dristigata roga and possible modern comparison

1. दृष्टिगत रोग

2. दृष्टिगतरोग – संख्या
• सुश्रुत – 12 - षट् च षट् च
• वागभि - 27
• भा.प्र. /यो.र – 14 (12+ सनिमित +अनिमित )
 6 – नतमिर/कांच/म ंगिाश – v/p/k/r /s/पाररम् ायी = याप्य

 2 – कफ / पपत पवदग्ध दृटिी = अशस्त्रकृ त
 धूिदशी – पपत – अशस्त्रकृ त
 हृस्त्वजाड्य – पपत – असाध्य
 िक
ु ाध्य – सिीपात – असाध्य
 गंभीरीका – वात – असाध्य

3. द्वे वर्तिमपि े पवद्याच्चर्तवायमन्यानि चाक्षिणि |
जायते नतमिरं येषु व्याधधिः परिदारुििः |
पि
2 वर्तिमपि + 4 अक्षिपि
 बाह्यं - तेजोज ाधश्रतं
 तेटवन्यत् - पपमशताधश्रति्
 तृतीयं – िेद आधश्रतं
 चापरि् – अष्स्त्ि आधश्रत
 डल्हि िे opposit बताया

4. मसरामभरमभसम्प्राप्य पवगुऽभ्यन्तरे भृशि् |
प्रििे पि े दोषो यस्त्य दृटिौ व्यवष्स्त्ितिः
अव्यक्तानि स रूपाणि सवामण्येव प्रप्यनत
प्रििपि गत नतमिर
दृष्टिभृमशं पवह्व नत द्पवतीयं पि ं गते
िक्षिका िशकाि् क
े शाञ्जा कानि च प्यनत
िण्ड ानि पताकां्च िरीचीिः क
ु ण्ड ानि च
पररप् वां्च पवपवधाि् वषमिभ्रं तिांमस च
दूरस्त्िान्यपप रूपाणि िन्यते च सिीपतिः
सिीपस्त्िानि दूरे च दृटिेगोचरपवभ्रिात्
यर्तिवािपप चार्तयिं सूचीपाशं ि प्यनत
द्पवतीयपि गत नतमिर Refrative error
SPASM OF ACCOMMODATION
PRESBYOPIA

5. ऊध्वं प्यनत िाधस्त्तात्तृतीयं पि ं गते |
िहान्र्तयपप च रूपाणि च्छाददतािीव वाससा ||
किमिासाक्षियुक्तानि पवपरीतानि वीिते |
यिादोषं च रज्येत दृष्टिदोषे ब ीयमस ||
अधिःष्स्त्िते सिीपस्त्िं दूरस्त्िं चोपररष्स्त्िते |
पा्वमष्स्त्िते तिा दोषे पा्वमस्त्िानि ि प्यनत ||
सिन्ततिः ष्स्त्िते दोषे सङ्क
ु ािीव प्यनत |
दृष्टििध्यगते दोषे स एक
ं िन्यते द्पवधा ||
द्पवधाष्स्त्िते त्ररधा प्येद्बहुधा चािवष्स्त्िते |
नतमिराख्यिः स वै दोषिः... |
तृतीयपि गत नतमिर
Immature
cataract

6. चतुिं पि ं गतिः
रुिद्धध सवमतो दृष्टिं म ङ्गिाशिः स उच्यते
तष्स्त्िन्िपप तिोभूते िानतरूढे िहागदे ||
चन्राददर्तयौ सििरावन्तरीिे च पवद्युतिः |
नििम ानि च तेजांमस भ्राष्जटिूनि च प्यनत
चतुिंपि ंगत नतमिर
स एव म ङ्गिाशस्त्तु िीम काकाचसष्ञ्ितिः
Mature
cataract

7. Note
 सुश्रुत चारों पि गत नतमिर िािता है परंतु पवशेष् रूप से तृतीय पि गत नतमिर
को नतमिर संिा की है
 चतुिम पि गत नतमिर को कांच,िीम का तिा म ंगिाश कहा है
 वागभि िे नतमिर कांच म ंगिाश को उतरोतर अवस्त्िा बताया है
नतमिर कांच म ंगिाश
राग राग
 वागभि द्पवतीय पि गत को नतमिर तृतीय पि गत को कांच तिा चतुिम पि गत
को म ंगिाश िािता है

8. तर वातेि रूपाणि भ्रिन्तीव स प्यनत
आपव ान्यरुिाभानि व्यापवद्धानि च िािविः
पपत्तेिाददर्तय खद्योत शक्रचाप तडडद्गुिाि्
मशणखबहमपवधचराणि िी कृ टिानि प्यनत
कफ
े ि प्येरूपाणि ष्स्त्िग्धानि च मसतानि च ||
गौरचािरगौराणि ्वेताभ्रप्रनतिानि च |
प्येदसूक्ष्िाण्यर्तयिं व्यभ्रे चैवाभ्रसम्प् वि ् ||
सम प् ापवतािीव पररजाड्यानि िािविः |
तिा रक्तेि रक्तानि तिांमस पवपवधानि च
हररत्यावकृ टिानि धूिधूम्राणि चेिते
वातज नतिीर
पपतज नतिीर
कफज नतिीर
रक्तज नतिीर
सष्न्िपातेि धचराणि पवप् ुतानि च प्यनत
बहुधा वा द्पवधा वाऽपप सवामण्येव सिन्ततिः |
हीिाधधकाङ्गान्यिवा ज्योतींटयपप च प्यनत
सष्न्िपात नतिीर
पपत्तं क
ु यामत् पररम् ानय िूष्च्छमतं रक्ततेजसा |
पीता ददशस्त्तिोद्यन्तिाददर्तयमिव प्यनत ||२५||
पवकीयमिािाि् खद्योतैवृमिांस्त्तेजोमभरेव च |
पररम् ानय नतमिर

9. • हरेदसृक्तेषु मसरापविोििैिः
• पवरेचयेच्चापप
• पुरािसपपमषा पवरेचिाङ्गोपदहतेि सवमदा
धचककर्तसा
 रागरदहत नतमिर
[विरेचनाङ्गोपहितेनेतत विरेचनद्रव्यसंस्कृ ते]
 विरेचन
[‘ततमिरे रागगणि मिषक् मसरािोक्षं वििर्जयेत्]
वातज नतमिर - एरण्ड + दूध
पपतज/रक्तज नतमिर - त्ररफ ा घृत
कफज नतमिर - त्ररवृत कल्क मसद्ध घृत
वातज नतमिर - त्ररफ ा + नत ते
पपतज नतमिर - त्ररफ ा + घृत
कफज नतमिर - त्ररफ ा + िधू
 ततमिर िे त्रिफला प्रयोग

10.  रागप्राप्त नतमिर
ततमिरे रागगणि मिषक् मसरािोक्षं वििर्जयेत्
रागप्राप्तेटवपप दहताष्स्त्तमिरेषु तिा कक्रयािः |
यापिािं यिोद्ददटिािः सेव्या्चापप ज ौकसिः
 नस्य प्रयोग
वातज नतमिर - बल्य ओषध मसद्ध ते से
पपतज नतमिर - ककोल्यादी गि मसद्ध ते
कफज नतमिर - उशीर ोध्र मसद्ध कल्क
 तपजि प्रयोग
 अंर्न
घृतं पुरािं त्ररफ ां शतावरीं पिो िुद्गाि क
ं यवािपप |
निषेविािस्त्य िरस्त्य यर्तितो भयं सुघोरापत्तमिरान्ि पवद्यते
 पथ्य

11. अराधग नतमिरं साध्यिाद्यं पि िाधश्रति् |
कृ च्रं द्पवतीये राधग स्त्यात्तृतीये याप्यिुच्यते
साध्य असाध्यता
प्रििपि िाधश्रति् + अरागी - साध्य
द्पवतीय पि गत + राग - कृ च्छ साध्य
तृतीय पि गत - याप्य
चतुिम पि गत म ंगिाश - असाध्य (कफज म ंगिाश को छोड़ कर )

12. defined as state of refraction, where in the parallel rays
of light coming from infinity are focused at the
sensitive layer of retina with the accommodation being
at rest
ERRORS OF REFRACTION
 Emmetropia - optically normal eye
• At birth, the eyeball is relatively short, having +2 to +3 hypermetropia.
• This is gradually reduced until by the age of 5-7 years the eye is emmetropic and
• remains so till the age of about 50 years.
• After this, there is tendency to develop hypermetropia again,
• This senile hypermetropia is due to changes in the crystalline lens.

