NEURO OPHTHALMOLOGY

AFFERENT  PUPILLARY DEFECT-

1. Absolute APD – AMAUROTIC PUPIL
2. Relative APD- MARCUS GUNN PUPIL

ABSOLUTE APD-

• Complete ON lesion
• Inv eye- No PL
• Both pupils- equal in size
• When the affected eye is stimulated→ neither pupil reacts
• When the nml eye is stimulated→ both pupils react nmlly
• Near reflex is nml

    RELATIVE APD-

• Caused by –incomplete ON lesion

                     -Sev retinal dis

                     -NEVER by a dense cataract

*  Swinging flashlight test-

When nml eye is stimulated→ Both pupils constrict

When abnml eye is stimulated→ Both pupils dilate

• This paradoxical dilatation of pupils occurs b’cos the dilatation produced by withdrawing the light from the nml eye outweighs the constriction produced by stimulating the abnml eye.
• Afferent /sensory lesions- Pupils are equal in size
• Efferent/ motor lesions-Anisocoria [unequal pupil size]

APD-

    Causes of APD-

1. AION
2. Optic neuritis
3. Glaucoma
4. CRAO / CRVO
5. Lesion of optic chiasma / optic tract
6. Amblyopia
7. VH
8. Macular degeneration
9. BRVO /BRAO

10.RD

OPTIC NERVE-

Length- 50mm

• Intraocular -1mm
• Intraorbital -25-30mm
• Intracanalicular- 6mm
• Intracranial- 10mm

                       OPTIC ATROPHY-case

DEF-

A condition characterized by loss of conducting function of the ON with pallor of the disc d/t gliosis & loss of capillaries.

PATHOGENESIS-

Degeneration of optic N fib→ Proliferation of astrocytes & glial tiss [Loss of transparency ] →When light enters the disc, instead of refraction , it gets reflected back→ so the disc appears pale.

VIVA-

CLASSIFICATION-

A] PATHOLOGICAL-

  1. Ascending OA

  2. Descending OA

     3. Inherited OA

B] OPHTHALMOSCOPIC-

  1. primary OA

  2. Secondary OA

  3.Consecutive OA

  4. Cavernous / glaucomatous OA

  5. Segmental / partial OA

PATHOLOGICAL-

ASCENDING OA-

• Also k/as Wallerian degeneration
• Prim lesion- ret,ON & choroids
• Atrophy proceeds towards the brain
• Eg

1. RP
2. CRAO
3. Papilloedema
4. Glaucoma
5. Toxic amb
6. Choroiditis

DESCENDING OA-

• Also k/as retrograde OA
• Brain/eye→ ON
• Eg- Chiasmal compression

        -Retrobulbar neuritis

INHERITED OA-

1. Congenital / Infantile OA-

Recessive form-

• OA shortly after birth
• Profound LOV
• Nystagmus
• Defective CV

Dominant form-

                       -blindness seldom occurs

                       -Vision slowly decreases

                      -central & paracentral scotoma

2. Leber’s OA- X –linked recessive

                      -men

                      -2-3 decade

-ul sudden LOV

-Fundus- Disc edema  + hyperaemia

            -telangiectatic BV s around disc

             -edematous NFL

             -Sec OA later

-Fields- dense central /centrocaecal scotoma

-Mild spasticity & gait disturbance

3. behr’s OA-

-Infancy

-AR

- Incomplete BL OA

-Temporal pallor

-Cerebellar ataxia

-Spasticity

-Pyramidal tr lesion

OPHTHALMOSCOPIC CLASSN-

CONSECUTIVE OA-

Follows dis of retina , choroid & retinal vasculature.

-Disc-Waxy pallor

       -nml margins

-Marked attenuation of As

-Nml physiological cup

-Asstd retinal pathology

• RP
• Choroiditis
• Chorioretinitis
• CRAO

TOXIC OA-

Tobacco ,ETB, streptomycin, INH, lead, arsenic.

Degeneration of axial portion of retrobulbar ON→ Fibrosis & gliosis in papillomacular bundle→ Temporal pallor.[ bcos PM fib enter the disc temporally]

PRIMARY OA-[viva]

-Orderly deg of nerve fib & replacement by glial tiss without alteration in the architecture of ONH

-Disc-chalky white

        -Sharply defined margins

        -Lamina cribrosa well seen        

        -surrounding ret is nml

        -Retinal BVs- nml

        -Retinal periphery-nml

Eg-

• Pituitary tum
• Retrobulbar neuritis
• Demyelinating dis
• Tabes dorsalis
• Toxic & nutritional neuropathies
• Hereditary neuropathies

-Lesions anterior to optic chiasma→ UL OA

-Lesions inv the chiasm & optic tract→ BL OA

BAND /BOWTIE OA-

• Chiasmal lesion
• -Pallor is on nasal & temporal side of disc ,sparing the sup & inf aspect
• Inv the PM bundle which enters the disc temporally

   KESTENBAUM SIGN-

Decrease in the number of capillaries on the disc surface

SECONDARY OA-

-Preceded by swelling of ONH

-Marked deg of optic n fib

-Excessive proliferation of glial tiss.

