Ophthalmology Notes @ OphthalNotes.blogspot.com

Ophthalmology Notes @ OphthalNotes.blogspot.com
A comprehensive collection of ophthalmology revision notes that cover a broad range of topics.

NEURO OPHTHALMOLOGY

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

  1. 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

  1. 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
  1. Inflamn which attacks the nerve proximal to this region & thus shows no ophthalmoscopic change.
  1. 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

  1. ORBITAL-
  • Tumours
  • Orbital abscess
  • Endocrine exophthalmos
  • Sinusitis

  1. 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

  1. 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}
  1. Papillitis
  2. Papilloedema
  3. 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.

  1. 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

  1. 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

  1. 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

  1. 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

  1. 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

  1. 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]

  1. 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

  1. 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

  1. CT scan-less sensitive
  2. 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

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