Neuro opthalmology

dr. Devi Azri Wahyuni, Sp.M

(K)
DEPARTMENT OPHTHALMOLOGY
UNIVERSITY OF SRIWIJAYA /
MOHAMMAD HOESIN HOSPITAL

Neurophysiology of
Optic Nerve

PREFACE

The eyes are intimately related to the

brain
The eyes give important diagnostic
clues to central nervous system
disorders.
Optic nerve is a part of the central
nervous system.

Anatomy and Topography of

Visual Pathway

Visual pathway consists of:

Retina
Optic nerve
Optic chiasm
Optic tract
Lateral geniculate nucleus (body)
Optic radiation ( geniculo calcarina tract )
Visual cortex

Retina

The retina is a thin, transparent

structure that develops from the
inner and outer layers of the optic
cup
It extends almost as far anteriorly
as the ciliary boby ending at that
point in aragged edge the ora
serata
It has ten layers

Ganglion cells fibers coming from

the nasal retina can travel
uninterrupted directly to the disc
Fibers from the temporal enter the
disc at superior or inferior pole
Macula fibers enter the disc on its
temporal side ( papillomacular
bundle )

Optic Nerve

Consists of more than 1 million

axon that originate in the ganglion
cell layer of the retina and extend
toward the occipital cortex

Has varies in length ;35 55

mm,usually about 50 mm from eye
to optic chiasma

The optic nerve four parts

Intraocular ( 1 mm)
Intraorbital ( 25 mm)
Intracanalicular ( 5 mm )
Intra cranial ( 10 mm)

Intraocular portion

Optic disk and optic nerve that lies

within sclera
Optic disc 3 mm nasal macula lutea
Nerve fibers exit through the
orifices of the lamina cribrosa

Intraorbital portion

20 mm to 30 mm long,elongated S
diameter 3-4 mm
Bermielin
Between the eyeball and the optic canal
Surrounded orbital fat,embedded the cilliary vessel
and nerve
Posteriorly,nasocilliari nerve and ophthalmic artery
cross above optic n. 25-30 mm
Surrounded anulus zinni in the orbital apex
Inflamation pain in the ocular movement

Intracanalicular potion

the optic canal lies withinthe lesser

ingof the sphenoid bone, 5 mm long
Passes through the optic canal
Surrounded by duramater,
arachnoid and piamater
Duramater pada bagian ini menyatu
dengan periosteum

Intracranial portion

Leaves the canal and pass

backward,upward and medially within the
subarachnoid space to reach the optic
chiasma
Related above to the olfactory tract, gyrus
rectus and anterior cerebrral a.
Panjang 5 - 16 mm
Sering mengalami kerusakan karena
gangguan dari struktur lain yang
berdekatan

Optic chiasma

Makes up part of the anterior

inferior floor of the third ventricle
Just antrior to the hypothalamus
Nasal retina fibers cross to the
opposite side to joint the
coresponding contralateral fibers

Optic tract

Contains ipsilateral temporal and

contralateral nasal fibers from the
optic nerves
Just prior to lateral geniculate body
Other fibers exit to the superficial
layers of the superior colliculus via
the brachium of the superior
colliculus

Lateral geniculated body

Is the synaptic zone for the higher

visual projection
Divided into six layers
The four superior levels are the
terminus of parvocellular axons are
responsible for mediating maximal
spatial resolution and color
perception

CGL

To inferior layers receive input from the

magnocellular fibers, that are more
sensitive to detecting motion
Contralateral eye terminate in layers
1,4,6
Ipsilateral fibers innervate 2,3 and 5

Optic radiations

Connect the lateral geniculate body

with the cortex of the occipital lobe
Loop of Meyer

Visual cortex

Area 17 Brodmann (striata area )

primary visual cortex
Area 18 Broadmann (para striata)
Area 19 Brodmann (peri striata)
secondary visual cortex

Primary visual area

Occupies the walls of the deep

calcarina sulcus
Superior retina quadrants (inferior
field) pass to the superior wall of
the calcarina sulcus
Inferior retinal quadrants pass to
the inferior wall of the calcarina
sulcus

Secondary visual area

Surround the primary visual area

Relate the visual information

Blood supply

Retina :a.ofthalmica,central retina a.