-Disc-

*  Dirty grey pallor

*  Poorly defined disc margin

*  Physiological cup obliterated [Cup is filled with proliferating fibroglial tiss→ lamina cribrosa cannot be seen]

*  Peripapillary sheathing of arteries

*  Tortuous & narrowed veins

Eg

• Papilloedema
• Papillitis
• AION

CAVERNOUS OA-

-Also k/as Glaucomatous / Schnabel’s OA

-Axonal deg without glial tiss proliferation→ Caverns → filled with hyaluronic acid

-Features-

*  Vertical enlargement of the cup

*  Notching of NRR

*  Laminar dot sign

*  Bayonetting sign

*  Backward bowing of lamina cribrosa

*  Nasal shifting of BV

*  Baring of circumlinear BVs

*  Splinter h’ages

*  Saucerization of disc

Eg-

• Glaucoma
• Methyl alcohol poisoning

ALTITUDINAL DISC PALLOR-

-Segmental disc swelling  fol by segmental OA

-AION

WEDGE SHAPED PALLOR-

BRVO

            OPTIC NEURITIS-case

DEF-Inflamn of ON

CLASS-

1. Inflamn affecting the ophthalmoscopically visible part of the nerve at the disc & thus showing obvious signs of disease

1. Papillitis
2. Neuroretinitis

2. Inflamn which attacks the nerve proximal to this region & thus shows no ophthalmoscopic change.

3. Retrobulbar neuritis

 PATHOLOGY-

3 types of neuritis-

1) PERINEURITIS / PERI-AXIAL NEURITIS-

   Leptomeningitis of the optic n & may represent a spread from the brain / orbit & sinuses.It may extend along the pial septa into the nerve parenchyma affecting the extramacular fib

2) AXIAL NEURITIS-

-Affects the Macular fib

-Causes a centrocaecal scotoma & temporal pallor of the disc

Eg-

• MS
• Toxic & nutritional neuropathies

3) TRANSVERSE NEURITIS

   Both axial & periaxial neuritis may progress to inv all the fib.

VIVA-

Q- MC type of ON in childn→ PAPILLITIS

Q-MCC of ON in childn→ POSTVIRAL

AETIO-

1. Idiopathic

             2. Demyelinating disorders

1. Multiple sclerosis
2. Acute Disseminated Encephalomyelitis [ADEM]
3. Neuromyelitis optica [Devic’s dis]
4. Diffuse Periaxial Encephalitis [ Schilder’s dis ]

3.Infections-

Local-

• Endophthalmitis
• Orbital cellulitis
• Sinusitis
• Contiguous spread from meninges, brain & base of skull

           Systemic-

     Bacterial-

• Tb
• Syphillis
• Cat-scratch dis
• Lyme’s dis

Viral-

• Influenza
• Measles
• Mumps
• Chickenpox
• HZV
• Infectious mononucleosis
• CMV

Protozoal-

• Toxocariasis
• Toxoplasmosis
• Malaria
• Pneumonia

Fungal-

• Cryptococcosis
• Histoplasmosis

Parasitic-Cysticercosis

4.Immune-mediated disorders

Local-

• Uveitis
• Sympathetic oph

Systemic-

• Sarcoidosis
• Wegener’s granulomatosis
• Ac Disseminated encephalomyelitis

C/F-

• Women
• 20-40 yrs
• Visual loss-usually UL-adults

                                   BL-childn

• Pain- Increases on eye movt-elev & adduction [d/t inv of SR &MR which share the same sheath with optic N]
• Uhthoff’s phen-Worsening of symptoms on exercise / rise in temp
• Pulfrich’s phen- Altered perception of moving objects
• Loss of colour vision [ Typically red desaturation]
• Reduced perception of light intensity
• RAPD
• Visual fields- central / centrocaecal scotoma
• Fundus-

-Vitreous opacities

-Retrobulbar neuritis-nml optic disc & NFL

-Papillitis- Disc-hyperaemia,

               -Peripapillary flame shaped h’ages

-Neuroretinitis-Disc hyperaemia + macular star

INV-

1. Visual fields-perimetry-central/centrocaecal scotoma
2. VEP-Prolonged latency
3. Complete bld count
4. Rapid plasma reagin
5. C-reactive protein
6. ESR
7. Fluorescent treponemal antibody –absorption [FTA-ABS]test
8. Anti-nuclear antibody [ANA] test
9. MRI-brain & orbit with gadolinium enhancement→For MS → periventricular plaques
10. Tb-X-ray chest

                -Montoux

                -sputum

11.Sarcoidosis-X-ray chest

                      -Gallium scan

12.Bld sugar

13. Sinusitis-X-ray –PNS

ATYPICAL ON-

• Out of typical age range
• No pain on eye movt
• Poor vision > 2wks

D/D-

1. Papilloedema
2. Optic N compression [Pituitary tum,meningioma]
3. AION
4. Toxic / nutritional def amblyopia
5. Non-organic visual loss
6. Leber’s hereditary OA

FEATURES	PAPILLOEDEMA	PAPILLITIS
LATERALITY	BL	UL
VISION	Transient LOV	Sudden LOV
OM	N	Restricted & painful
COLOR VISION	N	Affected
PUPILLARY REAC	N	RAPD
VITREOUS OPACITY	Absent	Present
DISC SWELLING	> + 3 D	+ 2D to + 3D
H’AGE & EXUD	More	Less
VISUAL FIELD	Constricted Enlarged blind spot	Central /centrocaecal scotoma
RECOVERY OF VISION	Usually not complete	Usually complete

T/T-

Pulsed steroid therapy-

IV Methyl prednisolone 1gm/day over 1 hour for 3 days→

Oral prednisolone 1 mg/kg/day for 11days

 ISCHEAMIC OPTIC NEUROPATHY-case

DEF-Acute painless optic neuropathy occurring sec to optic N ischaemia.

