आयुर्वेद मत अनुसार

बाह्य नेत्र रोग

आचार्य सुश्रुत ने दृष्टिगत रोगं के कारणों के वर्णन
प्रसङ़ में अनेक कारणों के साथ-साथ बाह्य दो कारणों
को भी माना है।

यथा-: बाह्यौ पुन विह सम्प्रदिष्टौ

निमित्तरचाव्यनिमित्तरच। सु.उ. 7/43
 सनिमित लिंगनाश अर्थात् सकारण लिद्गनाश ।
 अनिमित लिंगनाश अर्थात् कारणरहित लिड़नाश ।

 सनिमित लिंगनाशः
“निमित्ततस्त
शिरोभितापाज्ज्ञेयस्त्वभिष्यन्दनिदर्षनैश्च ।।’’
सु उ 7/43
 सनिमित्तज लिंगनाश का कारण शिरोभिताप स्वीकार
किया जाता है।
 यह लिंगनाश अभिष्यन्द समान लक्षणों वाला होता है।

 अनिमित्त लिंगनाश-:
“सुरर्शिगन्धर्वमहोरगाणां सन्दर्षनेनापि च
भास्वराणाम्। हन्येतदृष्टिर्मनुजस्य यस्य
सलिंगनाशस्त्वनिमित्तसंज्ञः ।।
तत्राक्षि विस्पष्टमिवावभाति वैदूर्यवर्णा विमला च
दृष्टि।’’ सु उ 7/44
 मनुष्य की दृष्टि देव, ऋषि, गन्धर्व, दिव्यसर्प अथवा
सूर्यदर्शन से अकस्मात नष्ट हो जाती है।
 नेत्र असामान्य रुप से स्पष्ट होकर वैदूर्य के
समान चमकने लगता है।
 नेत्र निर्मल रहते है।
आचार्य वागभट्ट द्वारा औपसर्गिक लिंगनाश का उल्लेख –
 औपसर्गिक लिङ्गनाश-
सहसैवाल्यसत्वस्यपश्यतो रूपमभूतम्।।
भास्वरं भास्करादि वा वाताद्य नयनाश्रिताः।
कुर्वन्ति तेजः संशोष्य दृष्टिं मुषितदर्शनाम्।
वैदूर्यवर्णं स्तिमितां प्रकृतिस्थामिवाव्यथम्।
औपसर्गिक इत्येष लिङ्गनाशः - (अ. हृ. उ. 12/30-31)

अचानक थोडे सत्व वाला व्यक्ति द्वारा अद्भुत चमकते

हुए या सूर्यादि प्रकाशवान वस्तु को देखने से वातादि
दोष नेत्र में आश्रित होकर तेज को सुखाकर दर्शन शक्ति
को नष्ट कर देते हैं। दृष्टि वैदूर्य वर्ण के समान
निर्मत निश्चल, स्वाभाविक और पीडारहित होती है, यह
औपसर्गिक लिङ्ङ्गनाश है।

OPTIC ATROPHY
Optic atrophy refers to degeneration of the optic nerve, which occurs
as an end result of any pathologic process that damages axons in the
anterior visual system, i.e. from retinal ganglion cells to the lateral
geniculate body.
The optic nerve contains approximately 1.2 million axons of the
ganglion cells of the retina. The axons possess a myelin sheath
provided by oligodendrocytes. Once damaged, the axons do not
regenerate.
Light incident from the ophthalmoscope undergoes total internal
reflection through the axonal fibers and subsequent reflection from
the capillaries on the disc surface gives rise to the characteristic
yellow-pink colour of a healthy optic disc.

