**Presentation on Optic Nerve, Neuritis, and Papilledema** The optic nerve (cranial nerve II) is essential for vision, transmitting visual information from the retina to the brain. Optic neuritis refers to inflammation of the optic nerve, often associated with conditions like multiple sclerosis, leading to vision loss, pain, and color desaturation. Papilledema, on the other hand, is optic disc swelling due to increased intracranial pressure, commonly linked to brain tumors, hydrocephalus, or meningitis. Both conditions require prompt diagnosis and management to prevent permanent vision impairment. This presentation will cover the anatomy, functions, pathologies, clinical manifestations, and diagnostic approaches related to these optic nerve disorders.

3. GROUP D
GANDAKI MEDICAL COLLEGE
TODAY’S TOPIC FOR PRESENTATION
ROLL
NO
TOPIC PRESENTERS
57 Anatomy of Optic Nerve
and Optic Neuritis
Roji Basnet
56 Papilloedema Rekha Sapkota

4. Anatomy of Optic Nerve and Optic
Neuritis
PRESENTER :
ROJI BASNET
Roll no: 57
GROUP - D

5. EMBRYOLOGY &
MORPHOLOGY
PARTS OF OPTIC
NERVES
INTRODUCTION
BLOOD SUPPLY OF
OPTIC NERVE
TOPICS ON OPTIC
NERVES

6. OPTIC NERVE

7. INTRODUCTION ON OPTIC NERVE
• Optic nerve : 2nd Cranial Nerve
• It starts from the optic disc & extends up to optic chiasma (where
each nerve meets).
• It is the backward continuation of the nerve fibre layer of retina
(axons of the ganglion cells).
• It also contains the afferent fibres of light reflex & some centrifugal
fibres.
• The optic nerve is about 47-50 mm in length.

9. Morphologically & Embryologically, the optic nerve is comparable to
the sensory tract (white matter) of the brain because :
1. The optic nerve is an outgrowth of the brain.
2. It is not covered by neurilemma (so does not regenerate when cut).
3. The fibres of the nerve (about 1 million in number) are very fine
about 2 to 10 μm in diameter.
4. Covered by meningial sheaths ( DAP).
5. Both the primary and secondary sensory neurons are in the retina.
 MORPHOLOGY AND EMBRYOLOGY

10. PARTS OF THE
OPTIC NERVE

11. Intraocular (1mm)
PARTS OF
OPTIC NERVES
Intraorbital
(30mm)
Intracranial
(10mm)
Intracanalicular(6-
9mm)

12. 1. Intraocular Part (Optic papilla/ Optic disc)
• Extends from optic disc to back of the eye ball.
• It is the shortest segment (1mm) and has a diameter of (1.5mm).
• Pierces choroid & sclera sieve like structure-LAMINACRIBOSA
• It is further divided into 4 portions :
(from anterior to posterior) :
a. Surface nerve fibre layer
b. Prelaminar layer
c. Lamina cribrosa region
d. Retrolaminar region

14. a) Surface Nerve Fibre Layer
• Composed of axonal bundles (nerve fibres
and astrocytes)
• ILM of Elschnig: Separates it from the
vitreous
. Central meniscus of kuhnt: Thickened
continuation of ILM
. Intermediary border tissue of Kuhnt:
Separates all layers of retina (except NFL)
from the optic nerve.

15. b. Prelaminar Region
• Main constituents- neuronal cells and astro-glial cells.
• Border tissue of Jacoby (astrocytes)- separates the choroid from the optic
nerve.