Intraocular :branches anastomose
circle of Zinn post. Cilliary a.
Intraorbital :ophtalmic a.
Intracanalicular : branch pial
ophthalmic a.

Intracranial : pial plexus sup.

Hypophyseal a. , carotid interna,
ophthalmic a.
Optic chiasma : pial plexus internal
carotid, sup hypophyseal, post and ant
comunicatting a., cerebral ant a.
Optic tract s : choroidal ant a.

LGB : choroidal ant and post a.

Optic radiation and occipital
cortex:middle and post cerebral a.

Evaluation of optic nerve disease

Signs of optic nerve dysfunction
I. Reduced visual acuity
2. Afferent pupillary defect
3. Dischromatopsia
4. Diminished light brightness
sensitivity.
5. Diminished contrast sensitivity,
6. Visual field defects

PUPILLARY PATHWAY

The pupil is a hole located in the center of

the iris of the eye allows light to enter the
retina

It appears black because most of the light

entering the pupil is absorbed by the
tissues inside the eye.

Size of the pupil depends on:

age, awareness, emotional status, retinal
ilumination, distan of sight ( near and far ),
acomodation,refraction status, IOP, patologic
proses in the eyes.

Changing of the pupil occurs with the sympathetic

fibers and parasympathetic fibers.
Sympathetics fibers dilatate pupils
Parasympathetic fibers constriction pupils .

ANATOMI & PHYSIOLOGY

The pupillary opening appears a central

location, but if carefully measured, it is actualy
situated slightly inferior and nasal to the center
of the cornea.

MAJOR FUNCTION OF THE PUPIL

FUNCTION :
1.

2.

Control of retinal illumination

reduction in optical aberrations

3.

Depth of focus

THE IRIS AND THE PUPIL

The iris can be divided into two main layers :

The
posterior
leaf

The
anterior
leaf

THE ANTERIOR LEAF CONSISTS

Conective tissue stroma with cells

Blood vessels
Nerves supplying the spincter and

dilator.

THE POSTERIOR IRIS LEAF

CONTAINS

The dilator muscle

The sphincter muscle
The posterior pigmented epithelium.

o Pupil diameter in dark adaptation is 4,5 mm

7,0 mm
in the bright adaptation:2,5 mm 6 mm.
o Miosis pupil diameter < 3 mm
o Midriasis pupil diameter > 6 mm

Isocoria if both pupil posses the same

diameter.
o Anisocoria pupil diameter difference
between two pupils > 0,3 mm and larger.
o

o size

of the pupil depends on:

age, emotion. Awareness, retina illumination,
acomodation stage,refraction status,IOP( intra ocular
pressure ), far & near sight, patologic proses
o Changing of the pupil diameter occurs with
the sympathetic fibers and parasympathetic
fibers.
o Sympathetics fibers function is to dilatate
pupils and parasympathetic fibers do
constriction the pupils .

AFFERENT PUPILLARY PATHWAY

pupillary fibers follows the optic tract and separate

from the optic tract just anterior to the lateral
geniculate body.

They

then enter the midbrain, where they synapse to

pretectal nucleus.
The

pupillary fibers leave pretectal nucleus and

distributes approximately equally to both EndingerWestphal nuclei

EFFERENT FIBERS PATHWAY

The

efferent pupillary light pathway

begins at the Endinger-Westphal (E-W)
nuclei.
The efferent pupillary pathway divided :

Parasymphatetic
pathway

Sympathetic
pathway

PARASYMPATHETIC PUPILLARY PATHWAY

Endinger Westphal Third nerve

cavernous sinus

Synapse

superior orbital
fissura
ciliary muscles
Ciliary ganglion
sphincter muscles

SYMPATHETIC PUPILLARY PATHWAY

The pupilodilator system is controlled by the

sympathetic nervous system.

