathy. For example:
o Rapid onset is characteristic of optic neuritis, ischemic optic
neuropathy, inflammatory (non-demyelinating) and traumatic optic
o Gradual onset over months is typical of compressive toxic/nutritional
o History over years is seen in compressive and hereditary optic
2. ASSOCIATED SYMPTOMS
o In young patient history of pain associated with eye movement,
paresthesia, limb weakness, and ataxia is suggestive of demyelinating
o In elderly patients transient visual loss, diplopia, temporal pain, jaw
claudication, fatigue, weight loss and myalgia suggestive of AION.
o In children, history of recent flu-like illness or vaccination days or weeks
before vision loss points to a para-infectious or post-vaccinial optic
o Symptoms such as diplopia and facial pain are suggestive of multiple
cranial neuropathies seen in inflammatory or neoplastic lesions of the
posterior orbit or parasellar region.
o Transient diplopia and headache should raise the suspicion of increased
3. DRUG HISTORY
o Some medications are either directly or indirectly toxic to the optic
nerve. These include drugs as ethambutol, amiodarone, alcohol, and
immunosuppressive medications such as methotrexate and
4. MEDICAL HISTORY
o DM, HrT and hypercholesterolemia is common in patients with non-
arteritic ischemic optic neuropathy (NAION).
o Patients who are being treated for or have history of malignancy may
have infiltrative or para-neoplastic optic neuropathy.
5. SOCIAL HABITS
o Such as (drinking, smoking) is important in suspected toxic/nutritional
6. FAMILY HISTORY
o A detailed family history is important in diagnosing hereditary
autosomal and mitochondrial optic neuropathies.
A. Establishment is with classical optic nerve dysfunction, which are:
1. VISUAL ACUITY (VA) can be normal or impaired depending on
whether the central visual field is affected. In many cases, visual
acuity is normal, yet the patient as a large visual field defect that
spares the central field.
2. COLOR VISION can be assessed by using the Ishihara color plates
or the American Optical Hardy-Ritter-Rand (AOHRR)
pseudoisochromatic color plates. Most patients with acquired optic
neuropathy will have dyschromatopsia.
3. A RAPD can be detected by performing the swinging light-pupil test.
In the presence of bilateral symmetric optic neuropathy, a RAPD may
be absent and the briskness of pupillary constriction to light will
reflect the degree of optic nerve dysfunction.
4. DIMINSHED CONTRAST SENSITIVITY
5. DIMINISHED LIGHT BRIGHTNESS SENSITIVITY, often persisting
after visual acuity returns to normal, for instance following the acute
stage of optic neuritis.
6. VISUAL FIELD, which vary with the underlying pathology.
B. The ophthalmologist should always look for evidence of uveitis such
as cells in the anterior vitreous or signs of posterior uveitis such as
retinal vasculitis, retinitis, and choroiditis. This would indicate that
the disc swelling is secondary to a uveitic process.
C. Fundus examination may show normal, swollen, pale or anomalous
The optic disc can be examined using a direct ophthalmoscope or at
the slit-lamp using a 78D or 90D lens.
Special attention should be paid to the colour of the disc, and whether
the whole disc is paler than usual, or only a segment.
The edge of the disc should be examined to see whether it is distinct or
Lastly the retinal blood vessels should be examined as they course
over the optic nerve head to see if they are distinct and of normal and
It is important to assess whether both optic discs are equally affected,
or whether one disc is normal, less affected or is swollen.
HOW TO EXAMINE THE OPTIC DISC
1. Visual filed testing: It is an integral component of the neuro-
ophthalmic examination and is critical in the diagnosis of optic
neuropathy. Both manual kinetic or automated static perimetry can be
2. Contrast sensitivity: It is usually reduced in patients with optic
neuropathy. Testing charts such as the perri-robson charts can be
useful in patients with normal snellen visual acuity. The sensitivity
and specificity of this tool, however, is yet to be determined.