2 types-

1] Anterior ischaemic ON

2] Posterior ischaemic ON

Anterior ION→ Arteritic

                     → Non-arteritic

NO	FEATURES	ARTERITIC	NON-ARTERITIC
1.	AGE	70 YRS	60 YRS
2.	SEX	3F> M	M=F
3.	SYMPTOMS	Headache Scalp tenderness Jaw claudication	Pain
4.	V/A	Upto 76% <6/60	Upto 61% < 6/60
5.	DISC	More pale	More hyperaemic
6.	CUP	N	Small
7.	ESR	70	20-40
8.	FFA	Disc & choroids filling delay	Disc filling delay

OCULAR FEATURES-

• rapid onset
• Painless
• UL LOV
• Visual field-Altitudinal defect,Arcuate scot,centrocecal def
• RAPD
• Disc edema
• Surface telangiectasia
• Flame-shaped h’ages
• Peri-papillary arterioles are narrowed

ARTERITC AION-

Giant cell arteritis-[ J-07-T/T]

• Headache
• Jaw claudication
• Scalp tenderness
• Prominent Temporal A
• Occult temporal arteritis-visual loss in the absence of overt systemic symptoms
• Pallor with disc edema
• Choroidal ischaemia→ peripapillary pallor & edema
• Fellow eye-N disc dia & cup

NON-ARTERITIC AION-

• Unrelated to temporal arteritis
• Visual impairment on awakening [Nocturnal hypotension]
• Hyperemic disc edema
• Telangiectasia-represents microvascular shunting from ischemic to non-ischemic region of ON→ c/as Luxury perfusion
• C/L eye-disc-small & Cup –small/absent→ k/as-‘Disc at risk’

INV-

1. ESR
2. Serum C-reactive protein
3. Superficial temporal A biopsy-

• Take biopsy from the ipsilateral side
• Ideal location is the temple, bcos it avoids damage to a major br of Auriculotemporal N
• Atleast 2.5cm section shud be taken & serial sections shud be examined b/o the pheno of ‘skip lesions’
• Patho-Thickening of the intima,Chr inflame infiltrate with giant cells

4.FFA- Prolonged choroidal filling time

Risk factors-

• HT
• DM
• IHD
• Thyroid dis
• COPD
• Carotid occlusive dis
• Vasculitis
• Migraine
• Nocturnal hypotension
• Hyperopia
• Smoking
• HLA-A29
• Hyperlipidemia

D/DS-

1.Non-arteritic ischemic ON-

-young

-less severe visual loss

-nml ESR

2. Optic neuritis-

-young

-painful ocular movts

-Hyperemic OD edema

3. Compressive optic N tum

-Slowly prog visual loss

4. CRVO

-Sev vis loss

-RAPD

-disc edema

-diffuse ret h’ages extending to periphery

5. CRAO-

-sudden painless,sev LOV

-RAPD

-no disc edema

-retinal edema

-cherry red spot

T/T-

1. Start systemic steroids.-Do not wait for temporal A biopsy report b’cos visual loss is permanent

IV methyl prednisolone 1 gm /day over 1 hour for 3 days

    → Foll by oral prednisolone 1mg/kg/day for 11 days

POSTERIOR ISCHEMIC ON-

D/t disorder of small pial Vs that supply the intraorbital portion of ON away from the eyeball.

ETIO-

• Giant cell arteritis
• SLE
• Sys hypotension /Shock optic neuropathy

   C/F-

• Visual loss
• RAPD
• No disc edema
• No h’ages

   T/T- Same

                      PAPILLOEDEMA-case

 

CSF CIRCULATION-

• CSF is formed by the choroid plexus in the ventricles of the brain
• Choroidal plexus→ Lateral ventricles → Foramen of Monro→ III ventricle→ Aqueduct of Sylvius→ IV ventricle→ Foramen of Luschka & Magendie→ SAS→Absorption by the arachnoid villi into the cerebral venous drainage system

NORMAL CSF PRESSURE-

• Infants- < 80 mm H2O
• Childn- < 90 mmH2O
• Adults- < 210 mmH2O

Papilloedema is also k/as ‘Choked disc’

DEF-

Swelling of the ONH d/t rise in ICP.

Passive edema without primary inflamn

Papilloedema→ Disc edema + rise in ICP

Disc swelling→ Disc edema -  rise in ICP

PATHOGENESIS-

• Lamina cribrosa divides the ON into –intraocular part  & retroocular part.
• Nmlly-Tiss press within the intraocular part is more than the retro-ocular part→ Disturbance in the press gradient across the lamina cribrosa→ i.e if the press in the IO part falls or press in the retro-ocular part becomes more→Disc edema
• Increase in CSF press in cranial SAS transmitted to SAS around the ON→ Alters the press gradient across the lamina cribrosa→Stasis of axoplasm in pre-laminar reg→ venous congestion→ Disc edema

AETIO-

1. Ocular
2. Orbital
3. Intracranial
4. Systemic
1. OCULAR CAUSES-Hypotension

                                      -Acute hypertension

Hypotension→ decrease tiss press in the pre-laminar region→ disc edema

Eg-

• Ocular trauma
• Parsplanitis
• Irvine – Gas syn
• CB & choroidal detachment

Acute hypertension-Eg –Acute angle closure glaucoma→ Obliteration of peripapillary Vs→ Anoxia→ disc edema