The symphatetic nervous system is divided

into :
1. Central (first-order) neuron.
2. Preganglionic (second-order) neuron.
3. Postganglionic (third-order) neuron.

Central (first-order) neuron

The symphatetic fibers arise in the

posterolateral area of the hipothalamus and
descend, uncrossed, in the lateral potion of
the midbrain, pons, medulla, and cervical
spinal cord to the ciliospinal center of budge
C8-T2.

Is located in the brainstem and cervical

cord.

Preganglion Neuron (second-order)

The preganglion fibers travel upward in

the symphatetic chain over the apex of the
lungs and through the stellata ganglion,
the inferior cervical ganglion, around the
subclavian artery and trough the middle
cervical ganglion to the superior cervical
ganglion at the carotic bifurcation.

Postganglion neuron (third-order)

The postganglion fibers travel to the

iris via the carotid plexus, the
cavernous sinus where they join
with the ophthalmic division of the
trigeminal nerve.

They emerge from the cavernous

sinus and pass into the orbit
through the nasocilliary branch of
the ophthalmic division.

o Finally entering the eye through the long

ciliary nerves and terminating at the iris
dilator muscle.
o The postganglion neuron starts from the
base of the skull and passes through the
cavernous sinus to the orbit.

PUPIL EXAMINATION

1.
2.
3.
4.
5.
6.
7.

Direct pupil reflex

Indirect pupil reflex ( konsensual)
RAPD
Pupil cycle time
Anisocoria
Pilocarpin 0,125%
Kokain 4% or 10%

Clinic manifestation defect

of the pupil pathway

Parasymphatetic defect :
1. Adies (tonic) pupil
2. Midriasis
Symphatetic defect :
1. Horner s syndrome
2. Argyll Robertson Pupil

Disease of optic nerve head

1. Papil Atrophy
-

primary
- secondary

2. Neuritis Optik:
- Typical
- Atypical
- Neuroretinitis

 3.
4.
5.
6.
7.

Neuroretinitis
Non arteritis AION
Arteritik AION
Posterior Ischaemic optic
neuropathy
Diabetic papillopathy

8. Leber hereditary optic neuropathy

9. Hereditary optic atrophy
10.Nutritional optic neuropathy
11.Toxic Optic Neuropathy
12.Papilloedema

Optic nerve atrophy

Classification of etiology:
Vascular
Degenerative
Secondary due to papillodema
Secondary due to optic neuritis
Optic compressive
Toxic
Matabolic
Traumatic
Glaucoma

Clinical finding:
- visual field loss, reduced of colour
vision
- pale optic disc
- Pupil reaction comparable with
decrease of visual acuity

Optic Atrophy

In children usually results from:

- anterior visual pathway disease,
such as inflammation (optic
neuritis), hereditary optic atrophy,
perinatal asphyxia, hydrocephalus,
and optic nerve tumors.

Dominant Optic Atrophy

Bilateral, slow loss of central vision in

childhood
Usually begins: age < 10 year with mild
visual loss (from 20/40 to 20/100)
Visual field: central or cecocentral scotoma
with normal peripheral isopters.
Color vision test a tritan dyschromatopsia.
Optic disc: temporal pallor with triangular
excavation.
Inheritance is usually autosomal dominant
but can be recessive.

Dominant Optic Atrophy

Long term prognosis: good, with

V.A. rarely reduced to the 20/200
50% : Nystagmus is present
Funduscopic: a pale optic disc with
vascular attenuation of the type
characteristically seen in retinal
degeneration.
ERG result are normal.

Leber Hereditary Optic Neurophaty

A maternally inherited (mitochondrial)

disease, leber hereditary optic neuropathy
(LHON).
Characterized by:
- acute or subacute bilateral loss of central
vision
- acquired red-green dyschromatopsia
- central or cecocentral scotoma in
otherwise patients (usually males) in
their second to fourth decade of life.