3. Electrophysiological tests: are VEP and ERG
4. OCT: optic nerve head, the peripapillary nerve fiber layer can be
analyzed. This has been useful in the follow up of patients with optic
neuritis, traumatic optic neuropathy, and Leber’s hereditary optic
Optic neuritis (ON) is a demyelinating inflammation of the optic nerve
that typically first occurs in young adulthood.
Demyelination is a pathological process in which normally myelinated
nerve fibres lose their insulating myelin layer. The myelin is
phagocytosed by microglia and macrophages, subsequent to which
astrocytes lay down fibrous tissue in plaques.
Demyelinating disease disrupts nervous conduction within the white
matter tracts of the brain, brainstem and spinal cord.
Occasionally, optic neuritis can result from an infectious process
involving the orbits or paranasal sinuses or occur in the course of a
systemic viral infection.
Demyelinating conditions that may involve the visual system include the
Isolated optic neuritis with no clinical evidence of generalized
demyelination, although in a high proportion of cases this subsequently
Multiple sclerosis (MS), by far the most common demyelinating
Devic disease (neuromyelitis optica), a very rare disease that may
occur at any age, characterized by bilateral optic neuritis and the
subsequent development of transverse myelitis (demyelination of the
spinal cord) within days or weeks.
Schilder disease, a very rare relentlessly progressive generalized
disease with an onset prior to the age of 10 years and death within 1–2
years. Bilateral optic neuritis without subsequent improvement may
According to ophthalmoscopic appearance
1. Retrobulbar neuritis,
According to aetiology
Multiple sclerosis (MS) is an idiopathic demyelinating disease involving
central nervous system white matter. Patients with multiple sclerosis
(MS) frequently have visual symptoms, and often the ophthalmologist is
the first physician consulted.
Familiarity with both the ocular and neurologic consequences of MS is
important in guiding the ophthalmologist to the appropriate diagnosis.
The prevalence of MS varies widely; it is more common in whites and in
individuals living in latitudes greater than 40 degrees from the equator.
Research is increasingly pointing to a reduced level of vitamin D in the
blood as a risk factor for development of MS.
The disease is 2-3 times more likely to affect women than men.
It is relatively uncommon in children under 10 years of age, and the
incidence is highest among young adults (25-40 years).
The onset even after the age of 50 years is not rare.
Although the cause of MS remains unknown, multiple factors appear
contributory. Epidemiologic studies suggest that genetic factors play a
Although there is a strong association with the HLA-DRB1 antigen, the
genetic associations are multifactorial.
MS significantly increased in first-degree relatives of patients with the
disease. Identical twins show a tenfold greater concordance of the
disease than do fraternal twins.
Although MS is classically considered a demyelinating disease, axonal
damage does occur early and is an integral part of the disease process.
This axonal loss manifests as "black holes" on the T1-weighted MRI
Myelin destruction is associated with local perivascular mononuclear cell
infiltration, myelin removal by macrophages, and astrocytic proliferation
with production of glial fibrils.
The term multiple sclerosis stems from the presence of these numerous
gliotic (sclerotic) plaque lesions.
Plaques are often situated in the white matter at the ventricular margins,
the optic nerves and chiasm, the corpus callosum, the spinal cord, and
throughout the brainstem and cerebellar peduncles.
PATHOLOGY IN MULTIPLE SCLEROSIS
Nonocular signs and symptoms attributable to MS may precede, follow,
or coincide with the ocular signs.
Initially, many symptoms of MS are so transient or benign that the
patient may fail to remember previous episodes.
Typically, significant episodes last for weeks or months.
The physician must ask specifically about transient diplopia, ataxia,
vertigo, patchy paresthesias, bladder or bowel dysfunction, and
Fatigue and depression are common and may precede the onset of
focal neurologic deficits.
The cerebellum, brainstem, and spinal cord may be involved singly or
simultaneously, thus producing single or multiple symptoms.