13.  defined as a state of refraction, when the parallel rays of light coming from infinity
(with accommodation at rest), are focused either in front or behind the sensitive
layer of retina, in one or both the meridians.
 ametropia includes - myopia, hypermetropia and astigmatism.
Ametropia- (a condition of refractive error),

14. Etiological classification
 Axial myopia
• increase in AP length of the eyeball - commonest form.
 Curvatural myopia
• due to increased curvature of the cornea, lens or both.
 Positional myopia
• Due to placement of crystalline lens in the eye.
 Index myopia
• Due to increase in the refractive index of crystalline lens associated
with nuclear sclerosis.
 Myopia due to excessive accommodation
• Due tospasm of accommodation.
MYOPIA
Myopia or short-sightedness is a type of refractive error in which parallel rays of light
coming from infinity are focused in front of the retina when accommodation is at rest .

15. 1. Congenital myopia
2. Simple or developmental myopia
3. Pathological or degenerative myopia
4. Acquired myopia which may be: (i) post-traumatic;(ii) post-keratitic; (iii) drug-induced,
(iv)pseudomyopia; (v) space myopia; (vii) Night myopia (viii) consecutive myopia
Clinical classification
Congenital myopia
• Congenital myopia is present since birth
• usually diagnosed by the age of 2-3 years.
• Most of the time the error is unilateral and manifests as anisometropia.
• Usually the error is of about 8 to 10 which mostly remains constant.
• The child may develop convergent squint
• May be associated with other congenital anomalies such as cataract,
microphthalmos, aniridia,megalocornea, etc.

16.  Simple or developmental myopia is the commonest variety.
 It is considered as a physiological error not associated with any disease of the eye.
 Its prevalence increases in school going age between 8 year to 12 years so, it is also
called school myopia
Simple myopia
• Axial type
• Curvatural type - due to underdevelopment of the eyeball.
• Role of diet in early childhood has also been reported.
• Role of genetics. - both parents myopic (20%), one parent myopic (10%) and
children with no parent myopic (5%).
• Theory of excessive near work in childhood was also put forward, but did not gain
much importance. In fact, there is no truth in the folklore that myopia is aggravated
by close work, watching television and by not using glasses.
Etiology.

17.  Symptoms
• Poor vision for distance (short-sightedness) - main symptom of myopia.
• Asthenopic symptoms may occur in patients with small degree of myopia.
• Half shutting of the eyes may be complained by parents of the child.
Clinicalpicture
Signs
• Prominent eyeballs - large
• Anterior chamber - slightly deeper than normal.
• Pupils - bit sluggishly reacting.
• Fundus is normal - rarely temporal myopic crescent .
Magnitude of refractive errror.
• Simple myopia usually occur between 5 and 10 year of age and increasing till
about 18-20 years of age at a rate of about –0.5 ± 0.30 every year.
• error does not exceed 6 to 8.

18.  Pathological/degenerative/progressive myopia
 rapidly progressive error which starts in childhood at 5-10 years of age and results in
high myopia during early adult life which is usually associated with degenerative
changes in the eye
Pathological myopia
Etiology.
• 2 factors (i) role of heredity (ii) role of general growth process.
It is now confirmed that genetic factors play a major role in the etiology, as the
progressive myopia is
(i) familial;
(ii) more common in certain races like Chinese, Japanese, Arabs and Jews,
(iii) uncommon among Negroes, Nubians and Sudanese.
Role of heredity

19. • Minor role , cannot be denied on the progress of myopia.
• Lengthening of the posterior segment of the globe only during the period of active
growth
• the factors which affect the general growth process - such as nutritional deficiency,
debilitating diseases, endocrinal disturbances and indifferent general health
Role of general growth process,
Genetic factors (play major role) General growth process (plays minor role)
↓
More growth of retina
↓
Stretching of sclera
↓ ↓
Increased axial length
↓
Degeneration of choroid Features of
↓
Pathological Degeneration of retina myopia
↓
Degeneration of vitreous

20. Symptoms
 Defective vision
- error is usually high Further, due to progressive degenerative changes,
an uncorrectable loss of vision may occur.
 Muscae volitantes
- floating black opacities in front of the eyes are also complained of patients.
These occur due to degenerated liquified vitreous.
 Night blindness
- may be complained by very high myopes having marked degenerative changes.
Clinical picture
Signs
 Prominent eye ball
 Cornea - large.
 Anterior chamber - deep.
 Pupils are slightly large and react sluggishly reactive

21.  Fundus examination reveals following characteristic signs :
• Optic disc
large and pale
its temporal edge a characteristic myopic crescent is present
• Degenerative changes in retina and choroid
common in progressive myopia characterised by white atrophic
patches at the macula with a little heaping up
• Foster-Fuchs' spot (dark red circular patch due to sub-retinal
neovas-cularization and choroidal haemorrhage) may be present
at the macula.
• Cystoid degeneration may be seen at the periphery
• Posterior staphyloma due to ectasia of sclera
• Degenerative changes in vitreous include: liquefaction, vitreous
opacities, and posterior vitreous detachment (PVD) appearing as
Weiss' reflex.

22. Optical treatment of myopia
• prescription of appropriate concave lenses,
The basic rule of correcting myopia
• the minimum acceptance providing maximum vision should be prescribed.
• In very high myopia undercorrection is always better to avoid the problem of
near vision and that of minification of images.
Treatment of myopia

23. General measures
 advising against marriage between two individuals with progressive myopia.
 However, if they do marry, they should not produce children.
Surgical treatment of myopia - very popular now-a-days
• balanced diet rich in vitamins and proteins
Low vision aids (LVA)
Prophylaxis (genetic counselling).
• Radial keratotomy (RK)
• Photorefractive keratectomy (PRK).
• Laser in-situ keratomileusis (LASIK).
• Intercorneal ring (ICR) implantation

24. long-sightedness is the refractive state of the eye wherein parallel rays of light coming
from infinity are focused behind the retina with accommodation being at rest .
HYPERMETROPIA
Etiology
 Axial hypermetropia - commonest form.
• About 1–mm shortening of the anteroposterior diameter of the eye results in 3
dioptres of hypermetropia.
 Curvatural hypermetropia
• curvature of cornea, lens or both is flatter than the normal
• About 1 mm increase in radius of curvature results in 6 dioptres of hypermetropia.
 Index hypermetropia
• occurs due to decrease in refractive index of the lens in old age.
 Positional hypermetropia
• results from posteriorly placed crystalline lens.
 Absence of crystalline lens - congenitally or acquired

25. There are three clinical types of hypermetropia:
Clinical types
Pathological hypermetropia
• either congenital or acquired conditions
It includes :
• Index hypermetropia (due to acquired cortical sclerosis),
• Positional hypermetropia (due to posterior subluxation of lens
Simple or developmental hypermetropia
• commonest form
• It results from normal biological variations in the development of eyeball.
• It includes axial and curvatural hypermetropia
• Aphakia (congenital or acquired absence of lens)
• Consecutive hypermetropia (due to surgically over-corrected myopia
Functional hypermetropia
• results from paralysis of accommodation

26.  Total hypermetropia = latent + manifest (facultative + absolute).
 Latent hypermetropia - amount of hypermetropia (about 1D) which is normally
corrected by the inherent tone of ciliary muscle.
 Facultative hypermetropia - can be corrected by the patient’s accommodative effort.
 Absolute hypermetropia - residual part of manifest hypermetropia which cannot be
corrected by the patient's accommodative effort

27. Symptoms
 Asymptomatic.
 small amount of refractive error corrected by accommodative effort without
producing any symptom.
 Asthenopic symptoms.
 hypermetropia is fully corrected but due to sustained accommodative efforts
patient develops asthenopic sysmtoms.
 These include: tiredness of eyes, frontal or fronto-temporal headache, watering
and mild photophobia.
 These asthenopic symptoms are especially associated with near work and
increase towards evening
 Defective vision with asthenopic symptoms.
 Defective vision only.