CLASSIFICATION
A. Primary versus secondary optic atrophy
a) Primary optic atrophy
1. Simple degeneration of the nerve fibers and are replaced by
columns of glial cells without alteration in the architecture of the
optic nerve head without any complicating process within the eye,
e.g. syphilitic optic atrophy of tabes dorsalis.
2. Commonly seen in
 Pituitary tumor-The pituitary gland is located just below the optic
chiasm, where the optic nerves from both eyes partially cross.
Because of this close relationship, a tumour growing upward from the
pituitary gland can compress the optic chiasm
 Optic nerve tumor- An optic nerve tumor, such as an optic glioma or
meningioma, causes optic atrophy by directly compressing the optic
nerve. This compression disrupts axoplasmic flow and impairs blood
supply, leading to degeneration of the retinal ganglion cell axons.
Over time, the nerve fibers die, resulting in pale optic discs.
 Traumatic optic neuropathy- Traumatic optic neuropathy occurs
when blunt or penetrating head trauma damages the optic nerve. The
injury may cause direct nerve fiber disruption or secondary swelling
and compression within the optic canal. This impairs axonal transport
and blood flow, leading to degeneration of the optic nerve. Over time,
this results in optic atrophy.
 Multiple sclerosis-In multiple sclerosis (MS), optic atrophy occurs due
to repeated episodes of optic neuritis, which is inflammation of the
optic nerve. The inflammation leads to demyelination (loss of the
myelin sheath) and axon damage in the optic nerve. Over time, this
results in degeneration of nerve fibers and impaired signal
 transmission. As the damaged axons die, the optic disc becomes pale
—known as optic atrophy
3. Optic nerve fibers degenerate in an orderly manner
4. The disc is chalky white and sharply demarcated, and the retinal
vessels are normal.
b) Secondary optic atrophy:
1. Atrophy is secondary to Papilledema and Papillitis.
2. Optic nerve fibers exhibit marked degeneration, with excessive
proliferation of glial tissue- Proliferation of glial tissue, also known as
gliosis, occurs in response to injury or degeneration of the optic nerve which
causes optic atrophy.
3. The disc is grey or dirty grey; the margins are poorly defined.

B. Ophthalmoscopic classification
 Consecutive optic atrophy:
1. Seen in
Retinitis pigmentosa-Retinitis pigmentosa (RP) causes optic atrophy through
progressive degeneration of the photoreceptor cells, mainly rods, followed by
cones. As these retinal cells die, there is reduced visual input to the optic nerve
Myopia-Pathological myopia can lead to optic atrophy due to elongation of the
eyeball, which stretches and thins the retina and optic nerve head. This
mechanical stretching can damage retinal ganglion cell axons and disrupt blood
supply. Over time, this leads to degeneration of optic nerve fibers, resulting in a
pale optic disc i.e. optic atrophy.
Central retinal artery occlusion- Central retinal artery occlusion (CRAO) causes
optic atrophy by suddenly cutting off the blood supply to the inner retina,
which includes the retinal ganglion cells. These cells send their axons through
the optic nerve. Without oxygen and nutrients, the ganglion cells quickly die,
and their axons degenerate. Over time, this leads to optic nerve fibre loss and
optic disc pallor, characteristic of optic atrophy.

2. It occurs following destruction of gang lion cells secondary to

degenerative or inflammatory lesions of the choroid and/ or retina
 causing Blurred or Decreased Vision, Scotomas (Blind Spots),
Distorted Vision (Metamorphopsia), Photopsia (Flashes of Light).
3. Disc is waxy pale with a normal disc margin, marked attenuation of
arteries, and a normal physiologic cup.

 Glaucomatous optic atrophy:

1. Marked cupping of the disc is observed in glaucomatous optic
atrophy.
2. It results from the effect of long-standing raised intraocular
pressure. (Normal-10-21 mmhg and >30mmhg -significant risk of
optic nerve damage)
3. Vertical enlargement of cup.
4. Visibility of the laminar cribeosa pores (laminar dot sign)

5. Nasal shifting of the retinal vessels.

6. Splinter hemorrhage at the disc margin may be observed.

 Post-neuritic optic atrophy.

1. It is secondary optic atrophy which develops as a sequel to
longstanding papilledema or papillitis.

 Vascular (ischemic) optic atrophy.

 1. It results from the conditions (other than glaucoma) producing disc
ischemia. These include: giant cell arteritis, severe haemorrhage,
severe anemia and quinine poisoning.

C. Ascending versus descending optic atrophy.

•Ascending or auto grade optic atrophy (Wallerian degeneration)
Follows damage to ganglion cells or nerve fibre layer due to diseases
of the retina or optic disc –
Eg of retinal disease- Diabetic retinopathy, Retinal detachment, Retinitis
pigmentosa, central serous retinopathy.
Eg of optic disc diseases-Glaucoma, optic neuritis, Ischemic optic neuropathy.
In it the nerve fibre degeneration progresses (ascends) from the
eyeball towards the geniculate body.

•Descending or retrograde optic atrophy

Proceeds from the region of the optic tract, chiasma or posterior
portion of the optic nerve towards the optic disc. Damage beyond
lateral geniculate nucleus (LGN) i.e. optic radiations and occipital
cortex does not cause optic atrophy as the second order neurons
(axons of ganglion cells) synapse in LGN.