PRESENTATION OF MS
Cerebellar dysfunction: ataxia, dysarthria, intention tremor, truncal or
head titubation, dysmetria (sometimes described by the patient as poor
Motor symptoms: extremity weakness, facial weakness, hemiparesis, or
Sensory symptoms: paresthesias of face or body (especially in a bandlike
distribution around the trunk), Lhermitte sign (an electric shock-like
sensation in the limbs and trunk produced by neck flexion), pain
(occasionally, trigeminal neuralgia)
Mental changes: emotional instability, depression, irritability, fatigue;
later in the course, cognitive dysfunction
Sphincter disturbances: frequency, urgency, hesitancy, incontinence;
urinary retention leading to urinary tract infection.
It has been suggested but not proved that environmental and infectious
agents may induce attacks of MS.
Multiple sclerosis is typically quiescent during the third trimester of
pregnancy but may flare up after delivery, suggesting hormonal influences.
SOME OF THE MORE COMMON NONOCULAR
Common. Optic neuritis (usually retrobulbar), internuclear
Uncommon. Skew deviation, ocular motor nerve palsies, hemianopia.
Rare. Intermediate uveitis and retinal periphlebitis.
Uhthoff symptom, transient deterioration of vision may be brought on by
exercise or even small elevations in body temperature.
Phosphenes (bright flashes of light) with movement of the affected eye.
Photisms (light induced by noise, smell, taste, or touch).
A. Laboratory evaluation of multiple sclerosis
No test unequivocally establishes the presence of MS, which remains a
The CSF in patients with definite MS is abnormal in more than 90% of
The most common abnormalities are elevation of immunoglobulin G (IgG)
level, elevation of the IgG/albumin index, and the presence of oligoclonal
IgG bands (in CSF but not in serum).
None of these findings, however, is specific for demyelinating disease.
B. Neuroimaging in multiple sclerosis
An MRI scan with fluid-attenuated inversion recovery (FLAIR) sequencing
and gadolinium infusion is the neuroimaging study of choice for the
diagnosis and management of MS.
The MRI scan is particularly sensitive for the identification of white matter
plaques in the CNS, and it is far superior to CT scan for visualizing the
posterior fossa and spinal cord.
INVESTIGATIONS IN MS
The overall 15-year risk of developing MS following an acute episode of
optic neuritis is about 50%.
With no lesions on MRI the risk is 25%, but over 70% in patients with one
or more lesions on MRI; the presence of MRI lesions is therefore a very
strong predictive factor.
A substantially lower risk of developing MS when there are no MRI lesions
is conferred by the following factors;
1. Male gender.
2. Absence of a viral syndrome preceding the optic neuritis.
3. Optic disc swelling, disc/peripapillary haemorrhages or macular
4. Vision reduced to no light perception.
5. Absence of periocular pain.
Optic neuritis is the presenting feature of MS in up to 25%.
Optic neuritis occurs at some point in 75% of patients with established MS.
ASSOCIATION BETWEEN OPTIC NEURITIS AND
○ Subacute monocular visual impairment.
○ Usual age range 25–40 years (mean around 30).
○ Some patients experience tiny white or Coloured flashes or sparkles
○ Discomfort or pain in or around the eye is present in over 90% and
typically exacerbated by ocular movement; it may precede or accompany
the visual loss and usually lasts a few days.
○ Frontal headache and tenderness of the globe may also be present.
○ Visual acuity (VA) is usually 6/18–6/60, but may rarely be worse.
○ Other signs of optic nerve dysfunction, particularly impaired colour vision
and a relative afferent pupillary defect.
PRESENTATION OF OPTIC NEURITIS
The optic disc is normal in the majority of cases (retrobulbar neuritis); the
remainder show papillitis.
○ Temporal disc pallor may be seen in the fellow eye, indicative of previous
Visual field defects
○ Diffuse depression of sensitivity in the entire central 30° is the most
○ Altitudinal/arcuate defects and focal central/centrocaecal scotomas are
○ Focal defects are frequently accompanied by an element of
superimposed generalized depression.