3. ORBITAL-

• Tumours
• Orbital abscess
• Endocrine exophthalmos
• Sinusitis

4. INTRACRANIAL-

1. Tumours-

Papilloedema + brain tum→”Plerocephalic edema”

Highest % in –Mid-brain

                     -Cerebellum

                     -Parieto-occipital region

2. Brain abscess

3. Cavernous sinus thrombosis

4 Aneurysm

5. SAH

6.Pseudotum cerebri

7. Malignant HT

8. Meningitis /Encephalitis

9. Tuberculomata & Gummata

10.Parasitic inf

11. Hydrocephalus

5. SYSTEMIC DIS-

• HT
• Bld dyscrasias- Pernicious anemia

                           -Polycythemia vera

                           -Thrombocytopenic purpura

                           -Leukemia

* Endocrine

UNILATERAL DISC EDEMA-

1. Papilloedema
2. Papillitis
3. AION
4. CRVO
5. Orbital tum
6. Ocular hypotony
7. Foster Kennedy syn→Frontal lobe tumour with I/L  OA & C/L  Papilloedema

PSEUDO FOSTER KENNEDY SYNDROME-

D/t giant cell arteritis involving both the discs at diff times.

    BILATERAL DISC EDEMA-

1. papilloedema
2. HTR
3. Diabetic papillopathy
4. TED
5. CCF
6. Leber’s on
7. Anaemia & Hypoxemia

    PSEUDOPAPILLOEDEMA-

1. Optic disc drusen
2. Hyperopia
3. Disc NV
4. Myelinated nerve fibres
5. Astrocytic hamartomas
6. Bergmister’s papilla

PATHOLOGY-

• Edematous swelling of NFL
• Infiltration of all the tiss with fld
• Lamina cribrosa bows forward with ant convexity
• Small / obliterated physiological cup
• Peripapillary ret displaced laterally & thrown into folds
• Both veins & capillaries distended
• Peripapillary h’ages
• SAS distended
• Swollen NFL contains cytoid bodies

C/F-

SYMPTOMS-

1. Transient LOV –Blackouts  [D/Ds]
2. Headache
3. Nausea/ vomitg
4. Diplopia [Rise in ICP→VI n palsy]

SIGNS-

1] EARLY PAPILLOEDEMA-

1. Symptoms are absent

2. V/A –N

3. Disc-Hyperaemia

          -Blurred margins [ nasal to begin with]

4. Swelling of peripapillary NFL

5.Loss of spontaneous venous pulsation

2] ESTABLISHED PAPILLOEDEMA

*  Transient LOV

*  Disc-Sev hyperemia

          -Mod elev

          -indistinct margins

          -Cup obscured

          -Small Vs obscured

* Venous engorgement

* flame-shaped h’ages

*  CW spots

*Circumferential ret folds

* Macular star [ DDs]

* Blind spot enlarged

TRANSIENT LOSS OF VISION-  viva  [MICA]

1] amaurosis fugax

2] Migraine

3] Impending CRVO & CRAO

4] Cerebrovascular insufficiency

MACULAR STAR –DDs-

• HTR
• DR
• CRVO
• CRAO
• Macular edema
• Neuroretinitis
• Juxtapapillary choroiditis

3] LONGSTANDING [ VINTAGE] PAPILLOEDEMA-

*  Variable V/A

* Visual fields begin to constrict

*  Disc- markedly elevated-‘CHAMPAIGNE CORK’

* CW spots –nt

* H’ages-nt

* Optociliary shunts

4] ATROPHIC PAPILLOEDEMA-

* Sec OA [DDs]

* Vision –sev impaired

* disc- Dirty grey

         -Slightly elevated

        -few crossing BVs

        -Indistinct margins

SECONDARY OA-{ D/Ds}

2. Papillitis
3. Papilloedema
4. AION

DD-Papilloedema-

• Papillitis
• Hyperopia
• Medullated NF
• Optic disc drusens

                    NYSTAGMUS-case

DEF-

Repetitive, Involuntary ,rhythmic ,to & fro oscillations of the eyeball.   [RIRO]

SACCADES-

Fixate on objects

PURSUIT S-

Maintain fixation

CLASS-

1. JERKY  NYSTAGMUS-

• Saccadic
• Slow defoveating movt & a fast refoveating movt.

2. PENDULAR NYSTAGMUS-

• Non-saccadic
• Both the foveating & defoveating movts are equal in velocity & amplitude.

Amplitude of nystagmus – means how far the eyes move

Frequency of nystagmus –means how often the eyes oscillate

3. MIXED NYSTAGMUS

Pendular nys in prim gaze & jerk nys on lateral gaze.

CLINICAL TYPES-

PHYSIOLOGICAL NYSTAGMUS- [ D-04]

1. END-GAZE NYSTAGMUS-

Fine jerky nystagmus in extreme gaze pos

B. OPTO-KINETIC NYSTAGMUS-

Jerk nys induced by moving repeatitive visual patterns across the visual field

C. VESTIBULAR NYSTAGMUS-

• Jerk nys
• Slow phase initiated by vestibular nuclei
• Fast phase initiated by brainstem & frontomesencephalic pathway
• COWS-
• Cold water poured into right ear-->Left jerk nys
• Warm water poured into right ear->Right jerk nys
• Cold water poured into both ears simultaneously→ jerk nys with fast phase upwards
• Warm water in both ears simultaneously→ Jerk nys with fast phase downwards.
• COLD SLOWS THINGS DOWN

MOTOR IMBALANCE NYSTAGMUS-

1.CONGENITAL NYSTAGMUS-

*  X-linked recessive or AD

*  Jerk or pendular type

* Binocular & similar amplitude in both the eyes

* good V/A

*  uniplanar

* Null zone present. So abnml head posture.