28. • Size of eyeball - small as a whole.
• Cornea - slightly smaller than the normal.
• Anterior chamber - shallow.
• Fundus examination - small optic disc
• The retina as a whole may shine due to greater brilliance of light reflections
(shot silk appearance).
• A-scan ultrasonography (biometry) - short antero-posterior length of the
eyeball
Signs
Treatment
 Optical treatment.
• prescribe convex (plus) lenses, so that the light rays are brought to focus on the retina .
 Surgical treatment • Holmium laser thermoplasty
• Hyperopic PRK
• Hyperopic LASIK

29. ASTIGMATISM
 Astigmatism is a type of refractive error wherein the refraction varies in the different
meridia.
 rays of light entering in the eye cannot converge to a point focus but form focal lines.
 two types of astigmatism: regular and irregular
REGULAR ASTIGMATISM
The astigmatism is regular when the refractive power changes uniformly from one
meridian to another (i.e., there are two principal meridia).
Etiology
1. Corneal astigmatism – most common
• Abnormalities of curvature of cornea.
2. Lenticular astigmatism - is rare:
i. Curvatural abnormalities
ii. Positional due to tilting or oblique placement
3. Retinal astigmatism due to oblique placement of macula may also be seen occasionally

30. types of regular astigmatism – 3 type
 Simple astigmatism
 Compound astigmatism.
 Mixed astigmatism
simple myopic
Simple hypermetropic
compound myopic
Compound hypermetropic
mixed

31.  Defective vision
 blurring of objects
 depending upon the type and degree of astigmatism, objects may
appear proportionately elongated
 asthenopic symptoms
Symptoms
 Different power in two meridia is revealed on retinoscopy or autorefractometry.
 Oval or tilted optic disc may be seen on ophthalmoscopy in high degree of
astigmatism.
 Head tilt.
 Half closure of the lid. Like myopes,
Signs

32.  Optical treatment
• prescribing appropriate cylindrical lens, discovered after accurate refraction.
i. Spectacles with full correction of cylindrical power
ii. Contact lenses.
• Rigid contact lenses may correct upto 2-3 of regular astigmatism, while soft
contact lenses can correct only little astigmatism.
 Surgical correction of astigmatism is quite effective.
Treatment
• Astigmatic keratotomy (AK)
• Photo-astigmatic refractive keratotomy (PARK)
• LASIK

33. It is characterized by an irregular change of refractive power in different meridia. There
are multiple meridian which admit no geometrical analysis.
IRREGULAR ASTIGMATISM
Etiological types
1. Curvatural irregular astigmatism - extensive corneal scars or keratoconus.
2. Index irregular astigmatism - refractive index in different parts of the crystalline
Symptoms
• Defective vision,
• Distortion of objects and
• Polyopia.
Investigations
1. Placido's disc
2. Photokerotoscopy and computerized corneal topography
Treatment
• contact lens which replaces the anterior surface of the cornea for refraction
• Phototherapeutic keratectomy
• keratoplasty.

34.  वातज – रागो ऽरुिो िारुतजिः
 पपतज -पपत्तात् पररम् ाय्यिवाऽपप िी िः
 कफज -मसतिः
 रक्तज - शोणितजस्त्तु रक्तिः
 सष्न्िपातज - सिस्त्तदोषोऽि पवधचर रूपिः
काच
 Immature cataract

35. - दृष्टिरागो भवेत् धचरों म ङ्गिाशे त्ररदोषजे |
- यिास्त्वं दोषम ङ्गानि सवेटवेव भवष्न्त दह
म ङ्गिाश
- अरुिं िण्ड ं वाताच्चञ्च ं परुषं तिा
- पपत्ता िण्ड ि िी ं कांस्त्याभं पीतिेव वा
- ् ेटििा बह ं ष्स्त्िग्धं शङ्खक
ु न्देन्दुपाण्डुरि ्
- च र्तपद्िप ाशस्त्ििः शुक् ो त्रबन्दुररवाम्भसिः |
सङ्क
ु चर्तयातपेऽर्तयिं छायायां पवस्त्तृतो भवेत्
िृद्यिािे च ियिे िण्ड ं तद्पवसपमनत
- प्रवा पद्िपराभं िण्ड ं शोणितार्तिकि्
 वातज म ङ्गिाश
 पपतज म ङ्गिाश
 कफज म ङ्गिाश
 रक्तज म ङ्गिाश
 सष्न्िपात
म ङ्गिाश

36. ् ैष्टिक
े म ङ्गिाशे तु किम वक्ष्यामि मसद्धये
ि चेदधेन्दु घिामम्बुत्रबन्दु िुक्ताकृ नतिः ष्स्त्िरिः
पवषिो वा तिुिमध्ये राष्जिाि् वा बहुप्रभिः
दृष्टिस्त्िो क्ष्यते दोषिः सरुजो वा स ोदहतिः
 धचककर्तसा - असाध्य (कफज म ंगिाश को छोड़ कर )
 ष्स्त्िग्ध ष्स्त्वन्िस्त्य
 का े िार्तयुटिशीत े यष्न्रतस्त्योपपवटिस्त्य स्त्वां
 िासां प्यतिः सिि ्
 िनतिाि् शुक् भागौ द्वौ कृ टिान्िुक्र्तवा ह्यपाङ्गतिः
 मसराजा पववष्जमते िाधो िोध्वं ि पा्वामभ्यां नछरे दैवकृ ते ततिः
 श ाकया प्रयर्तिेि पव्वस्त्तं यववक्रया िध्यप्रदेमशन्यङ्गुटठष्स्त्िरहस्त्तगृहीतया
 दक्षििेि मभषक् सव्यं पवध्येत् सव्येि चेतरत्
 वाररत्रबन्द्वागििः सम्यग् भवेच शब्द स्त्तिा व्यधे
 संमसच्य पवद्धिारं तु योपषर्तस्त्तन्येि कोपवदिः
 निरभ्र इव घिांशुयमदा दृष्टििः प्रकाशते
शस्त्र किम

37.  घृतेिाभ्यज्य ियिं वस्त्रपट्िेि वेटियेत्
 ततो गृहे निराबाधे शयीतोत्ताि एव
 उद्गार कास िविुटठीविोर्तकम्पिानि
 तर्तका ं िाचरेदूध्वं यन्रिा स्त्िेहपीतवत्
 त्र्यहात् त्र्यहाच्च धावेत कषायैरनि ापहैिः
 दशाहिेवं संयम्य दहतं दृष्टिप्रसादिि्