Vision worsens over several days to 3 weeks and then begins to improve.
Initial recovery is fairly rapid and then slower over 6–12 months.
○ More than 90% of patients recover visual acuity to 6/9 or better.
○ Subtle parameters of visual function, such as colour vision, may
○ A mild relative afferent pupillary defect may persist.
○ Temporal optic disc pallor or more marked optic atrophy may ensue.
○ About 10% develop chronic optic neuritis with slowly progressive or
stepwise visual loss.
Indications for steroid treatment
When visual acuity within the first week of onset is worse than 6/12,
treatment may speed up recovery by 2–3 weeks and may delay the onset of
clinical MS over the short term
This may be relevant in the patients with poor vision in the fellow eye or
those with occupational requirements, but the limited benefit must be
balanced against the risks of high-dose steroids.
Therapy does not influence the eventual visual outcome and the great
majority of patients do not require treatment.
Intravenous methylprednisolone sodium succinate 1 g daily for 3 days,
followed by oral prednisolone (1 mg/kg daily) for 11 days, subsequently
tapered over 3 days.
Oral prednisolone may increase the risk of recurrence of optic neuritis if
used without prior intravenous steroid.
TREATMENT OF OPTIC NEURITIS
(IMT) reduces the risk of progression to clinical MS in some patients,
but the risk versus benefit ratio has not yet been fully defined with the
options available, which include interferon beta, teriflunomide and
A decision should be individualized, based on risk profile – particularly
the presence of brain lesions – and patient preference; most do not
commence IMT until a second episode of clinical demyelination has
occurred, though there may be an increasing tendency towards a lower
Para-infectious optic neuritis
Optic neuritis may be associated with viral infections such as measles,
mumps, chickenpox, rubella, whooping cough and glandular fever, and may
also occur following immunization.
Children are affected much more frequently than adults
Presentation is usually 1–3 weeks after a viral infection, with acute severe
visual loss generally involving both eyes.
Bilateral papillitis is the rule.
The prognosis for spontaneous visual recovery is very good, and treatment
is not required in the majority of patients.
However, when visual loss is severe and bilateral or involves an only
seeing eye, intravenous steroids should be considered, with antiviral cover
OTHER CAUSES OF OPTIC NEURITIS
Non-infectious optic neuritis
Optic neuritis affects 1–5% of patients with neurosarcoid. It may
occasionally be the presenting feature of sarcoidosis but usually develops
during the course of established systemic disease.
The optic nerve head may exhibit a lumpy appearance suggestive of
granulomatous infiltration and there may be associated vitritis.
Autoimmune optic nerve involvement may take the form of retrobulbar
neuritis or anterior ischaemic optic neuropathy.
Neuroretinitis refers to the combination of optic neuritis and signs of retinal,
usually macular, inflammation.
Cat-scratch fever is responsible for 60% of cases.
About 25% of cases are idiopathic.
Other notable causes include syphilis, Lyme disease, mumps and
Painless unilateral visual impairment, usually gradually worsening over about
○ Papillitis associated with peripapillary and macular oedema.
○ A macular star typically appears as disc swelling settles; the macular star
resolves with a return to normal or near-normal visual acuity over 6–12
Treatment: This is specific to the cause, and often consists of antibiotics.
Recurrent idiopathic cases may require treatment with steroids and/or other
Non-arteritic anterior ischaemic optic neuropathy (NAION) is caused by
occlusion of the short posterior ciliary arteries resulting in partial or total
infarction of the optic nerve head.
Predispositions include structural crowding of the optic nerve head so that
the physiological cup is either very small or absent.
Hypertension (very common), DM, hyperlipidaemia, collagen vascular
disease, antiphospholipid antibody syndrome, hyperhomocysteinaemia,
sudden hypotensive events, cataract surgery and sleep apnoea syndrome.