* High astigmatism→ Rx –contact lens

*   Horizontal

*  Dampened by eye closure [sleep] & convergence

*  Persists thru out life.

2.SPASMAS MUTANS-

*   Pendular nys

*   Abnml head posture

*   Head nodding

*   Occurs bet 4mo & 2yrs of age

*    diff in maintaining fixation

*  Insufficient control d/t instable motor cortical centres

3.LATENT NYSTAGMUS-

*  Bil, jerk & horizontal nys

*  With both eyes open-No nys

*   Nys on covering one eye

* Fast phase in dir of uncovered eye

* Asstd with-Esotropia & DVD

4.PERIODIC ALTERNATING NYSTAGMUS-

* Conjugate horizontal jerk nys that periodically reverses its direction

* Causes- Demyelination

             -Brainstem dis

5.CONVERGENCE RETRACTION NYSTAGMUS-

*  Caused by co-contraction of EO ms

* Jerk nys induced by passing an OKN tape downwards

*  Upwards refixation saccade brings the two eyes towards each other

* Asstd with globe retraction

* Lesion-Pe-tectal area

5. DOWNBEAT NYSTAGMUS-

• Vertical nys with fast phase downwards
• Increases in lateral gaze
• Lesion- Cervico-medullary juncn at the foramen magnum
• Causes-Arnold Chiari malformn

               -Syringobulbia

               -Wernicke’s encephalopathy

               -Hydrocephalus

               -Demyelination

                -Lithium,phenytoin,carbemazepine,barbiturates,alcohol

6.UPBEAT NYSTAGMUS-

*  Vertical nys with fast phase upwards

*   Causes- Posterior fossa lesion

               -Wernicke’s encephalopathy

7.SEE-SAW NYSTAGMUS-

*  Pendular nys in which one eye elevates & intorts & the other eye depresses & extorts.

*  Cause- Chiasmal lesion with bitemporal hemianopia

            -III ventricle

             -syringobulbia

             -brainstem stroke

8. ATAXIC NYSTAGMUS-

• Horizontal jerk nys which occurs in the abducting eye.
• * Cause-INO

    9.MINER’S NYSTAGMUS-

    *  Rotatory rapid nys

    * Defective vision at night with dancing  movt of light            objects.

*   pendular nys in prim pos & later jerky nys in lateral gaze

* due to low illumination in mine workers

    10.NYSTAGMUS BLOCKAGE SNY-

    *  Purposive esotropia  dampens the nys

    * compensatory phen

T/T-

A] General Rx-

*  Rx of cause

*  good food

*  Visual hygiene

B] Specific Rx-

A) CONSERVATIVE-

1)  OPTICAL-

* Correction of refractive error

*  Stimulating accommodative convergence- by overcorrecting minus lenses

*  Gallilean arrangement of contact lenses & spec

*  CL-For high ref error.They give good visual stim for fusional control

B) PRISMOTHERAPY-

1. Base –out prism [7PD]- For fusional convergence→ Decreases nystagmus in congenital nys

2. Apex in prefered dir of gaze [ base towards face turn]

C) MEDICAL THERAPY-

1.  Cyclopentolate 1 % BD

2.  Botulinum A toxin –Retrobulbar space [ 10-25 U in 0.1-1ml every 3-4 mo]

3.  Baclofen -5mg TDS

                   -Increase every 3days

                   -max 80 mg/day

                   - Periodic alternating nys

4. clonazepam- Downbeat nys

5. Carbamezepine- Sup obl myokymia

3. Propranolol- opsoclonus

D)ORTHOPTICS

  1. Pleoptics

2. Penalization

3. Occlusion-

Partial occlusion of sound eye with a neutral density filter to reduce the V/A in the fixing eye below that of the amblyopic eye

B]SURGICAL-

1) Faden’s posterior fixation suture

Ind-

1. Abnml head posture
2. nystagmus blockage syn
3. for decreasing nys intensity

Tech- The muscle creating the nys is sutured to the sclera at the equator

2) Modified Kestenbaum surg-

-Indicated in all cases with 20 % face turn

- Recession-resection of all 4 recti [ equal amt of 5mm for all recti]

- Similarly vertical ms recession-resection for chin elevation / depression of 25 deg or more

       VISUAL FIELD DEFECTS-spot

Notes-diag

1. OPTIC N-

A )CENTRAL SCOTOMA- Depressed area of visual field inv the fixation point.

UNILATERAL CENTRAL SCOTOMA-

• Optic neuritis
• Compressive lesion of ON

   BILATERAL CENTRAL SCOTOMA-

• Nutrional ON
• Hereditary ON
• Toxic ON

B )CECOCENTRAL SCOTOMA- Involves fixation pt + blind  spot

• Toxic ON
• Serous RD
• Optic pit

C ) ARCUATE SCOTOMA- Inv superior & inf arcuate nerve fibres  

*  Glaucoma

* AION

* Papilloedema

* Optic disc drusen

* Optic pits

* BRVO

D ) ALTITUDINAL SCOTOMA-Inv the upper / lower half of visual field in one / both eyes

1. AION

2.ONH Drusen

3. Chr papilloedema

4. ONH coloboma

5. Hemiretinal V occlusion

Strongly suggests a vascular etio

2. CHIASMAL LESIONS- BITEMPORAL HEMIANOPIA

• Infrachiasmatic- Pituitary adenoma
• Suprachiasmatic- Meningioma, craniopharyngioma
• Intrachiasmatic-Glioma

PITUITARY ADENOMA-

• Typical field defect- Bitemporal hemianopia
• Bitemporal hemianopia→ Scotomatous

                                         → Non-scotomatous

• Scotomatous-

• Stops at the vertical meridian
• Progresses Clockwise-RE

                     Anticlockwise-LE

-Junctional scotoma of Traquair-

Central scot in one eye & superotemporal scot in other eye.