16. c. Lamina Cribrosa
• Sieve like structure
• Bundles of optic nerve fibres leave through it
• Border tissue of Elchnig : collagenous tissue with astrocytes

17. d. Retrolaminar region
• O.N acquires myelin sheath in this region thus there is characteristic
increase in diameter of optic nerve from 1.5 to 3mm.
• ASTROCYTES COUNT- decrease

18. 2. Intra Orbital Part
• Extends from back of the eyeball to the optic foramina
• sinuous course (wavy) to give play for eye movements
• Optic nerve in this part is covered by dura, arachnoid and pia mater.
• Posteriorly, near the optic foramina, it is closely surrounded by the
annulus of Zinn and the origin of 4 rectus muscles. Some fibres of
superios rectus muscle are adherent to its sheath here, and accounts
for the painful ocular movements seen in retrobulbar neuritis.
• Anteriorly, the nerve is separated from the ocular muscles by the
orbital fat.

19. • Inferomedially, central retinal artery & vein enter the nerve about
10mm from the eyeball.
• Superiorly from lateral to medial side, the ophthalmic artery, vein and
nasociliary nerve cross the optic nerve.

20. 3. Intracanalicular Part
• This part is closely related to ophthalmic artery
which lies inferolateral to it.
• Sphenoid & posterior ethmoidal sinuses lie
medially & are separated by only thin bony
lamina (optic nerve is therefore involved in sinus
infection )
Applied : This accounts for retrobulbar neuritis
following infection of the sinuses.

21. 4. Intracranial Part
• Lies above the cavernous sinus and converges with its fellow to form
optic chiasma.
• Ensheaths in pia mater
• Receives arachnoid and dural sheaths at the point of entry into the
optic canal.

22. BLOOD SUPPLY
OF OPTIC NERVE

23. BLOOD SUPPLY OF OPTIC NERVES
• Intraocular (Optic Nerve Head)
Arterial supply :
Surface layer - through the Capillaries from retinal arterioles
Prelaminar region- centripetal branches of peripapillary choroid
Laminar region
Retrolaminar part - Centrifugal branches of central retinal artery ,
centripetal contribution from pial branches of choroidal arteries
Venous drainage - central retinal vein
short post. ciliary arteries & arterial circle of
zinn haller

24. • Intraorbital part
Arterial supply- by periaxial system and axial system of vessels
Venous drainage- by central retinal vein
• Intracanalicular part
Arterial supply- central retinal artery
Venous drainage- central retinal vein
• Intracranial part
Arterial supply- by perichiasmal and ophthalmic artery
Venous drainage- central retinal vein

25. Figure Showing Blood supply in different
parts of Optic Nerve

26. INTRODUCTION
TOPICS ON OPTIC
NEURITIS
ETIOLOGICAL CLASSIFICATION
PATHOPHYSIOLOGY AND SIGNS
Differential Diagnosis,
Investigations
ANATOMICAL TYPES,
Ophthalmoscopic features
Evolution, Recovery and
Complications
TREATMENT

27.  Optic Neuritis
• Optic neuritis includes inflammatory and demyelinating
disorders of the optic nerve.
• It causes acute, usually monocular visual loss.
• Highly associated with Multiple Sclerosis(15-20% cases)
• Usually between 20-40 years of age.

28.  Etiological classification:
1. Idiopathic : In a large proportion of cases, the underlying cause is
unidentifiable.
2. Hereditary optic neuritis (Leber's disease)
3. Demyelinating disorders : These are by far the most common cause of
optic neuritis. These include :
Multiple sclerosis,
Neuromyelitis optica (Devic's disease)
Diffuse periaxial encephalitis of Schilder.
4. Parainfectious optic neuritis : It is associated with various viral infections
such as measles, mumps, chickenpox, whooping cough and glandular fever.

29. 5. Infectious optic neuritis : may be sinus related (with acute ethmoiditis) or
associated with cat scratch fever, syphilis (during primary or secondary
stage), tuberculosis, lyme disease and cryptococcal meningitis in patients
with AIDS.
6. Autoimmune disorders : Associated with optic neuritis include :
Sarcoidosis,
Systemic lupus erythematosus,
Polyarteritis nodosa,
GuillainBarre syndrome & Wegener's granulomatosis.
7. Toxic optic neuritis/ Toxic Amblyopia :
Agents include: Tobacco, Ethyl Alcohol, Methyl Alcohol, Lead Arsenic,
Cannabis
Drugs include: Quinine, Chloroquine