PATHOLOGICAL FEATURES
i. Degeneration of the optic nerve fibers is associated with
attempted but unsuccessful regeneration which is characterized by
proliferation of astrocytes and glial tissue.
ii. Ophthalmoscopic appearance of the atrophic optic disc depends
upon the degree of loss of nerve tissue vis gliosis. following three
situations may occur:
1. Degeneration of the nerve fibers may be associated with excessive
gliosis. These changes are pathological features of the consecutive
and post neuritic optic atrophy.
2. Degeneration and gliosis may be orderly and the proliferating
astrocytes arrange themselves in longitudinal columns replacing the
nerve fibers (columnar gliosis). Such pathological features are seen in
primary optic atrophy.
3. Degeneration of the nerve fibres may be associated with
negligible gliosis. It occurs due to progressive decrease in blood
supply. Such pathological changes are labelled as cavernous
(Schnabel's) optic atrophy and are features of glaucomatous and
ischemic (vascular) optic atrophy.

CLINICAL FEATURES OF OPTIC ATROPHY

1.Loss of vision
 Sudden or gradual onset - depending upon the cause of optic
atrophy and
 Partial or total - depending upon the degree of atrophy.

2.Pupil is semi dilated and direct light reflex is very sluggish or

absent. Swinging flash light test depicts Marcus Gunn pupil (RAPD).

Marcus Gunn pupil

It’s a condition where one eye has reduced ability to perceive light due to a
problem in the afferent (sensory) pathway — mainly the optic nerve or severe
retinal disease.
Despite having normal pupil muscles, the affected eye doesn't trigger a normal
constriction when exposed to light.
What is the Swinging Flashlight Test
This is the key clinical test used to detect a Marcus Gunn pupil.
Here's how it's done:
 1. The patient looks straight ahead in a dim room.
2. A light is shone into one eye for about 2–3 seconds.
3. Then the light is quickly swung to the other eye.
4. This is repeated several times.
Normal Response:
 When light enters either eye, both pupils constrict equally (due to the
consensual light reflex).
In Marcus Gunn Pupil:
 When the light is moved from the normal eye to the affected eye, both
pupils paradoxically dilate instead of constricting further.
 Because the affected eye perceives less light, so it sends a weaker signal
to the brain, leading the pupils to relax (dilate) slightly, as if they are in
darkness.
Anatomy Behind It
Afferent Pathway:
 Light → Retina → Optic nerve → Pretectal nucleus (midbrain)
Efferent Pathway:
 From the pretectal area → Edinger-Westphal nucleus → Oculomotor
nerve (CN III) → Pupil constrictor muscles
In Marcus Gunn pupil, the afferent input from one eye is weaker, so the
pupillary constriction response is reduced on both sides when light shines in
that eye.

3. Visual field loss in general, the field loss is peripheral in systemic

infections, central in focal optic neuritis and eccentric when the
nerve tracts are compressed.

4. Ophthalmoscopic appearance ophthalmoscopic features of optic

atrophy in general are pallor of the disc and decrease in the number
of small blood vessels (Kestenbaum index). The pallor is not due to
atrophy of the nerve fibres but to loss of vasculature.
(A)Kestenbaum's sign in severe optic atrophy. A score of 1 highlight severe disease.
(B) Kestenbaum's sign in borderline optic atrophy. The optic disc here may be passed
as normal. However, if the number of small vessels traversing the disc margin (which
are not obviously arteries, veins or branches thereof) is counted, only 2–3 (arrowed)
can be scored, which is well below the normal level of 9–10.
(C) An early glaucomatous disc with a Kestenbaum score of 6.
(D) A healthy optic disc. Numerous capillaries can be counted (Kestenbaum score: 9–
10). Their course from disc surface arterioles to peripapillary retinal capillaries is
evident.
Ophthalmoscopic features of different types of optic atrophy are: -
i. Primary optic atrophy - Colour of the disc is chalky white or white
with bluish hue. Its edges (margins) are sharply outlined.
ii. Consecutive optic atrophy - Disc appears yellow waxy. Its edges are
not so sharply defined as in primary optic atrophy. Retinal vessels are
attenuated.
iii.Post-neuritic optic atrophy - Optic disc looks dirty white in colour.
Due to gliosis, its edges are blurred, physiological cup is obliterated
and lamina cribrosa is not visible.
iv. Glaucomatous optic atrophy. It is characterised by deep and wide
cupping of the optic disc and nasal shift of the blood vessels.
v. lschaemic optic atrophy. Ophthalmoscopic features are pallor of
the optic disc associated with marked attenuation of the vessels.