D/t inv of Von Willibrandt’s knee [ i.e lower nasal fib of ipsilateral side loop into the C/L side]

• Non-scotomatous –

• Upper temporal quad are symmetrically depressed→ LT→ cross the vertical midline→ LN→ UN
• Return of funcn is in opp dir.

SUPRACHIASMATIC-

1. Those that impinge on the chisma from anterosuperior dir→ Meningioma
2. Those that attack from posterosuperior dir→ Craniopharyngioma

INFRACHIASMATIC- Craniopharyngioma

PSEUDO-BITEMPORAL HEMIANOPIA-

• Bil sectoral retinitis pigmentosa
• Bil inferotemporal retinoschisis
• Tilted disc

3. OPTIC TRACT-

• Retrochiasmal lesions cause homonymous hemianopia i.e occur in each eye on the same side of visual field
• Respect the vertical meridian
• Nerve fib from corresponding retinal elements in each eye are not closely aligned in either the optic tract / LGB→ Incongruous homonymous hemiaopia [ i.e Dissimiliar field defect]

4. RETROGENICULATE-

1. OPTIC RADIATION-

• Homonymous hemianopia
• TEMPORAL LOBE- ‘PIE IN THE SKY’

                                     -Inv inferior fib of optic radiation

                                     -Lesion-Infarction

                                                 -Tum

                                                 -Abscess

                                      -Seizures

                                      -Visual hallucinations

*  PARIETAL LOBE- ‘PIE ON THE FLOOR’

                                  -Inv superior fib of optic radn

                                  -Lesion-Infarction

                                              -Tum

                                              -Abscess

                                 -Hemiparesis

     Gertsman syn -Acalculia

                            -Agnosia

                            -Rt-Lt confusion

                           -Dyslexia-inability to read letters

                          

GERTSMAN SYN-acalculia & inability to name fingers from left to right.

B. OCCIPITAL CORTEX-

*  Extremely congruous

* Very complex, like pieces in a jig-saw puzzle

*  Macular sparing.

Reasons-

1. Large macular projection in occipital cortex
2. Dual bld supply-Middle & posterior cerebral cir
3. Possibility of dual macular innervation also exists

• Occipital lesions are vascular
• Occipital lobe → Nml OKN
• Parietal lobe→ Abnml OKN
• RIDDOCH PHEN-

Specific for occipital lobe lesions

Ability to detect movts & not an object in an area of visual field.

CALCRINE FISSURE-

• Lesion→ UL loss of temporal crescent
• Sparing→ Preservation of temporal crescent
• Thus preservatn or loss of temporal crescent proves that the lesion is in occipital cortex
• CORTICAL BLINDNESS- ANTON’S SYN

Denial of blindness

Complete blindness + nml pupillary response

              PUPILLARY REACTIONS

LIGHT REFLEX

Afferent- Optic N

Efferent- III N

Rods & cones → Ganglion cells → Optic N → optic chiasma [Nasal fib decussate & temporal fib remain uncrossed ]

→ Pre-tectal nucleus [Nasal fib go to C/L nu & temporal fib to I/L nu ]→ EW nu. These are the internuncial fib responsible for consensual light reflex.--> III N [inf div ]→

N to IO→ ciliary ganglion→ short ciliary Ns→ sphincter pupillae

* Normally, there is a tonic inhibitory input from the cerebral cortex to the EW nu.

*  During sleep, there is dimunitionof this input resulting in papillary constriction.

FUNCTIONS OF LIGHT REFLEX-

1. Light ref→ pupillary constriction →less amt of light enters the eye → protects the eye against bleaching
2. Helps in light & dark adaptation

-Large pupil → admits more light → allows greater acuity in dim illumination.

-Small pupil → limits ref aberrations → greater acuity

WERNICKE’S PUPIL-

• Lesion of optic tract
• Light reflex [direct+consensual] is absent when light is thrown on the temporal retina of affected side & nasal retina of opposite side. Vice versa it is present

ILL-SUSTAINED PUPILLARY REAC-

Optic neuritis

OPTIC ATROPHY- Direct light rea -nt

                               -Consensual +nt

NEAR REFLEX-

TRIAD-Convergence

           -Accomodation

           -Pupillary constriction

SYMPATHETIC SUPPLY-

Post Hypothalamus [1st neuron ]→ Brainstem→ Ciliospinal centre of Budge [2nd neuron ]→ Sup cervical ganglion [3rd neuron ]→ ascends along the ICA→ skull→Joins oph div of V n→ via nasociliary & Long ciliary N→ ciliary body & dilator pupillae

LIGHT  NEAR DISSOCIATION

• Light reflex – absent / sluggish
• Near reflex – nml

CAUSES-

UNILATERAL-

1. Afferent conduction defect
2. Adie’s pupil                                          3As + H
3. HZO
4. Aberrant regeneration of III N