30. Association between optic neuritis and multiple sclerosis
• MS is a chronic condition in which the immune system mistakenly
attacksTrusted Source the protective myelin sheath that surrounds the nerve
cells. These attacks damage these cells, causing inflammation and
permanent scarring in the brain, spinal cord, and other nerves.
• In MS, optic neuritis occurs when the immune cells attack the healthy,
protective myelin sheath that surrounds the optic nerve, mistaking them for
invading cells. This causes the myelin to swell up, which can lead to optic
nerve damage.
• The swelling disrupts the signals between the eye and the brain, causing
visual disturbances that can include double vision, blurred vision, or blind
spots of MS in up to 30%.

31. Pathophysiology

32.  Anatomical Types:
Optic neuritis can be classified into three anatomical types:
1. Papillilis (Optic Discs) : It refers to involvement of the optic disc in
inflammatory and demyelinating disorders. This condition is usually
unilateral but sometimes may be bilateral.
2. Neuroretinitis (Optic Disc + Retina) :refers to combined involvement of
optic disc and surrounding retina in the macular area.
3. Retrobulbar neuritis :is characterized by involvement of optic nerve
behind the eyeball. Clinical features of acute retrobulbar neuritis are
essentially similar to that of acute papillitis except for the fundus
changes and ocular changes

34. Typical and Atypical optic neuritis
The term typical optic neuritis refers to the one associated with
demyelination, particularly multiple sclerosis.
Whereas,
The term atypical neuritis is labeled for the one associated with causes
other than demyelination disorders.

35.  Clinical features
Symptoms
Optic neuritis may be asymptomatic or may be associated with following
symptoms:
 Visual loss : Monocular sudden, progressive and profound visual loss.
 Dark adaptation may be lowered.
 Visual obscuration in bright light is a typical symptom of acute optic
neuritis.

36. Visual loss in Optic neuritis

37.  Impairment of colour vision is always present in optic neuritis.
Typically, the patients observe reduced vividness of saturated colours.
 Movement phosphenes and sound induced phosphenes may be
perceived by patients with optic neuritis.
 Uhthoff’s symptom : Episodic transient obscuration of vision on
exertion and on exposure to heat, which recovers on resting or moving
away from the heat occurs in patient with isolated optic neuritis.

38.  Pulfrich's phenomenon : Depth perception;
Particularly for the moving object may be
impaired.
 Pain : Patients may complain of mild dull eye
ache. lt is more marked in patients with
retrobulbar neuritis than with papillitis. Pain is
usually aggravated by ocular movements,
especially in upward or downward.

39. The most common symptom of optic neuritis is decreased vision, which
happens suddenly or quickly over the course of 1-3 days. Many people
describe the blurring and darkening of their vision as “dimming” or like
“the brightness is turned down.” Optic neuritis does not affect your glasses
prescription.

40.  Signs
• Visual acuity is usually reduced markedly.
• Colour vision is often severely impaired
• Pupil shows ill-sustained constriction to light. Marcus Gunn pupil
which indicates relative afferent pupillary defect (RAPD) is a
diagnostic sign. It is detected by the swinging flash light test.
• Visual field changes: The most common field defect in optic neuritis is
a relative central or centrocaecal scotoma.

41.  Ophthalmoscopic features:
• Papillitis is characterized by hyperaemia of the disc and blurring of the
margins. Disc becomes oedematous and physiological cup is obliterated.
Retinal vein are congested and tortuous. Splinter hemorrhages and fine
exudates may be seen on the disc. Slit lamp examination may reveal
inflammatory cells in the vitreous.
• Inflammatory signs may also be present in the surrounding retina when
papillitis is associated with macular star formation and the condition is
labelled as 'neuoretinitis’.
• ln majority of the cases, with retro-bulbar neuritis fundus appears
normal and the condition is typically defined as a disease where neither
the ophthalmologist nor the patient sees anything. Occasionally,
temporal pallor of the disc may be seen.