Leber Hereditary Optic Neurophaty

Progressive atrophy : a flat, pale disc with

dense central scotoma.
Clinical: a low grade optic neuritis with
circumpapillary telangiectasia, pseudoedema
of the disc, and absence of fluorescein
staining.
Pallor of the entiredisc indistinguishable
from primary atrophy generally develops
within a few weeks after onset of visul
disturbance

Leber Hereditary Optic

Neurophaty

Final visual acuity is rarely better

than 20/200.
Associated neurologic
abnormalities:
- paraplegia, dementia, deafness,
migraines, vertigo, spasticity, and
cardiac preexcitation arrhythmia
(Wolff-Parkinson-While) syndrome.

Leber Hereditary Optic

Neurophaty

Transmitted by female carriers and

involves the mitochondrial DNA,
mutations in the mitochondrial
genome responsible for complex I
(NADH:ubiquinone oxidoreductase)
No effective treatment exists,
although a small percentage of
patients will demonstrate
spontaneous improvement.

Primary optic atrophy

Lesion at retrolamelar optic nerve to

geniculate corpus laterale
Pale with clearly margin, diffuse or
sectoral
Etiology:
Retrobulbar

neuritis
Compression of tumor or aneurysm
Hereditary optic neuropathy
Toxic optic neuropathy

Secondary optic atrophy

Preceded by swelling of ONH

White or dirty grey, poorly
delineated margin
Reduced of vascular at surface ONH
Etiology :
Papilloedema,

papilitis, AION

Demyelinating optic neuritis

(Typical Optic Neuritis)

Age 30-50,
Subacute monocular visual
impairment
Discomfort surounding eye with
movement
Normal papil optic nerve
temporal pale recurrent attact
VA worsen in few days 2 weeks,
improvement with in 2-4 weeks.
Relationship with MS

Atypical optic Neuritis

Visual loss from secondary demyelination

of optic nerve
Common causes:
sarcoidosis nonmultiple sclerosis
(MS) autoimmune disorders uveitis
infectious retinitis and meningitis
idiopathic disorders

Atypical optic Neuritis

Diagnosed by clinical and/or imaging

features consistent with a systemic
disorder and not consistent with MS.
Unlike typical optic neuritis, visual loss
often improves with corticosteroid
treatment (corticosteroid-responsive) and
worsens when corticosteroids are
tapered or withdrawn (corticosteroiddependent

Swollen left optic disc and peripapillary retina with

choroidal infi ltrates in a patient with sarcoidosis. Caution: most patients
with sarcoidosis affecting the optic nerves show no fundus abnormalities

Neuroretinitis

Clinical syndrome : sudden decease of

vision, painless, papil edema and macular
star feature.
Idiopatik : 25 %
Cat scratch disease : 60%
Other etiology: syphilis dan lyme disease

Anterior ischemic optic neuropathy

age >50 th
Due to ischaemic process
Painless monocular visual loss
Visual field deffect : altitudinal or
arcuate
Divided into Arteritic AION and Non
Arteritic AION

Diabetic papillopathy

type 1 dan 2 DM
Blurred vision, painless
RAPD +/VF defect : enlargement of blind spot
Papilledema, hyperemia, and surface
telangiectasis.