38. Definition
• Derived from Greek word – katarraktes which means ‘waterfall’ assuming that
abnormal humour developed in front of lens but it is misnomer
• The crystalline lens is a transparent structure.
• Its transparency may be disturbed due to degenerative process leading to
opacification of lens fibres.
• Development of an opacity in the lens is known as cataract.
CATARACT
Etiological classification
I. Congenital and developmental cataract
II. Acquired cataract
Classification
 Senile cataract
 Traumatic cataract
 Complicated cataract
 Metabolic cataract
 Electric cataract
 Radiational cataract
 Toxic cataract

39.  Capsular cataract.
i. Anterior capsular cataract
ii. Posterior capsular cataract
 Subcapsular cataract.
i. Anterior subcapsular cataract
ii. Posterior subcapsular cataract
 Cortical cataract.
 Supranuclear cataract.
 Nuclear cataract.
Morphological classification
Polar cataract.
i. Anterior polar cataract
ii. Posterior polar cataract

40. congenital and developmental cataracts occur due to disturbance in the
formation of the lens fibres
acquired cataract, opacification occurs due to degeneration of the already
formed normal fibres.
The exact mechanism and reasons for the degeneration of lens fibers are yet
not clear.
However, in general any factor, physical, chemical or biological, which
disturbs the critical intra and extracellular equilibrium of water and
electrolytes or deranges the colloid system within the lens fibers, tends to
bring about opacification.
The factors responsible for disturbing such an equilibrium of the lens fibres
vary in different types of acquired catract

41.  Also called as ‘age-related cataract’
 this is the commonest type of acquired cataract
 affecting usually above the age of 50 years
 The condition is usually bilateral, but almost always one eye is affected earlier than the
other.
SENILE CATARACT
- cuneiform
- cupuliform cataract.
Morphologically, the senile cataract occurs in two forms,
1.cortical (soft cataract)
2. nuclear (hard cataract).

42. Etiology
Senile cataract is essentially an ageing process its precise etiopathogenesis is not clear, the
various factors implicated are as follows:
A.Risk Factors
1. Heredity..
2. Ultraviolet irradiations. More exposure to UV irradiation from sunlight
3. Dietary factors. Diet deficient
4. Dehydrational crisis. An association with prior episode of severe dehydrational crisis
(due to diarrhoea, cholera etc.) and age of onset and maturation of cataract.
5. Smoking- Smoking causes accumulation of pigmented molecules—3 hydroxykynurinine
and chromophores
6. Diabetes mellitus.
7. Myotonic dystrophy

43. Maturation of Cortical senile cataract
Stages of maturation
 The earliest senile change is demarcation of cortical fibres owing to their separation by
fluid.
 demonstrated by slit-lamp examination only.
 These changes are reversible.
 Stage of lamellar separation
• Early detectable opacities with clear areas between them are seen.
Stage of incipient cataract.
Cuneiform senile cortical cataract.
• characterised by wedge-shaped opacities with clear areas in between.
• These extend from equator towards centre and in early stages can only be demonstrated
• These opacities are present both in anterior and posterior cortex
• present a typical radial spoke-like pattern of greyish white opacities

44. • saucer shaped opacity develops just below the capsule
Cupuliform senile cortical cataract.
• usually in the central part of posterior cortex which gradually extends outwards.
• There is usually a definite demarcation between the cataract and the surrounding
clear cortex.
• Cupuliform cataract lies right in the pathway of the axial rays and thus causes an
early loss of visual acuity

45. • In this stage, opacification progresses further.
• The lens appears greyish white but clear cortex is still present and
so iris shadow is visible.
• In some patients, at this stage, lens may become swollen due to
continued hydration. This condition is called ‘intumescent
cataract'..
 Stage of Immature senile cataract (ISC).
• In this stage, opacification becomes complete, i.e., whole
of the cortex is involved.
• Lens becomes pearly white in colour.
• Such a cataract is also labelled as ‘ripe cataract’ .
 Stage of Mature senile cataract (MSC).

46.  Stage of Hypermature senile cataract (HMSC).
• When the mature cataract is left in situ, the stage of hypermaturity sets in.
• The hypermature cataract may occur - two forms:
• Morgagnian hypermature cataract:
• Sclerotic type hypermature cataract:
 Morgagnian hypermature cataract:
• after maturity the whole cortex liquefies and the lens is
converted into a bag of milky fluid.
• small brownish nucleus settles at the bottom, altering its
position with change in the position of the head. Such a
cataract is called Morgagnian cataract

47. • Sometimes after the stage of maturity, the cortex becomes disintegrated and
the lens becomes shrunken due to leakage of water.
• The anterior capsule is wrinkled and thickened due to proliferation of
anterior cells and a dense white capsular cataract may be formed in the
pupillary area.
 Sclerotic type hypermature cataract:
• In it, the sclerotic process lens inelastic and hard, decreases its ability to accommodate
and obstructs the light rays.
• These changes begin centrally and slowly spread peripherally , a very thin layer of clear
cortex may remain unaffected.
• The nucleus may become diffusely cloudy (greyish) or tinted (yellow to black) due to
deposition of pigments.
• In practice, the commonly observed pigmented nuclear cataracts are either amber,
brown (cataracta brunescens) or black (cataracta nigra) and rarely reddish (cataracta
rubra) in colour
Maturation of nuclear senile cataract

48. Clinical features
Symptoms.
• An opacity of the lens may be present without causing any symptoms; and may be
discovered on routine ocular examination.
Common symptoms of cataract are as follows:
1. Glare. One of the earliest visual disturbances with the cataract is glare or intolerance
of bright light; such as direct sunlight or the headlights of an oncoming motor vehicle.
2. Uniocular polyopia doubling or trebling of objects:
It occurs due to irregular refraction by the lens owing to variable refractive index
as a result of cataractous process.
3. Coloured halos.
4. Black spots in front of eyes. Stationary black spots may be perceived by some patients.
5. Image blur, distortion of images and misty vision
6. Loss of vision.
• It is painless and gradually progressive in nature.

49. • Paitents with central opacities (e.g., cupuliform cataract) have early loss of
vision.
• These patients see better when pupil is dilated due to dim light in the evening
(day blindness).
• In patients with peripheral opacities (e.g. cuneiform cataract) visual loss is
delayed and the vision is improved in bright light when pupil is contracted.
• In patients with nuclear sclerosis, distant vision deteriorates due to progressive
index myopia. Such patients may be able to read without presbyopic glasses.
This improvement in near vision is referred to as ‘second sight'.

50. Visual acuity testing.
• Depending upon the location and maturation of cataract, the visual acuity may range
from 6/9 to just PL +
Oblique illumination examination.
• It reveals colour of the lens in pupillary area which varies in different types of cataracts
•
Test for iris shadow.
• When an oblique beam of light is thrown on the pupil, a crescentric shadow of
pupillary margin of the iris will be formed on the greyish opacity of the lens, as long as
clear cortex is present between the opacity and the pupillary margin .
• When lens is completely transparent or completely opaque, no iris shadow is formed.
• presence of iris shadow is a sign of immature cataract.
Distant direct ophthalmoscopic examination
Signs

51. Slit-lamp examination
Grade of hardness Description of hardness Colour of nucleus
Grade I Soft White or greenish yellow
Grade II Soft-medium Yellowish
Grade III Medium-hard Amber
Grade IV Hard Brownish
Grade V Ultrahard Blackish
(rock-hard)

52. Examination Nuclear cataract ISC MSC HMSC(M) HMSC(S)
Visual acuity 6/9 to PL+ 6/9 to FC+ HM+ to PL+ PL+ PL+
Colour of
lens
Grey, amber Greyish white Pearly white Milky white Dirty white
Iris shadow Seen Seen Not seen Not seen Not seen
Distant direct Central dark Multiple dark No red glow No red glow No red glow