42. Hs
B
Optic disc
Hyperemia
Hemorrhage
Blurring of Disc
margins
Papillitis

43. Neuroretinitis
MACULAR STAR
FORMATION

44. Retrobulbar

45. • Contrast sensitivity is impaired.
• Visually evoked response (VER) shows reduced amplitude and delay
in the transmission time.
• Fundus fluorescein angiography reveals mild to moderate leak in
early phase which increases with the time.

46.  Differential Diagnosis
• Papillitis should be differentiated from:
Papilloedema
Ischaemic optic neuropathy,
Anterior orbital compressive neuropathy
Pseudopapilloedema
• Acute retrobulbar neuritis should be differentiated from:
Hysterical blindness
Cortical blindness
Indirect optic neuropathy.

47.  Investigations
1. Multifocal VEP is helpful in making early diagnosis of optic neuritis.
2. MRI scan of brain and orbit should preferably be performed in each
case presenting with acute optic neuritis.
• Optic nerve MRI scan may show gadolinium enhancement, increased
signal, and sometimes swelling of the affected nerve.
• Brain MRI may show cerebral, brainstem, and/or cerebellar white
matter lesions (plaques).

48.  Evolution, Recovery and Complications
• Evolution.
In optic neuritis, typically, the visual acuity and colour vision is lost
progressively over 2- 5 days.
• Recovery
The rate of visual recovery is slower than the rate of visual loss and
usually starts within 2 weeks and takes between 4 and 6 weeks. About
75 to 90% cases get good visual recovery.
• Complications.
Recurrent attacks of acute retrobulbar neuritis are followed by primary
optic atrophy and recurrent attack of papillitis are followed by
postneuritic optic atrophy leading to complete blindness.

49.  Treatment
1. Efforts should be made to find out and treat the underlying cause.
There is no effective treatment for idiopathic and hereditary optic
neuritis and that associated with demyelinating disorders.
2. CORTICOSTEROID THERAPY
• Oral prednisolone therapy alone is contraindicated in the treatment of
acute optic neuritis.
• If the MRI brain shows lesions supportive of multiple sclerosis, each
patient should receive immediate intravenous methylprednisolone ( 1
gm daily) for 3 days followed by oral prednisolone (1mg/ kg/ day) for 11
days. Then taper prednisolone over 4 days.

50. Indications for iv methylprednisolone in acute optic neuritis patients
with a normal brain MRI scan are:
• Visual loss in both eyes simultaneously or subsequently within hours or
days of each other.
•When the only good eye is affected.
•When the slow progressive visual loss continues to occur.
3. Interferon therapy
It has been reported to reduce recurrences in patients with multiple
sclerosis. However, the treatment is very expensive and with unknown
long term benefits

51. Thank You

52. Papilloedema

53.  Papilloedema is defined as swelling or edema of the optic nerve head
secondary to raised intracranial pressure.
 Usually bilateral; may be unilateral.
 Optic disc swelling in the absence of raised intracranial pressure is
referred to as optic disc edema. Causes are papillitis, neuroretinitis,
CRVO, Diabetic papillopathy, orbital cellulitis, leukaemias, lymphomas.
Introduction

54. CSF Production and Circulation
Daily CSF production: 500ml
Total amount of CSF: 140ml
Normal pressure: 6-25 cm H2O

55. Causes of Papilloedema
1.Intracranial space occupying lesions (ICSOLs)
These include brain tumors,abscess,tuberculoma, gumma, subdural haematoma
and aneurysms.ICSOLs at any position may induced papilloedema except medulla
oblongata (because of foramen magnum). Papilloedema is most frequently associated
with tumors arising in posterior fossa, which obstruct Aqueduct of Sylvius. Thus,
the ICSOLs of cerebellum, midbrain and parieto-occipital region produce
papilloedema more rapidly than other regions.
Etiopathogenesis

56. 2. Congenital conditions include aqueductal stenosis and
craniosynostosis.
3. Intracranial infections such as meningitis and encephalitis.
4.Intracranial hemorrhages: Cerebral as well as subarachnoid
hemorrhage (worst headache) can give rise to papilloedema.
5.Obstruction of CSF absorption via arachnoid villi which have been
damaged previously.
6.Tumors of spinal cord occasionally give rise to papilloedema.