Nutritional optic neuropathy

Deff protein and complex vit B

Progresive dan bilateral visual impairment
Dischromatopsia
Papil optic nerve : normal
atrophy(temporal)

Nutritional optic neuropathy

Visual field defect :

Cecocentral

scotoma

Toxic optic neuropathy

Characterized : gradual,
progressive, bilateral and painless
Central or cecocentral scotoma
Decrease of visual acuity and colour
vision
Mild to moderate papil edema
Cause : > methanol
medication : INH,
ethambutol

METHANOL TOXIC OPTIC NEUROPATHY

INTRODUCTION

Methanol Toxic Optic Neuropathy :

a group of medical disorders defined by
visual impairment due to optic nerve
damage secondary to a methanol

CHALLENGES

ETHANOL
ethyl alcohol, drinking alcohol,
grain alcohol
Very rare,Chronis, Liver dissorder,
Malnutrition
Fermentation alcohol low
concentration
Distilation alcohol high concentration

METHANOL
methyl alcohol, wood
alcohol, wood naphta or wood
spirits
CHEAP, SWEET
Formic acid Neurotoxin Optic nerve
damage
Serum levels 20 mg/dL ocular
injury

PATOPHYSIOLOGY

Methanol
Methanol

Alcohol dehydrogenase

Formaldehyde
Formaldehyde

Formaldehyde dehydrogenase

Formic acid
Formic acid
Mitochondrial RGC disruption
Mitochondrial RGC disruption
ROS
ROS

Cytochrom C
Cytochrom C
release
release
Caspase 2, 9activation
Caspase 2, 9activation
Caspase 3
Caspase 3
activation
activation

Apoptosis
SGR
Apoptosis SGR
11/6/16

Visual acuity
Visual acuity

Caspase 8
Caspase 8
activation
activation

ATP
ATP

GSH
GSH
Death receptor
Death receptor

89

How to establish the diagnosis ?

symptoms

91

signs

Decreased visual acuity

Pupils sluggish, no RAPD
Reduced contrast sensitivity
and color vision
Optic disc normal, swollen, or
hyperemic ( early)
Temporal disc pallor optic
atrophy (late)
Centrocaecal scotoma

92

Management
MANAGEMENT

CORRECTION OF METABOLIC ACIDOSIS

CORRECTION OF METABOLIC ACIDOSIS
Sodium bicarbonate
Sodium bicarbonate
Selective Hemodyalisis
Selective Hemodyalisis

ANTIDOTE TO INHIBIT THE METABOLISM OF

ANTIDOTE TO
TO FORMATE
INHIBIT THE METABOLISM OF
METHANOL
METHANOL TO FORMATE

Ethanol (Ethyl alcohol)

Ethanol (Ethyl alcohol)
Fomepizole
(4-Methylpyrazole)
Fomepizole (4-Methylpyrazole)

93

MANAGEMENT
SUPPLEMENTATION
SUPPLEMENTATION

Folic
acid
Folic acid
Vitamin
VitaminBB
Adenosin
AdenosinTri
TriPhosphat
Phosphat(ATP)
(ATP)
Steroid
Steroid

94

Intravenous pulse steroids

The result still controversy(side effect >>)

Anti-inflammatory and immunosupresan
effect
Inhibit TNF secretion
Methylprednisolone 1 gr/ day, devided 4
doses for 3 days MP oral 1 mg / kg bw/day
tappering off

95

Folic acid
Compensation of deficiency Hepatic H4 folat
to counter / enhance the metabolism of
formate side effect <<
acute : 4 x 1 mg/kgbw ( max 50 mg) oral 3
x 1 tablet
Mitochondrial protector
Ubiquinone, L-carnitine, Co enzyme Q 10
Gingko biloba
96

Morbidity

Depends on the risk factors, the

underlying etiology, and the duration
of symptoms before the institution of
treatment.
Advanced optic atrophy is less likely
to recover visual function than a
patient who does not have such
pathologic changes.

97

Prognosis

Variable
Depends upon the nature of the
agent, total exposure prior to
removal
Degree of vision loss at the time of
diagnosis.

98

Neuroimaging

Almost always are indicated, unless one is

absolutely certain of the diagnosis.
Magnetic resonance imaging (MRI) most
appropiate to evaluate of the optic nerves
and chiasm with and without gadolinium
enhancement.

99

Ethambutol Optic Neuropathy

INTRODUCTION

Tuberculosis caused by
mycobacterium tuberculosis.