53. MANAGEMENT
Non-surgical measures
 Treatment of cause of cataract.
• control of diabetes mellitus
• Removal of cataractogenic drugs such as corticosteroids.
• Removal of irradiation (infrared or X-rays)
• Early and adequate treatment of ocular diseases
 Measures to delay progression.
• iodide salts of calcium and potassium are being prescribed in early stage - till
date no conclusive results available.
• Role of vitamin E and aspirin

54.  Measures to improve vision in the presence of incipient and immature cataract
• Refraction,
• Arrangement of illumination.
o Patients with peripheral opacities - instructed to use brilliant illumination.
o presence of central opacities, a dull light placed beside and slightly behind the
patient’s head will give the best result
• Use of dark goggles
Surgical management
• INTRACAPSULAR CATARACT EXTRACTION
 CONVENTIONAL EXTRACAPSULAR CATARACT EXTRACTION (ECCE)
• EXTRA CAPSULAR CATARACT EXTRACTION
small incision cataract surgery (SICS)
 Phacoemulsification

55. Surgical steps of conventional ECCE
1. Superior rectus (bridle) suture
2. Conjunctival flap
3. Partial thickness groove or gutter
4. Corneoscleral section.
5. Injection of viscoelastic substance in
anterior chamber
6. Anterior capsulotomy.
7. Removal of anterior capsule.
8. Hydrodissection.
9. Removal of nucleus.
10.Aspiration of the cortex.
11.Implantation of IOL.
12.Closure of the incision
13.Conjunctival flap is reposited
14.Patching of eye

56. पपत्तेि दुटिेि गतेि दृष्टिं पीता भवेद्यस्त्य िरस्त्य दृष्टििः
पीतानि रूपाणि च िन्यते यिः स िािविः पपत्तपवदग्धदृष्टििः
प्राप्ते तृतीयं पि ं तु दोषे ददवा ि प्येष्न्िमश वीिते च
रारौ स शीतािुगृहीतदृष्टििः पपत्ताल्पभावादपप तानि प्येत्
पपतपवदग्धदृटिी
 स्त्िाि
 दोष
 िि
 धचककर्तसा
 Hemeralopia

57. धचककर्तसा
 अशस्त्रकृ त
 गुदिकांजि
 क
ु ब्जकान्जि
 ददिरात्र्यन्ध
गैररक
ं सैन्धवं कृ टिा गोदन्तस्त्य िषी तिा
गोिांसं िररचं बीजं मशरीषस्त्य िििःमश ा
वृन्तं कपपर्तिान्िधुिा स्त्वयङ्गुप्ताफ ानि च
चर्तवार एते योगािः स्त्युरुभयोरञ्जिे दह
 चार योग – उभय दहता

58.  Hemeralopia (from Greek word hemera- "day", and alaos, - "blindness")
 inability to see clearly in bright light
Hemeralopia
Cause
 Cone dystrophy
 anti-epileptic drug trimethadione are typical causes.
 which fails to constrict in response to light;
 aniridia
 Albinism
 Cancer-associated retinopathy(CAR
Management – according to cause

59. तिा िरिः ् ेटिपवदग्धदृष्टिस्त्तान्येव शुक् ानि दह िन्यते तु
त्ररषु ष्स्त्ितोल्पिः पि ेषु दोषो िक्तान्ध्यिापादयनत प्रसह्य
ददवा स सूयामिुगृहीतचिुररिेत रूपाणि कफाल्पभावात्
 स्त्िाि
 दोष
 िि
 धचककर्तसा
 NIGHT BLINDNESS
(NYCTALOPIA)
कफपवदग्धदृटिी

60. • Night (scotopic) vision is a function of rods.
• the conditions in which functioning of these nerve endings is deranged will
result in night blindness.
Cause
 vitamin A deficiency,
 retinal degenerations (e.g., retinitis pigmentosa), congenital high myopia,
familial congenital night blindness and Oguchi’s disease.
 ocular media interfering with the light rays in dim light (i.e. With dilated
pupils).
 These include paracentral lenticular and corneal opacities.
 In advanced cases of primary open angle glaucoma
NIGHT BLINDNESS (NYCTALOPIA)

61.  स्त्िाि
 दोष
 िि
 धचककर्तसा
पवद्योतते येि िरस्त्य दृष्टिदोषामभपन्िा िक
ु स्त्य यद्वत्
धचराणि रूपाणि ददवा स प्येत् स वै पवकारो िक
ु ान्ध्यसञ्ििः
िक
ु ान्ध्य

62. This primary pigmentary retinal dystrophy is a hereditary disorder predominantly
affecting the rods more than the cones.
Inheritance
 autosomal recessive, followed by autosomal dominant.
 X-linked recessive is the least common.
RETINITIS PIGMENTOSA
Incidence
 It occurs in 5 persons per 1000 of the world population.
 Age. - childhood and progresses slowly, often blindness in advanced middle age.
 Sex. - Males are more commonly affected than females in a ratio of 3:2.
 Laterality. - Bilateral and both the eyes are equally affected.

63. Clinical features
(A) Visual symptoms
1. Night blindness. It is the characteristic feature It occurs due to degeneration
of the rods.
2. Dark adaptation
3. Tubular vision occurs in advanced cases.
Fundus changes
Retinal pigmentary changes.
Retinal arterioles are attenuated
Optic disc becomes pale and waxy
Visual field changes
 Annular or ring-shaped scotoma

64. Treatment
It is most unsatisfactory; rather we can say that till date there is no effective
treatment for the disease.
1. Measures to stop progression,
 Vasodilators
 placental extracts
 light exclusion therapy,
 ultrasonic therapy and acupuncture therapy.
 Recently vitamin A and E.
2. Low vision aids (LVA)
3. Rehabilitation - as per his socio-economic background.
4. Prophylaxis.- Genetic counselling

65. स ह्रस्त्वजाड्यो ददवसेषु कृ च्राद्ध्रस्त्वानि रूपाणि च येि प्येत्
 स्त्िाि
 दोष
 िि
 धचककर्तसा
 Micropsia
ह्रस्त्वजाड्यो

66. MICROPSIA
o objects are perceived smaller than they are actually
cause
• Retinal odema
• Macular degeneration
• Central serous retinopathy
• Traumatic brain injury, epilepsy, migraine

67. दृष्टिपवमरूपा ्वसिोपसृटिा सङ्क
ु च्यतेऽभ्यन्तरत्च यानत
रुजावगाढा च तिक्षिरोगं गम्भीररक
े नत प्रवदष्न्त तज्िािः
गम्भीररका
 स्त्िाि
 दोष
 िि
 धचककर्तसा
 pthesis bulbi

68. PTHESIS BULBI
 pthesis bulbi is small, shrunken and nonfuntional eye
 its occur as the end stage of severe ocular disease
 ETIOLOGY
INFLAMMATION
panuveitis
acute and chronic uveitis
Wegener granulomatous
INFECTION
endopthalmitis
ulcerative keratitis
TRUMA
POST SURGICAL

69. शोकज्वरायासमशरोमभतापैरभ्याहता यस्त्य िरस्त्य दृष्टििः |
सधूिकाि् प्यनत सवमभावांस्त्तं धूिदशीनत वदष्न्त रोगि ्
 स्त्िाि
 दोष
 िि
 धचककर्तसा
 पपतज पवसपम िाशक
 रक्त पपत िाशक
 शीत उपक्रि
धूिदशी
युञ्ज्यात् सपपमधूमिदशी िरस्त्तु शेषं क
ु यामरक्तपपत्ते पवधािि ् |
यच्चैवान्यत् पपत्तहृच्चापप सवं यद्वीसपे पैपत्तक
े वै पवधािि ्