Patients are usually over the age of 50, but are typically younger than
those who develop arteritic ION
NON-ARTERITIC ANTERIOR ISCHAEMIC
OPTIC NEUROPATHY NAION
○ Sudden painless monocular visual loss; this is frequently discovered on
awakening, suggesting a causative role for nocturnal hypotension.
○ VA is normal or only slightly reduced in about 30%. The remainder has
moderate to severe impairment.
○ Visual field defects are typically inferior altitudinal but central,
paracentral, quadrantic and arcuate defects may also be seen.
○ Dyschromatopsia is usually proportional to the level of visual impairment,
in contrast to optic neuritis in which colour vision may be severely impaired
when VA is reasonably good.
○ Diffuse or sectoral hyperaemic disc swelling, often associated with a few
peripapillary splinter haemorrhages.
○ Disc swelling gradually resolves and pallor ensues 3–6 weeks after onset.
should include blood pressure, a fasting lipid profile and blood glucose.
It is also very important to exclude occult giant cell arteritis with
symptomatic enquiry and testing as appropriate.
Atypical features may prompt special investigations, such as neuroimaging.
Improvement in vision is common although recurrence occurs in about 6%.
About 50% of eyes achieve 6/9 or better, though 25% will only reach 6/60 or
• Fellow eye
Involvement of the fellow eye occurs in about 10% of patients after 2 years
and 15% after 5 years.
When the second eye becomes involved, optic atrophy in one eye and disc
oedema in the other gives rise to the ‘pseudo-Foster Kennedy syndrome’.
• There is no definitive treatment.
• Optic nerve fenestration has not been shown to be of benefit.
• Some authorities advocate short-term systemic steroid treatment.
• Any underlying systemic predispositions should be treated.
• Although aspirin is effective in reducing systemic vascular events and
is frequently prescribed in patients with NAION, it does not appear to
reduce the risk of involvement of the fellow eye.
Arteritic anterior ischaemic optic neuropathy (AAION) is caused by giant cell
About 50% of patients with GCA have polymyalgia rheumatica (PMR) at
diagnosis, while around 20% of PMR patients will develop GCA.
PMR is characterized by pain and stiffness in proximal muscle groups,
typically the shoulders and biceps, that is worse on waking.
Symptoms can be severe but generally respond dramatically to a low–
medium dose (initially 15–20 mg daily) of oral prednisolone.
The causative relationship between GCA and PMR remains uncertain, though
many suspect them to be different presentations of the same underlying
Arteritic anterior ischaemic optic neuropathy (AAION) affects 30–50% of
untreated patients with GCA, of whom one-third develop involvement of the
fellow eye, usually within a week of the first.
ARTERITIC ANTERIOR ISCHAEMIC
OPTIC NEUROPATHY (AAION)
○ Sudden, profound unilateral visual loss not uncommonly preceded by
transient visual obscurations (amaurosis fugax) and sometimes by double
○ Periocular pain is common.
○ Other GCA symptoms are common; most cases of AAION occur within a few
weeks of the onset of GCA, although at presentation about 20% do not have
○ Simultaneous bilateral involvement is rare but rapid involvement of the
second eye, with resultant total blindness, should always be regarded as a
○ Severe visual loss is the rule, commonly to only perception of light or worse.
○ A strikingly pale ‘chalky white’ oedematous disc is particularly suggestive of
○ Over 1–2 months, the swelling gradually resolves and severe optic atrophy
It is very poor. Visual loss is usually permanent, although, very rarely,
prompt administration of systemic steroids may be associated with partial
It is aimed at preventing blindness of the fellow eye, as visual loss in the
index eye is unlikely to improve even with immediate treatment; the second
eye may still become involved in 25% despite early steroid administration.
The regimen is as follows:
Intravenous methylprednisolone, 500 mg to 1 g/day for 3 days followed by
oral prednisolone 1–2 mg/kg/day. After 3 more days the oral dose is reduced
to 50–60 mg (not less than 0.75 mg/kg) for 4 weeks or until symptom
resolution and ESR/CRP normalization.