Optic atrophy: A Primary; B Consecutive (in a patient with retinitis pigmentosa); C,

Postneuritic; D, Ischaemic ;E glaucomatous optic atrophy

ETIOLOGIC CLASSIFICATION:
1.Hereditary: This is divided into congenital or infantile optic atrophy
(recessive or dominant form), Behr hereditary optic atrophy
(autosomal recessive), and Leber optic atrophy.

2. Consecutive atrophy: Consecutive atrophy is an ascending type of

atrophy (eg. chorioretinitis, pigmentary retinal dystrophy, Cerebro
macular degeneration) that usually follows diseases of the choroid or
the retina.
3. Circulatory atrophy: Circulatory is an ischemic optic neuropathy
observed when the perfusion pressure of the ciliary body falls below
the intraocular pressure. Circulatory atrophy is observed in central
retinal artery occlusion, carotid artery occlusion, and cranial arteritis,

4. Metabolic atrophy is observed in disorders such as thyroid

ophthalmopathy, juvenile diabetes mellitus, nutritional
amblyopia, toxic amblyopia, tobacco, methyl alcohol, and drugs.

5. Demyelinating-atrophy is observed in diseases such as multiple

sclerosis

6. Pressure or traction atrophy is observed in diseases such as

glaucoma and Papilledema.

7. Post inflammatory atrophy is observed in diseases such as optic

neuritis, peri neuritis secondary to inflammation of
the meninges, and sinus and orbital cellulites.

8. Traumatic optic neuropathy.

DIAGNOSIS:

1. Visual acuity by Snellen chart

2. Ishihara color blindness test
3. Pupillary function: Pupil size should be noted, as well as the
magnitude and the latency of the direct and consensual responses to
light and near stimulation.
A relative afferent pupillary defect (RAPD) is a hallmark of unilateral
afferent sensory abnormality or bilateral asymmetric visual loss.
Occasionally, RAPD is the only objective sign of anterior visual
pathway dysfunction. It is a sensitive optic nerve function test.

4. Optic disc:
a. Optic disc changes can present with temporal pallor (as seen
in toxic neuropathy and nutritional deficiency), focal pallor or
bow-tie pallor (as seen in compression of the optic chiasm), and
cupping (as seen in glaucomatous optic atrophy).
b. In the end stages of the atrophic process, the retinal vessels
of the normal caliber still emerge centrally through the
otherwise avascular disc.
c. Thinning of the neuroretinal rim.
d. In most cases of optic atrophy, the retinal arteries are
narrowed or attenuated.

5. Visual field testing: visual field changes can include enlargement of

the blind spot and paracentral scotoma, altitudinal defects and
bitemporal defects.

6. Electroretinogram

DIFFERENTIAL DIAGNOSIS:
•Axial myopia
•Myelinated nerve fibers
•Optic disc drusen
• Optic nerve hypoplasia
• Optic nerve pit

MANAGEMENT
• No proven treatment exists for optic atrophy. However, treatment
that is initiated before the development atrophy can be helpful in
saving useful vision
• Intravenous steroids
 IV Methylprednisolone: 1 gram per day
Given over 60–90 minutes
For 3 consecutive days
 Followed by:
Oral Prednisolone:1 mg/kg/day
For 11 days, then taper over 3–5 days
 • Idebenone Quinone analog, has been used for Leber hereditary
optic neuropathy.
900 mg/day orally (300 mg three times daily) for at least 6–12
months.
• Stem cell treatment: Neural progenitor cells delivered to the
vitreous can integrate into the ganglion the retina, turn on
neurofilament genes, and migrate into the host optic nerve.
•DeoxyadenosyIcobalamin and hydroxocobalamin are active forms of
vitamin B-12 which are also used for the management of optic
atrophy.

INDEX

SNO. CONTENT PAGE NO.

1 बाह्य नेत्र रोग 1-2

2 OPTIC ATROPHY INTRODUCTION 3

3 CLASSIFICATION 3-6

4 PATHOLOGICAL FEATURES 7

5 CLINICAL FEATURES 7-10

6 ETIOLOGIC CLASSIFICATION 11

7 DIAGNOSIS 12

8 DIFFERENTIAL DIAGNOSIS 13

9 MANAGEMENT 13