    BILATERAL-

1. Neurosyphyllis
2. DM
3. myotonic dystrophy
4. Parinaud’s dorsal midbrain syn
5. Familial amyloidosis
6. Encephalitis
7. Chr alcoholism

ARGYLL ROBERTSON PUPIL

• Lesion –tectum-interfere with light reflex fibres
• BL
• pupils –small & irreg
• Light rea- Absent
• Accomodation rea – present
• Good vision in both eyes
• Atrophic depigmented patches on iris
• Pupils do not dilate with mydriatics
• Causes-

Syphillitic-tabes dorsalis

Non-syphyillitic-DM

                         -MS

                         -H’age

                         Tum of pre-tectal area

Site of lesion-Internuncial neuroes bet pre-tectal Nu & EW nu

\

                 ADIE’S  TONIC PUPIL

• Caused by denervation of the postganglionic supply to sphincter pupillae and ciliary ms
• UL
• Healthy young women
• Pupil-large & regular-anisocoria
• Light rea –absent / sluggish
• Near ref –slow & tonic
• Redilatation occurs slowly
• Vermiform movts of pupillary border
• With 0.125% pilocarpine-tonic pupil constricts rapidly

                                            -nml pupil does not constrict

    This is d/ super-sensitivity of cholinergic stim

• With atropine-Tonic pupil dilates

                         -Argyll Robertson pupil does not

* HOLMES-ADIE PUPIL-

 Adie’s pupil + Absent knee / ankle jerks

                        HIPPUS

• Alternate rhythmic dilatation & constriction of pupil
• Depends upon rhythmic activity of CNS
• Seen in Multiple sclerosis

                        HORNER’S SYNDROME

Oculosympathetic syn

C/F-

• Ptosis –d/t weakness of Muller’s ms
• Elev of LL- d/t weakness of inferior tarsal ms
• Miosis- d/t unopposed action of sphincter pupillae [ sphincter pup-III n,Dilator pup- Sympathetic chain ]
• Nml rea to light & near
• Anhydrosis
• Hypochromic heterochromia
• IOP is lower than 5mmHg on nml side
• Accomodation is decreased
• Enophthalmos

CAUSES-

CENTRAL [1st order neuron ]-post hypothalamus

• Brainstem dis
• Syringomyelia
• Lateral medullary syn
• Spinal cord tum

PRE-GANGLIONIC [2nd order ]-cilio-spinal centre of Budge

• Pancoast tum
• Carotid & aortic aneurysms & dissections
• Neck lesions [glds,trauma,postsurg]

POSTGANGLIONIC [3rd neuron]-Superior cervical ganglion

• Cluster headache
• Internal carotid A dissection
• Nasopharyngeal tum
• Otitis media
• Cavernous sinus mass

COCAINE TEST-

Cocaine 4 %- Nml pupil dilates

                   -Horner’s pupil does not dilate

Cocaine blocks the uptake of adrenaline that causes papillary dilatation. Since no adrenaline is available, no dilatation occurs in Horner’s syn.

HYDROXYAMPHETAMINE TEST [1%]-

• To diff pre-ganglionic from post-ganglionic
• Pre-ganglionic- Both pupils will dilate
• Post-ganglionic-Horner’s pupil will not
• Hydroxyamphetamine potentiates the release of NA from post-gang N endings.If the neuron is intact,[ 1st or 2nd order] NA will be released & pupil will dilate.In a lesion of III order neuron there will be no dilatation since the neuron is destroyed.

ADRENALINE 1: 1000-

-Opposite to the response in 1 % hydroxyamphetamine.

MIOSIS-

[< 2mm]

1. Bright light
2. Acute iritis
3. Opium
4. Morphine
5. Pontine H’age
6. Pilocarpine
7. Sleep

MYDRIASIS-

1. Dark
2. Angle closure glaucoma
3. Absolute glaucoma
4. Coma
5. Head inj
6. Mydriatics [atropine,homatropine]
7. OA
8. III n palsy

                                         MIOTICS-spot

1. Cholinergic miotics
2. Sympathetic miotics

1. CHOLINERGIC / PARASYMPATHOMIMETIC /PARASYMPATHETIC  MIOTICS-

      2Types-

I]  Direct stimulant at the myoneural junctn as acetylcholine-

    *   Pilocarpine

    *   Methacholine

II]  Indirect stimulants-By abolishing the effect of cholinesterase [ Anticholinesterase]-

• Eserine (0.25-1%)
• Neostigmine
• Demecarium bromide
• Phospholine iodide (0.06-0.25%)

III] Combination of direct & indirect-

• Carbachol
• Urecholine

2. SYMPATHETIC MIOTICS-

• Or sympatholytic
• Adrenergic blocking agent→Inhibits pupillary dilatation→leaves the sphincter pupillae unopposed
• Thymoxamine (0.5%)

USES OF MIOTICS-

1. Glaucoma
2. Accomodative esotropia
3. Accomodation failure
4. In cat surg before AC  IOL implantation
5. Pre-operatively for keratoplasty
6. amblyopia Rx-penalisation

SIDE-EFFECTS

1.Impaired night vision

2.Reduced V/A in the presence of axial lens opacity

3.Generalised constriction of visual field

4.Spasm of accommodation→ myopia

5,Increased permeability of BAB→ Transfer of proteins, fibrin & cells into aq .In chr ant uveitis , this effect along with miosis promotes Post synechiae.