70.  Age-related macular degeneration (ARMD), also called senile
macular degeneration,
 it is a bilateral disease of persons of 59 years of age or older.
 It is of two types non-exudative and exudative.
Etiopathogenesis
ARMD is an age-related disease
 risk factors
• heredity, nutrition, smoking, hypertension and exposure to sun light.
• The disease is most prevalent in caucasians.
AGE-RELATED MACULAR DEGENERATION

71. Non-exudative or atrophic ARMD.
• dry or geographic ARMD
• responsible for 90 percent cases.
symptoms
• mild to moderate, gradual loss of vision
• distorted vision,Metamorphsia
• difficulty in reading due to central
shadowing.
Ophthalmoscopically
• drusens (colloid bodies),
• pale areas of retinal pigment epithelium
• atrophy and irregular pigmentation.
Exudative ARMD.
• wet or neovascular ARMD.
• responsible for only 10 percent cases of ARMD
symptoms
• rapidly progressive marked loss of vision.
• More metamorphosia
course of exudative ARMD passes through many stages.
• Stage of drusen formation,
• Stage of retinal pigment epithelium (RPE) detachment,
• Stage of choroidal neovascularisation (CNV)
• Stage of haemorrhagic detachment of RPE,
• Stage of haemorrhagic detachment of neurosensory
retina
• Stage of disciform (scarring) macular degeneration

72. Treatment
There is no effective treatment for non-exudative ARMD.
 Role of dietary supplements and antioxidants in prevention or
treatment of ARMD.
• antioxidants, vitamins and minerals (vitamin C and E, beta carotene,
zinc and copper)
 Treatment modalities available to treat exudative(neovascular) ARMD
• Argon green-laser photocoagulation
• Photodynamic therapy (PDT)
.
Diagnosis
 Fundoscopy
 F.F.A.
 Amsler grid test –
• for progression of disease

73. - निमित्ततस्त्तर मशरोमभतापात् ज्िेयस्त्त ् अमभटयन्द निदशमिै्च
बाह्य िेररोग
1. सनिमित्त म ंगिाश 2. अनिमित्त म ंगिाश
सनिमित्त म ंगिाश
 कारि – मशरोअमभताप
 दोष
 िि – अमभटयन्द सिाि
 धचककर्तसा
 Optic neuritis

74. Etiology
1. Idiopathic
2. Hereditary optic neuritis (Leber’s disease)
3. Demyelinating disorders - multiple sclerosis, neuromyelitis optica
4. Parainfectious optic neuritis - various viral infections such as measles, mumps,
chickenpox, whooping cough and glandular fever.
6. Toxic optic neuritis
OPTIC NEURITIS
 Optic neuritis includes inflammatory and demyelinating disorders of the optic nerve.
Anatomical types. 3 anatomical types:
 Papillitis. - involvement of the optic disc in inflammatory and
demyelinating disorders.
 Neuroretinitis - combined involvement of optic disc and surrounding
retina in the macular area.
 Retrobulbar neuritis - involvement of optic nerve behind the eyeball.

75. Symptoms.
Optic neuritis may be asymptomatic or may be associated with following symptoms:
 Visual loss. Sudden, progressive and profound visual loss
 Dark adaptation
 Visual obscuration in bright light is a typical symptom of acute optic neuritis.
 Impairment of colour vision
 Movement phosphenes and sound induced phosphenes
 Depth perception, particularly for the moving object may be impaired (Pulfrich’s
phenomenon).
 Pain. - mild dull eyeache.
Signs:
1. Visual acuity - reduced markedly.
2. Colour vision - severely impaired.
3. 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.

76. 4. Ophthalmoscopic features
• hyperaemia of the disc and blurring of the margins.
• Disc becomes oedematous
• Splinter haemorrhages
• fine exudates .
• Inflammatory cells in the vitreous
• Inflammatory signs in the surrounding retina when papillitis is
associated with macular star formation
• PAPILLITIS
• neuroretinitis
• fundus appears normal
• retrobulbar neuritis

77. • Efforts should be made to find out and treat the underlying cause.
• There is no effective treatment for idiopathic and hereditary optic
• Corticosteroid therapy may shorten the period of visual loss, but will not influence
the ultimate level of visual recovery in patients with optic neuritis.
• Optic neuritis treatment trial (ONTT) group has made following recommendations
for the use of corticosteroids
Treatment
 Oral prednisolone therapy alone is contraindicated in the treatment of acute
optic neuritis
 patient with acute optic neuritis should have brain MRI scan.
 If the brain shows lesions supportive of multiple sclerosis (MS),
• IV methylprednisolone (1 gm daily) for 3 days
• followed by oral prednisolone (1 mg/kg/day) for 11 days.
• intravenous methylprednisolone in acute optic neuritis patients with a normal
brain MRI scan

78. हन्येत दृष्टििमिुजस्त्य यस्त्य स म ङ्गिाशस्त्र्तवनिमित्तसञ्ििः
तराक्षि पवस्त्पटिमिव अवभानत वैदूयमविाम पवि ा च दृष्टििः
 कारि –
 दोष
 िि –
 धचककर्तसा
 SOLAR RETINOPATHY
अनिमित्त म ंगिाश/ओपसधगमक म ंगिाश
सुरपषमगन्धवमिहोरगािां सन्दशमिेिापप च भास्त्वरािाि्

79.  Photoretinitis, also known as solar retinopathy or eclipse retinopathy
 retinal injury induced by direct or indirect sun viewing.
 Solar retinopathy is associated with religious sun gazing, solar eclipse observing,
telescopic solar viewing, sun bathing and sun watching in psychiatric disorders.
PHOTORETINITIS
Causes of photic retinopathy
- other than solar retinopathy, are:
• Welding arc exposure,
• Lightening retinopathy
• Retinal phototoxicity from ophthalmic instruments like operating
microscope

80. Pathogenesis
Solar radiations damage the retina through:
 Photochemical effects
• produced by UV and visible blue light
 Thermal effects
• may enhance the photochemical effects.
• The long visible wave length and infrared rays from the sun are absorbed by the
pigment epithelium producing a thermal effect.
Clinical features
Symptoms.
• Unilateral or bilateral deceased vision (6/12–6/60) which develops within 1 to 4
hours after solar exposure,
• usually improves to 6/6 –6/12 within six months.

81. Signs.
• Initially the fundus may appear normal.
• Shortly after exposure a small yellow spot with gray
margin may be noted in the foveolar and parafoveolar
region.
• typical lesion appears later- central burnt-out hole in the
pigment epithelium
• In worst cases, typical macular hole may appear
Treatment
• There is no effective treatment for photoretinitis, so emphasis should be on
prevention.
• Eclipse viewing should be use of protective eye wear filters (which absorb UV
and infrared wave lengths).

82.  It refers to retinal changes seen in patients with diabetes mellitus
 In Western countries, it is the leading cause of blindness
DIABETICRETINOPATHY
Etiopathogenesis
Risk factors :
Duration of diabetes- is the most important determining factor.
• Roughly 50 percent of patients develop DR after 10 years,
• 70 percent after 20 years
• 90 percent after 30 years of onset of the disease.
Sex. - Incidence is more in females than males (4:3).
Poor metabolic control.
Heredity.
Pregnancy may accelerate the changes of diabetic retinopathy.
Hypertension, when associated
Other risk factors - smoking, obesity and hyperlipidemia.