WHO : 9,2 million new cases of

tuberculosis each year.

About 55% ethambutol

Estimate 2% will experince

significant and irreversible vision
loss.

The annual incidence of this

serious iatrogenic complication is
100,000.

Indonesia is thrid position in the

world after India and China.
Prevalence : 0,2 0,65%
Pulmonary Hospital in Palembang
2.955 cases (2010)
501 new cases.

Ethambutol toxic Neuropathy

> 25mg/kg/day.

Standard dosage 15-25 mg/kg/day

1% visual loss .

ETHAMBUTOL

Structure of ethambutol
dihydrochloride

Synthetic compound, soluble in water,

stable in high temperature, sold in
sodium hidrochloride.

PATHOGENESIS

Ethambutol destroy bacteria by

chelating the metal ions that are
involved in prokaryotic ribosomes.

The metabolite of ethambutol,

ethylenediiminodibutyric acid, is a
strong chelator of copper and Zinc.

...Pathogenesis

Copper a cofactor for cytochrome

c oxidase ( enzyme in the electron
transport chain and cellular oxidative
metabolism within mitochondria )

Ethambutol decrease the levels of

copper avaible for cytochrome c
oxidase mitochondrial issufisiency

Ethambutol decreased of energy that

required for axonal transport in optic
nerve optic nerve damage optic
neuropathy

Mitochondria provide most of the

ATP required by cell.
Energy depletion and oxidative
stress mitochondrial damage
opening of the mitochondrial
permeability transition pore (MPTP)
leakage of cytocrome C
apoptotic death pathways in the
cytosol.

The mitochondrial pathway

apoptosis

CLINICAL PRESENTATION

Decreased Vision.
bilateral progressive painless visual
blurring ( minimal reduction
NLP ).
Onset ocular symptoms 2 - 5
months
Pupil response
Bilaterally sluggish to light with no
RAPD.

Decreased colour perception

Dyschromatopsia may be the earliest
sign of toxicity.
Classicaly red-green colour changes

Visual field defect

Central scotoma is the most common
visual field defect, but bitemporal
defect or periferal field constriction
have been reported

Optic nerve
fundoscopic is usually normal, but
showed swelling and hyperemia
follow with splinter haemorhage
later.

ADDITIONAL EXAMINATION

OCT (Optical Coherence tomography)

To evaluate retinal nerve fiber layer
(RNFL) thickness in early stage
ethambutol optic neuropathy
Humphrey Field Analyzer
The most common of visual field
defect in ethambutol toxicity is central
and cecocentral scotoma

CHARACTERISTIC OCULAR TOXICITY

ETHAMBUTOL
a.

Dose-related
Incidence of ethambutol related
retrobulbar neuritis of
18% >35mg/kg/day
5-6% 25mg/kg/day
<1% 15mg/kg/day
in patient receiving ethambutol for
more than two months.

b. Duration-related
Manifestation of ocular toxicity is
usually delayed, which generally
doesnt develop until after
treatment for at least 1,5
months.
Variable mean interval between
onset of therapy and toxic effect
3 5 months

c. Reversibility
Classically described as reversible on
discontinuation of ethambutol ( weeks
to months ).
Studies have reported permanent
visual impairment without recovery in
some patients with prompt
ethambutol discontinuation.

DIAGNOSIS
1.

2.
3.
4.
5.

Receiving treatment of
ethambutol.
Decreased visual acuity
Earliest sign of dyscrhomatopsia
Optic disc : normal/swelling/pallor
Visual field defect :
central/secocentral, bilateral
hemianopsia, perifer contriction

MANAGEMENT

Ethambutol induced ocular toxicity

--- must be immediately
discontinued

Therapy discontinuation is the only

effective management

PREVENTIVE
a. Patient should be assessed for:
- Feasibility and contraindication of
using ethambutol.
b. Patient with difficulty in appreciating
and reporting visual symptoms or
change of vision like young children,
person with language difficulties
contraindicated

c.
d.