Systemic miotic→ Morphine

                        MYDRIATICS-spot

1. PARASYMPATHOLYTIC MYDRIATIC
2. SYMPATHOMIMETIC  MYDRIATIC

1. PARASYMPATHOLYTIC MYDRIATIC-

Abolish the action of acetylcholine by destroying cholinesterase→ Paralysis of sphincter pupillae & ciliary ms

DRUGS-

1. Atropine 1%
2. Homatropine 1-2%
3. Hyosine 0.1-1%
4. Cyclopentolate 0.5-1%
5. Tropicamide 0.5-1%

USES-

1.Mydriatic uses-

*  To dilate the pupil for fundus, lens,periphery & vitreous exam

*  Fundus photography,FFA & photocoagn

*  uveitis

*  Nuclear sclerotic or posterior polar cat

*  Pre-oper

2.Cycloplegic uses-

*  Refraction

*  Amblyopia

*   Uveitis

*  Post –oper

*  Corneal abrasion

SIDE-EFFECTS-

1. Photophobia
2. Reduced accommodation
3. Acute ACG
4. Dry mucous memb
5. Tachycardia

ATROPINE-

• Long-acting
• Strongest
• Complete dilatation in 30-40 min
• Cycloplegia in 2 hrs
• Effect lasts for 21 days

HOMATROPINE- 2%

• short acting
• Cycloplegia + mydriasis in 45-60 min
• Effect lasts for 48 hrs

CYCLOPENTOLATE-1%

• Short acting
• Myd + cyc in 1 hr
• Effect lasts for 6-12 hrs

TROPICAMIDE-1%

• Short acting

SYMPATHOMIMETIC MYDRIATICS-

Act on postsynaptic receptors→release of NA→mydriasis

DRUGS-

1. Adrenaline [1 in 10,000] as intracameral
2. Phenyephrine 5-10%
3. Cocaine 2-4 %

SIDE-EFFECTS-

1. HT
2. Reflex bradycardia
3. headache,trembling,stinging
4. Liberate iris granules→ rise in IOP
5. Loss of cor microvilli
6. Desquamation of cells
7. Ischaemia  d/t vessel blanching

USES-

1. Fundus exam
2. ECCE + / -  PCIOL
3. Break post synechiae

C/I OF MYDRIATICS-

1. ACG
2. Very shallow AC
3. Iris –fixated IOL

CONGENITAL ON ANOMALIES

OPTIC DISC DRUSENS-

DEF- OD drusens composed of hyaline like calcific material within the substance of ONH

-Bil

-Result from intracellular calcification within the axons

C/F-

Buried drusens-

-Early childhood

-Elevated disc with scalloped margins

-Blurred disc margins

-No physiological cup

-No hyperaemia of disc surface

-surface Vs are not obscured

-Anomalous vascular pattern

-Spontaneous venous pulsation

Exposed drusens-

• Early teens
• Emerge on the disc surf as waxy pearl like irregularities

Complications-

1.Juxtapapillary CNV

Associations-

• RP
• Angioid streaks
• Allagille syn

INV-

1. USG- high acoustic reflectivity

2. CT scan-less sensitive
3. FA-Exposed drusen show autofluorescence prior to dye injection & buried drusen- late localized hyperfluorescence

d/t staining

-no leakage

[papilloedema- hyperfluorescence & late leakage]

OPTIC DISC COLOBOMA

DEF-Results from incomplete closure of choroidal fissure

-Mostly sporadic, AD may occur

-UL /BL

C/F-

-Reduced V/A

-Disc- focal,discrete,white ,bowl shaped excavation,decentered inferiorly so that inf NRR is thin or absent & nml disc tiss is confined to a small superior wedge

-Retinal vasculature nml

-Fields- superior defect

COMPLICATIONS-

1. Serous RD at the macula
2. progressive enlargement of the excavation
3. RRD

OCULAR ASSOCN

1. Microphthalmos
2. coloboma –iris,CB & fundus

    SYSTEMIC ASSOTN

1. Chromosomal anomalies-Patau’s syn

                                            -Edward’s syn

                                            - Cat’s eye synn

2. CHARGE-

   C- Coloboma

    H-Heart defect

    A-choanal Atresia

    R- Retarded growth

    G- Genital anomalies

    E –Ear anomalies

MORNING  GLORY SYNDROME

-Very rare

-Usually UL & sporadic

-BL & hereditary are still rarer

C/F-

• V/A –very poor
• Disc- enlarged with a funnel shaped excavation

           -central core of whitish glial tiss at the base of the excavation-represents persistent hyaloid remnants

-Disc is surrounded by an elevated annulus of chorioretinal pigmentary disturbance

-BVs emerge from the rim of the excavation like spokes of a wheel

COMPLICATION- Serous RD

SYSTEMIC ASSN-

1.Frontonasal dysplasia

2. NF-2

OPTIC NERVE HYPOPLASIA

-UL /BL

DEF- Decreased no of nerve fibres

Caused by ingestion of foll drugs by mother during gestation

-Alcohol

-LSD

-Quinine

- protamine zinc insulin

-steroids

-Diuretics

-cold remedies

-anticonvulsants

Superior segmental hypoplasia may be asstd with maternal DM

C/F-

• V/A- normal to no PL
• Disc –small & grey surrounded by a halo of hypopigmentation caused by concentric chorioretinal atrophy [double ring sign]
• Distance from the fovea to the temporal border of the disc equals or exceeds 3 times the disc dia.This strongly suggests disc hypoplasia
• BV?
  s are of normal caliber
• aQO98cp’p l\   ojiy