83. Pathogenesis.
it is a microangiopathy affecting retinal precapillary arterioles, capillaries and venules
Vascular changes seen in diabetes mellitus
Thickening of capillary basement membrane
Changes in RBCs
Loss of capillary pericytes
Microvascular occlusion
Retinal ischaemia
Capillary leakage
Microaneurysms
Haemorrhage,Retinal oedema,Hard exudates,Arteriovenous shunts
(Intraretinal microvascular abnormalities — IRMA), Neovascularisation

84.  Non-proliferative diabetic retinopathy (NPDR)
• Mild NPDR
• Moderate NPDR
• Severe NPDR
• Very severe NPDR
 Proliferative diabetic retinopathy (PDR)
 Diabetic maculopathy
 Advanced diabetic eye disease (ADED)
Classification

85. Ophthalmoscopic features of NPDR include:
• Microaneurysms - in macular area (the earliest detectable lesion).
• Retinal haemorrhages - both deep (dot and blot haemorrhages) and
superficial haemorrhages (flame-shaped).
Non-proliferative diabetic retinopathy (NPDR)
• Hard exudates-yellowish-white waxy-looking patches
• Retinal oedema
• Cotton-wool spots (if > 8, there is high risk of developing PDR).
• Venous abnormalities,- beading, looping and dilatation.
• Intraretinal microvascular abnormalities (IRMA).

86. Mild NPDR .
• At least one microaneurysm or intraretinal
hemorrhage.
• Hard/soft exudates may or may not be present.
Moderate NPDR
• Moderate microaneurysms/intraretinal
hemorrhage.
• Early mild IRMA.
• Hard/soft exudates may or may not present.
 On the basis of severity of the above findings the NPDR has been further classified

87. Severe NPDR. -Any one of the following (4-2-1 Rule)
• Four quadrants of severe microaneurysms/intraretinal
hemorrhages.
• Two quadrants of venous beading.
• One quadrant of IRMA changes.
Very severe NPDR. - Any two of the following (4-2-1 Rule):
• Four quadrants of severe microaneurysms/intraretinal
hemorrhages.
• Two quadrants of venous beading
• One quadrant of IRMA changes.

88. Proliferative diabetic retinopathy (PDR)
Proliferative diabetic retinopathy develops in more than 50 percent of cases
after about 25 years of the onset of disease.
Therefore, it is more common in patients with juvenile onset diabetes.
It is characterised by proliferation of new vessels from the capillaries, in the
form of neovascularisation at the optic disc (NVD) and/or elsewhere (NVE)
in the fundus,
Types.
1. PDR without HRCs (Early PDR) ,
2. PDR with HRCs (Advanced PDR).
High risk characteristics (HRC) of PDR are as follows
: NVD 1/4 to 1/3 of disc area with or without vitreous haemorrhage (VH) or pre-retinal
haemorrhage (PRH)
NVD < 1/4 disc area with VH or PRH
NVE > 1/2 disc area with VH or PRH
Later on condensation of connective tissue around the new vessels results in
formation of fibrovascular epiretinal membrane.
Vitreous detachment and vitreous haemorrhage may occur in this stage.

89. Investigations
 Urine examination,
 Blood sugar estimation.
 Fundus fluorescein angiography should be carried out to areas of
neovascularisation,
Management
I. Screening for diabetic retinopathy.
 To prevent visual loss occurring from diabetic retinopathy a periodic follow-up is
very important.
 The recommendations for periodic fundus examination are as follows:
• Every year, till there is no diabetic retinopathy or there is mild NPDR.
• Every 6 months, in moderate NPDR.
• Every 3 months, in severe NPDR.
• Every 2 months, in PDR with no high risk characteristic.

90. Medical treatment
 Control of systemic risk
• Strict metabolic control of blood sugar, Lipid reduction, Control of anaemia
 Role of pharmacological modulation.
• Protein kinase C (PKC) inhbitors,
• Vascular endothelial growth factors (VEGF) inhibitors,
• Antioxidants such as vitamin E
 Role of intravitreal steroids
• Flucinolone acetonide intravitreal implant
• Intravitreal injection of triamcinolone (2 to 4 mg)

91.  Macular photocoagulation.
Photocoagulation.
• Macula is treated by laser only if there is clinically significant macular oedema (CSME)
• two laser techniques
 Focal treatment
 Grid treatment.
Panretinal photocoagulation (PRP)
 Surgical treatment - It is required in advanced cases of PDR
• Pars plana vitrectomy
indicated for dense persistent vitreous haemorrhage, tractional retinal detachment,

92. • It refers to fundus changes occurring in patients suffering from systemic hypertension
HYPERTENSIVE RETINOPATHY
Pathogenesis
Three factors which play role in the pathogenesis vasoconstriction, arteriosclerosis and
increased vascular permeability.
Vasoconstriction
• Primary response of the retinal arterioles to raised blood pressure is narrowing
(vasoconstriction)
• It occurs in pure form in young individuals, but is affected by the pre-existing
sclerosis in older patients.
Arteriosclerotic changes
• manifest as changes in arteriolar reflex and A-V nipping result from thickening of
the vessel wall.

93. Increased vascular permeability
• results from hypoxia and is responsible for haemorrhages, exudates and focal retinal
oedema.
Grading of hypertensive retinopathy
• Keith and Wegner (1939) have classified hypertensive retinopathy
Grade I
• mild generalized arteriolar attenuation, particularly
of small branches
Grade II
• Marked generalized narrowing and arterioles
associated with deflection of veins at arteriovenous
crossings (Salus’ sign).

94. Grade III
• Grade II changes + copper-wiring of arterioles, banking of veins distal to
arteriovenous crossings (Bonnet sign)
• tapering of veins on either side of the crossings (Gunn sign)
• Flame-shaped haemorrhages, cotton-wool spots and hard exudates are also present
Grade IV
• changes of Grade III + silver-wiring of arterioles
• papilloedema

95. Clinical types
 Hypertension with involutionary (senile) sclerosis.
• When hypertension occurs in elderly patients (after the age of 50 years) in the
presence of involutionary sclerosis
 Hypertension without sclerosis.
• It occurs in young people
• where elastic retinal arterioles are exposed to raised blood pressure for a short
duration.
• There are minimal signs of arteriovenous crossing.
Hypertension with compensatory arteriolar sclerosis.
• This condition is seen in young patients with prolonged benign hypertension
 Malignant hypertension

96. Managment hypertension retinopathy
• Mild – only blood pressure control
• Moderate – bp control + cholestrol control
• Malignant - physician control stepwise reduction blood pressure and avoid
sudden reduction because it may cause perfution of optic nerve

97. RETINAL VASCULITIS - Inflammation of the retinal vessels may be primary (Eales’ disease) or secondary to
uveitis.
Eales’ disease
 It is an idiopathic inflammation of the peripheral retinal veins.
 It is characterised by recurrent vitreous haemorrhage.
Clinical features.
• It is a bilateral disease, typically affecting young adult males.
• The common presenting symptoms are sudden appearance of floaters (black spots)
in front of the eye
• painless loss of vision due to vitreous haemorrhage.
Etiology.
• It is not known exactly.

98. Clinical course of the Eales’ disease can be described in four stages:
 Stage of inflammation
• peripheral veins are congested and perivascular exudates
• sheathing are seen along their surface.
• Superficial haemorrhages.
 Stage of ischaemia
• Obliteration of the involved vessels and development of avascular areas in the
periphery
Stage of retinal neovascularization
• marked by development of abnormal vessels at the retina.
Stage of sequelae
• Development of complications such as proliferative vitreoretinopathy, tractional
retinal detachment, rubeosis iridis and neovascular glaucoma.

99. Treatment
 Medical treatment.
• Course of oral corticosteroids for extended periods is the main stay of treatment
during active inflammation.
• A course of antitubercular therapy has also been recommended in selective
cases.
 Laser photocoagulation
• indicated in stage of neovascularizion.
 Vitreoretinal surgery is required for non resolving
• vitreous haemorrhage
• tractional retinal detachment.