57. 7. Idiopathic intracranial hypertension (IIH)
 known as pseudotumor cerebri (PTC), also an important cause of raised
intracranial pressure. Usually found in yound obese women . It is characterized by
chronic headache and bilateral papilloedema without any ICSOLs or enlargement of
the ventricles due to hydrocephalus.
8.Systemic conditions includes malignant hypertension, pregnancy induced
hypertension(PIH),cardiopulmonary insufficiency, blood dyscrasias and nephritis.
9. Diffuse cerebral edema from blunt head trauma may cause papilloedma.
10. Cerebral venous sinus thrombosis may also cause papilloedma.

58. In majority of the cases with raised intracranial pressure, papilloedema is bilateral.
Disc swelling due to ocular and orbital lesions is usually unilateral.
However, unilateral cases as well as of unequal change do occur with raised intracranial pressure.
Few conditions are as follows:
1.Foster- Kennedy Syndrome
It is associated with olfactory or sphenoidal meningiomata and frontal lobe tumors. In this
condition, there occurs pressure optic atrophy on the side of lesion and papilloedema on the
other side (due to raised ICP).
2. Pseudo-Foster-Kennedy Syndrome
It is characterized by occurrence of unilateral papilloedema associated with raised ICP(due to
any cause) and a pre-existing optic atrophy on the other side.
Bilateral versus Unilateral Papilloedema

59. Till date, Hayreh’s theory is the most accepted one.
It states that, “Papilloedema develops as a result of stasis of axoplasm in the prelaminar region
of optic disc, due to an alteration in the pressure gradient across the lamina cribrosa.”
Pathogenesis

60. Papilloedema usually develops quickly, appearing within 1-5 days of raised
intracranial pressure.
In cases with acute subarachnoid haemorrhage it may develop even more rapidly
within 2-8 hrs.
However, recovery from fully developed papilloedema is rather slow. It takes
about 6-8 weeks to subside after the intracranial pressure is normalised.
Evolution and Recovery

61. A. General Features
 Headache (occipital, throbbing, worsens with straining, coughing,sneezing and
valsalva procedure).
 Projectile vomiting
 Diplopia ( false localizing sign due to 6th
nerve palsy)
B. Ocular Features
 Transient blackout of vision (amaurosis fugax)
 Visual acuity and pupillary reactions usually remain normal until the late stages
of diseases when optic atrophy sets, so loss of vision is not a common feature of
papilloedema.
Clinical Features

62. Mechanical
 Elevation of the optic disc
 Blurring of the optic disc margin
 Filling in the physiological cup
 Edema of the peripapillary nerve
fiber layer
 Retinal folds(Paton’s lines)
 Macular fan
Signs

63. Vascular
 Hyperemia of the optic disc
 Vascular congestion
 Peripapillary hemorrhage
 Exudates in the disc or
peripapillary area
 Nerve fiber layer infracts
Signs

64. Clinical features of papilloedema can be described under four stages:
1. Early Papilloedema
Symptoms: usually absent and visual acuity is normal. Patients may give history of
recurrent attacks of transient blackout of vision(amaurosis fugax).
Pupillary reactions are normal.
Ophthalmoscopic features :
 Obscuration of the disc margins (nasal margin
are involved first followed by the superior,
inferior, temporal).
 Blurring of peripapillary nerve fiber layer.
 Absence of spontaneous venous pulsation at
the disc.
 Mild hyperaemia of the disc.
 Splinter haemorrhages in the peripapillary
region may be present.
 Tortuous Vessels, possibly small haemorrhages
‘C-Shaped Halo’
Visual fields : fairly normal.