A typical subsequent regimen consists of reducing the daily dose by 10
mg/day every 2 weeks until 20 mg/day is reached, with tapering afterwards
titrated against ESR/CRP and symptoms, e.g. a 2.5 mg reduction every 2–4
weeks to 10 mg then a 1 mg reduction every 1–2 months.
Optic atrophy is not a disease in itself but a clinical sign.
It refers to pallor of the optic disc which results from irreversible damage to
the retinal ganglion cells and axons.
The axons of the retinal ganglion cells make up the optic nerve and continue
onto the optic chiasm, optic tract and up to the lateral geniculate body before
Injury to the retinal ganglion cells and axons anywhere along their course
from the retina to the lateral geniculate body may result in optic atrophy.
The causes of optic atrophy are numerous; they include:
3. Compression, including raised intracranial pressure
4. Nutritional deficiencies / effect of toxins, including epidemic
6. Hereditary conditions and childhood optic atrophy
Diminution of vision (central acuity/colour vision/visual field defects)
Afferent pupil defect
Optic disc pallor
Reduced number of small blood vessels on the disc surface
Attenuation (thinning) of blood vessels around the disc
Thinning of the retinal nerve fiber layer.
CLINICAL FEATURES IN OPTIC ATROPHY
Non pathologic causes of a pale disc:
1. Disc is examined with very bright light
2. Large physiologic cup in axial myopia
3. Post-cataract extraction
Other (non optic atrophy) causes of a pale disc:
1. Myelinated retinal nerve fibers
2. Optic disc coloboma
3. Optic disc hypoplasia
CAUSES OF PSEUDO OPTIC ATROPHY
Primary optic atrophy occurs without antecedent swelling of the optic
It may be caused by lesions affecting the visual pathways at any point
from the retrolaminar portion of the optic nerve to the lateral geniculate
Lesions anterior to the optic chiasm result in unilateral optic atrophy,
whereas those involving the chiasm and optic tract will cause bilateral
Compression by tumours and aneurysms
Hereditary optic neuropathies
Toxic and nutritional optic neuropathies; these may give temporal pallor,
particularly in early/milder cases when the papillomacular fibres are
PRIMARY OPTIC ATROPHY
Flat white disc with clearly delineated margins.
Reduction in the number of small blood vessels on the disc surface.
Attenuation of peripapillary blood vessels and thinning of the retinal
nerve fibre layer (RNFL).
The atrophy may be diffuse or sectoral depending on the cause and
level of the lesion.
Temporal pallor of the optic nerve head may indicate atrophy of fibres
of the papillomacular bundle, and is classically seen following
demyelinating optic neuritis.
Band atrophy is a similar phenomenon caused by involvement of the
fibres entering the optic disc nasally and temporally; it occurs in
lesions of the optic chiasm or tract and gives nasal as well as temporal
Secondary optic atrophy is preceded by long-standing swelling of the
optic nerve head.
Signs vary according to the cause and its course.
Slightly or moderately raised white or greyish disc with poorly
delineated margins due to gliosis.
Obscuration of the lamina cribrosa.
Reduction in the number of small blood vessels on the disc surface.
Peripapillary circumferential retinochoroidal folds, especially temporal
to the disc (Paton lines), sheathing of arterioles and venous tortuosity
may be present.
Include chronic papilloedema, anterior ischaemic optic neuropathy and
Intraocular inflammatory causes of marked disc swelling are sometimes
considered to cause secondary rather than consecutive atrophy.
SECONDARY OPTIC ATROPHY
Consecutive optic atrophy is caused by disease of the inner retina or
its blood supply.
The cause is usually obvious on fundus examination, e.g. extensive
retinal photocoagulation, retinitis pigmentosa or prior central retinal
The disc appears waxy, with reasonably preserved architecture.
CONSECUTIVE OPTIC ATROPHY