100. amblyogeneic factors operating during the critical period of visual development
Amblyopia/lazy eye
Definition
Partial loss of vision in one or both eyes, in the absence of any organic disease of
ocular media, retina and visual pathway.
Pathogenesis
 The most sensitive period for development of amblyopia is first six months
of life and it usually does not develop after the age of 6 years.
Amblyogenic factors
• Visual (form sense) deprivation as occurs in anisometropia,
• Light deprivation e.g., due to congenital cataract
• Abnormal binocular interaction e.g., in strabismus

101. Strabismic amblyopia
Stimulus deprivation amblyopia - congenital or traumatic cataract, complete
ptosis and dense central corneal opacity
Anisometropic amblyopia
Isoametropic amblyopia - bilateral amblyopia occurring in children with
bilateral uncorrected high refractive error.
Meridional amblyopia - uncorrected astigmatic refractive error. It is a
selective amblyopia for a specific visual meridian.
Types - Depending upon the cause,

102.  Visual acuity - reduced.
• Recognition acuity is more affected than resolution acuity.
 Effect of neutral density filter.
• Visual acuity when tested through neutral density filter improves by
one or two lines in amblyopia and decreases in patients with organic
lesions.
 Crowding phenomenon
• visual acuity is less when tested with multiple letter charts
(e.g.Snellen’s chart) than when tested with single charts (optotype).
 Colour vision - is usually normal
CLINICAL CHARACTERISTICS

103. amblyopia should be started as early as possible (younger the child, better the prognosis).
 Occlusion therapy
occlusion of the sound eye, to force use of amblyopic eye is the main stay in the
treatment of amblyopia.
Treatment
 before the occlusion therapy is started, it should be ensured that:
 Simplified schedule for occlusion therapy depending up on the age is as below
 Upto 2 years - occlusion done in 2:1, 2 days in sound eye and one day in amblyopic
eye.
 At the age of 3 years, 3:1,
 At the age of 4 years, 4:1,
 At the age of 5 years, 5:1
 After the age of 6 years, 6:1

104.  Normally visual axis of the two eyes are parallel to each other in the ‘primary
position of gaze’ and this alignment is maintained in all positions of gaze.
STRABISMUS
Definition
 misalignment of the visual axes of the two eyes is called squint or strabismus

105. The rectus muscles
originate from a common tendinous ring (the annulus of Zinn)
• Medial rectus arises from the medial part of the ring
• superior rectus from the superior part
• inferior rectus from the inferior part
• lateral rectus from the lateral part by two heads which join in a
‘V’ form.
 All the four recti run forward around the eyeball and are
inserted into the sclera
Superior rectus
Medial
rectus
Inferior
rectus
Lateral
rectus
The superior oblique muscle
• arises from the bone above and medial to the optic foramina.
• It runs forward and turns around a pulley — ‘the trochlea’
• inserted in upper and outer part sclera behind the equator
The inferior oblique muscle
• arises from the orbital plate of maxilla just lateral to
the orifice of the nasolacrimal duct.
• It passes laterally and backward
• inserted into lower and outer part of the sclera behind
the equator

106. Muscle Primary action Secondary action Tertiary action
MR Adduction — —
LR Abduction — —
SR Elevation Intorsion Adduction
IR Depression Extorsion Adduction
SO Intorsion Depression Abduction
IO Extorsion Elevation Abduction
1. Adduction. It is inward movement (medial rotation)
2. Abduction. It is outward movement (lateral rotation)
3. Supraduction. It is upward movement (elevation)
4. Infraduction. It is downward movement (depression).
5. Incycloduction (intorsion). It is a rotatory movement
6. Excycloduction (extorsion). It is a rotatory movement
Types of ocular movements
 Uniocular movements - called ‘ductions’ :

107.  Binocular movements- two types: versions and vergences.
o Versions - conjugate movements - symmetric movements of both eyes in the same
direction
 Dextroversion.
• It is the movement of both eyes to the right.
• It results due to simultaneous contraction of right lateral rectus and left medial rectus.
 Levoversion.
• movement of both eyes to the left.
• It is produced by simultaneous contraction of left lateral rectus and right medial rectus.
 Supraversion
• upward movement
• simultaneous contraction of bilateral superior recti and inferior obliques
 Infraversion.
• downward movement of both eyes
• due to simultaneous contraction of bilateral inferior recti and superior obliques

108.  Dextrocycloversion
• It is rotational movement around the anteroposterior axis
• superior pole of cornea of both the eyes tilts towards the right
 Levocycloversion.
o Vergences - also called disjugate movements
• Convergence.
 It is simultaneous inward movement of both eyes which results from
contraction of the medial recti.
• Divergence.
 It is simultaneous outward movement of both eyes produced by contraction of
the lateral recti.
symmetric movements of both eyes in opposite directions

109. Definition
When a normal individual fixes his visual attention on an object of regard, the image is
formed on the fovea of both the eyes separately; but the individual perceives a single
image. This state is called binocular single vision
BINOCULAR SINGLE VISION
Visual development
• At birth there - no central fixation and the eyes move randomly.
• first month of life - fixation reflex starts developing and established by 6
months.
• in 6 months - macular stereopsis and accommodation reflex is fully
developed.
• in 6 year of age full visual acuity (6/6) is attained and binocular single vision
is well developed.

110. Grades of binocular single vision
• There are three grades of binocular single vision, which tested by synoptophore
 Grade I — Simultaneous perception.
• It is the power to see two dissimilar objects simultaneously.
• It is tested by projecting two dissimilar objects in front of the two eyes.
 Grade II—Fusion.
• It consists of the power to superimpose two incomplete but similar images to form one complete image
 Grade III— Stereopsis.
• It consists of the ability to perceive the third dimension (depth perception).
• It can be tested with stereopsis slides in synoptophore

111. Broadly, strabismus can be classified as below:
I. Apparent squint or pseudo strabismus.
II. Latent squint (Heterophoria)
III. Manifest squint (Heterotropia)
 Concomitant squint
 Incomitant squint.
Classification of strabismus
In pseudostrabismus the visual axes are in fact parallel, but the eyes seem to have a squint:
PSEUDOSTRABISMUS
Pseudoesotropia or apparent convergent squint
• prominent epicanthal fold and negative angle kappa.
Pseudoexotropia or apparent divergent squint
• may be associated with hypertelorism and positive angle kappa.

112.  Heterophoria also known as ‘latent strabismus’, is a condition in which the
tendency of the eyes to deviate is kept latent by fusion.
 Therefore, when the influence of fusion is removed the visual axis of one eye
deviates away.
 Orthophoria is a condition of perfect alignment of the two eyes which is
maintained even after the removal of influence of fusion.
 orthophoria is a theoretical ideal.
 Practically a small amount of heterophoria is of universal occurrence and is
known as ‘physiological heterophoria
HETEROPHORIA

113.  Esophoria - It is a tendency to converge.
 Exophoria - It is a tendency to diverge.
 Hyperphoria. It is a tendency to deviate upwards,
 Hypophoria - is a tendency to deviate
 Cyclophoria. - It is a tendency to rotate around the anteroposterior axis
Types of heterophoria
Etiology
A. Anatomical factors
1. Orbital asymmetry.
2. Abnormal interpupillary distance - wide IPD is associated with exophoria and small with
esophoria.
3. Faulty insertion of extraocular muscle.
4. A mild degree of extraocular muscle weakness.
5. Anatomical variation in the position of the macula in relation to the optical axis of the
eye.

114. B. Physiological factors
1. Age. - Esophoria is more common in younger age and exophoria which is
more in elderly.
2. Role of accommodation.
• Increased accommodation is associated with esophoria and decreased
accommodation with exophoria.
3. Role of convergence.
• Excessive use of convergence may cause esophoria while decreased use of
convergence is often associated with exophoria
4. Dissociation factor
• prolonged constant use of one eye may result in exophoria (as occurs in
individuals using uniocular microscope and watch makers using uniocular
magnifying glass).