65. 2. Established Papilloedema
Symptoms: Patient may give history of
transient visual obscurations in one or both
eyes, lasting a few seconds, after standing.
Visual acuity is usually normal.
Pupillary reaction remain fairly normal.
Ophthalmoscopic Features
 Cup Filled Obliteration- filled up with exudates
 Severe Disc Hyperaemia
 Venous engorgement, peripapillary flame
haemorrhages
 Cotton Wool Spots
 Circumferential Retinal Folds (Paton Lines)
 Hard exudates radiate outward
Visual fields: show enlargement of blind spot.

66. 3. Chronic Papilloedema
Symptoms: visual acuity is variably reduced depending upon the duration
of the papilloedema.
Pupillary reactions are usually normal.
Ophthalmoscopic features
 Acute haemorrhages and cotton wool
spots resolve, and peripapillary edema
is resorbed.
 The optic disc give appearance of the
dome of a champagne cork. The central
cup remains obliterated. Small drusen like
crystalline deposits (corpora amylacea)
may appear on the disc surface.
Visual fields: Blind spot is enlarged and the
visual fields begin to constrict.

67. 4. Atrophic Papilloedema
Symptoms: Atrophic papilloedema develops after 6-9 months of chronic
papilloedema and is characterized by severely impaired visual acuity.
Pupillary reaction: Light reflex is impaired.
Ophthalmoscopic features
 There occur greyish white discolouration
and pallor of the disc due to atrophy of the
neurons and associated gliosis.
 Prominence of the disc decreases in spite of
persistent raised ICP.
 Retinal arterioles are narrowed and veins become
less congested. Whitish sheathing develops
around the vessels.
Visual fields: Concentric contraction of peripheral
fields becomes apparent as atrophy
sets in.

68. Differential Diagnosis
 Pseudopapilloedema
Its is a non-specific term used to describe elevation of the disc similar to
papilloedema, in conditions such as optic disc drusen, hypermetropia and persistent
hyaloid tissue.
 Papillitis
 Tilted optic disc
 Hypoplastic disc
 Myelinated nerve fibers

70. Investigations
History and physical examination including blood pressure measurement.
Ophthalmic examination: Fundus examination, assessment of visual acuity, pupillary examination,
ocular motility&alignment and visual fields.
1.MRI with or with out contrast is the investigation of choice.
2.CT Scan
 To rule out :
 Intracranial lesions
 Obstructive hydrocephalus
 Can detect :
 Subarachnoid, epidural & subdural haemorrhage
 Acute infractions
 Cerebral edema
 Where MRI is contraindicated(pacemaker, metallic clip)

71. 3. MRI venography or CT venography: for venous sinus thrombosis.
4.Lumbar Puncture: is diagnostic in recording opening pressure.
 CSF for microbial and infectious causes.
 Therapeutic procedure for Psuedotumor cerebri.
5. Fundus flouroscence angiography: to detect disc leakage in true
optic disc edema.
6. B-scan ultrasonography: show pseudopapilloedema (e.g. optic disc
drusen).

72. Medical
 For IIH:
 Oral acetazolamide (second line drugs are furosemide and topiramate if
acetazolamide is intolerant.)
 Weight loss
 Salt restricted diet
 For CVT:
 Oral anticoagulants
Treatment
Treatment is directed at underlying causes.

73. Surgery
 For mass or haemorrhage : Neuro-surgical consultation and removal of
mass.
 For IIH:
 Optic nerve sheath fenestration
 CSF shunting:
 Lumbo-peritoneal shunting
 Ventriculo-peritoneal shunting

74. Optic nerve sheath fenestration

77. CSF Shunting
Ventriculo-peritoneal Shunting Lumbo-peritoneal Shunting

78. More severe papilloedema- worse visual prognosis.
Disc pallor with papilloedema- indication of poor visual prognosis, even if
ICP is lowered immediately because the pallor is caused by loss of axons.
Visual Prognosis

79. THANK YOU