Health education
Baseline vision test
visual acuity and colour perception
should be conducted before starting
treatment.
Especially high dosage
>25mg/kg/day

PROGNOSIS

Is good following cesation of

treatment although recovery may
take up to 12 months.
A minority of patients develop
permanent visual impairment as a
result of optic atropy

SCREENING

Frequency of examination is
monthly
- Doses 15mg/kg/day .
- Patients at increased risk for
toxicity:
DM, Chronic renal failure,
alcoholism,eldrerly, children, other
ocular defects, induced periperal
neuropathy.

SCREENING

Screening should be every 3 6

months for lower doses.
The drug should be stopped
immediately if symptoms develop.

PAPILLOEDEMA

Congestive non inflamatory optic disc

due to increase of intracranial pressurre

Children : Increased intracranial

pressure can be hydrocephalus
from a mass lesion or pseudotumor
cerebri.
Infants: Increased intracranial
pressure results in firmness and
distension of the open fontanelles,
usually accompanied by nausea,
vomiting, and headaches.

Older child may have transient

visual obscuration.
Esotropia and diplopia injury to
the sixth nerve, which usually
resolver once intracranial pressure
is reduced

Mechanisme of papilloedema

2.

ICP compressed the optic

nerve sheath stasse of retinal
vein and optic disc
Mechanical optic nerve and disc
to anteriorly

Etiology of Papilloedema

Cerebral Tumors
Abcess
Subdural hematome
Acquired hydrocephalus
Arteriovenous malformation
Malignan hypertension
Spinal tumor
Uremia
mucopolisacharidosis

Ophthalmoscopic finding
Optic disc edema :
>3D
non delineated
margin, Spot
haemorrhage
turtous vein

Chiasm lesions

Etiology
1. Tumor

2. Non neoplastic masses

Pituitary adenoma, craniopharyngioma

Aneurysma, arachnoid cysts

3. others:

Inflamatory, demyelinating disease,,

trauma

Chiasm lesion

Ussually compresive
Pediatric
Hypothalamic

glioma
Craniopharyngioma

Adult
Pituitary

adenoma
Meningioma
Craniopharyngioma
Aneurysm

Retrochiasmal lesion

Children : neoplasm > vascular >

trauma

Adults : vascular > neoplasm >

trauma

Retrochiasmal Lesions
Optic tract
1. Incongruous homonimous
hemianopia
2. Wernicke hemianopic pupil
3. Optic atrophy
4. Contralateral pyramidal sign

Temporal optic radiation

1. VF defect : contralateral
homonimous, superior quadrant
anopia
2. Associated feature
Contralateral hemisensory
disturbance, mild hemiparesis,
paroxysmal olfactory and
gustatory hallucination

Anterior parietal radiation

1. VF defect : incongruous,
contralateral, homonimous,
quadrantanopia
2. Associated feature:
Of

inferior

dominant parietal lobe disease:

agraphia, left right disorientation, and
finger agnosia
Of non dominan : apraxia and spatial
neglect

Main Radiation
1.VF defect : complete
homonimous hemianopia
2.Optokinetic nystagmus

Striate cortex
1. VF defect : Macular sparing
congruous homonimous hemianopia
2. Associated feature : visual
hallucination, denial of blindness
3. causes : vascular disease,
migraine, tumor and trauma.

Lintasan Impuls visual dan Gangguan Lapang Penglihatan Akibat

Berbagai Lesi di Lintasan Visual

LAPANG PANDANG
Dinilai menggunakan :

PERIMETERI :
- Statik ( Humprey )
- Kinetik ( Goldman )
Untuk diagnostik dan evaluasi terapi
Dokter Umum Konfrontasi

Lapang pandang glaukoma

Pemeriksaan LP dg alat khusus :

* Perimeter Goldmann

LP normal dg Goldmann

Automated perimeter : Humphrey visual field analyzer

THANK YOU

THANK U