NEURO OPHTHALMOLOGY

OPEX REVIEW SERIES

Christian Luna M.D.
May 5, 2011
OUTLINE
 Anatomy
 Signs of Optic Nerve dysfunction

 Diagnostic Tests

 Neuro Ophtha AVF

BONY ANATOMY - ORBITAL WALLS
SINUSES
 ANATOMY OF THE OPTIC NERVE

 Carries 1.2 M afferent

fibers originating from the
retinal ganglion cells

 50 cm long from globe to

the chiasm
ANATOMICAL SUBDIVISIONS OF THE OPTIC NERVE

 Intra-ocular
 Shortest (3-4mm)
 Papillitis, optic disc edema,
and abnormal deposits
(drusen)
 Intra-orbital
 25-30mm long
 Globe to optic foramen
 Thicker-- + myelin
 S-shaped
 May cause pain on eye
movement when inflamed
 ANATOMICAL SUBDIVISIONS OF OPTIC NERVE

 Intracanalicular
 Traverses the optic canal
 6mm
 Fixed
 Dura mater fuses with the
periosteum
 Intracranial
 Joins
the chiasm
 10mm
PATHWAY OF LIGHT REFLEX
PUPILLARY CONSTRICTION
SIGNS OF OPTIC NERVE DYSFUNCTION
 Reduced visual acuity
 Afferent pupillary defect

 Dyschromatopsia

 Diminished light brightness sensitivity

 Visual field defects

PRIMARY OPTIC ATROPHY
 Caused by lesions from the
retrolaminar portion of ON to LGB
 No antecedent swelling
 Causes:
 Compression of tumors/aneurysms
 Retrobulbar neuritis
 Hereditary, toxic, or nutritional optic
neuropathies
 Signs:
 Pale, flat disc
 Distinct disc borders
  vessels on disc surface
(Kestenbaum sign)
SECONDARY OPTIC ATROPHY
 Preceded by swelling of the
optic nerve head
 Causes:
 Chronic papilledema
 AION

 papillitis

 Signs:
 White, dirty grey disc
 Disc is elevated

 Indistinct disc borders

NON-ARTERITIC ANTERIOR ISCHEMIC
OPTIC NEUROPATHY (NAION)
 Most common in elderly
 Infarction of optic nerve
head due to occlusion of
short posterior ciliary
arteries
NON-ARTERITIC ANTERIOR ISCHEMIC
OPTIC NEUROPATHY (NAION)
 Sudden, painless,  Predispositions:
monocular visual HPN
loss not associated DM
with premonitory Sudden
visual obscurations hypotensive
episodes
Sildenafil intake
Collagen vascular diseases
Sleep apnea syndrome
NON-ARTERITIC ANTERIOR ISCHEMIC
OPTIC NEUROPATHY (NAION)
Signs:
 Hyperemic disc swelling
with splinter-shaped
hemorrhages
 Pallor ensues after 3-6
weeks
 Fellow eye involvement in
10% after 2 years, 15% in
5 years
ARTERITIC ANTERIOR ISCHEMIC OPTIC
NEUROPATHY
 Occlusion of the
posterior ciliary arteries
due to GCA
 8th-9th decade
 Sudden, profound visual
loss, preceded by visual
obscurations
 Systemic signs of GCA
ARTERITIC ANTERIOR ISCHEMIC OPTIC
NEUROPATHY
 Chalky white,
edematous optic disc
 Optic atrophy ensues in
1-2 month
 Tx:
 Systemic steroids
 PAPILLEDEMA

 Passive,non-inflammatory
edema of ONH
 Secondary to increased ICP

 Early Papilledema:
 No visual symptoms
 Disc hyperemia, mild elevation,
slightly indistinct borders
 PAPILLEDEMA
 Signs
 Severe disc hyperemia and
edema
 Venous engorgement,
hemorrhages and CWS
 PAPILLEDEMA
 Chronic Papilledema
 “champagne cork”
appearance
 Absent CWS, hemorrhages

 Atrophic papilledema
 Greyish disc elevation
 PAPILLITIS VS PAPILLEDEMA
Papillitis Papilledema

Unilateral Bilateral

Sudden onset Insidious onset

Sudden LOV Gradual LOV

Central scotoma Contraction of VF

Fine opacities seen in posterior Clear posterior vitreous

vitreous
LEBER HEREDITARY OPTIC NEUROPATHY
 Mitochondrial DNA
mutation
 2nd-4th decade, males

 Unilateral, severe, painless

loss of central vision
 Disc hyperemia, dilated
surface capillaries, and
swelling of peripapillary
nerve fiber layer
POST-TRAUMATIC OPTIC NEUROPATHY
 Unexplained decrease in vision
 (+) history of trauma

 RAPD

 Decrease color perception

 Fundus:
 Hyperemic disc
 Indistinct, elevated disc borders

 Treatment: Steroids within 6 hrs of injury

 OCULOMOTOR NERVE
 Anatomy
 Clinical Features
CRANIAL NERVE III
CLINICAL FEATURES
 Profound ptosis
 Abducted eye in primary
position
 Limited adduction,
depression, elevation
 Dilated pupils
 TROCHLEAR NERVE
 Anatomy

 ClinicalFeatures
 Special Test
 Parks 3-step test
 Bielschowsky’s Head Tilting test
IMPORTANT FEATURES
 Only CN that emerges
dorsally
 Crossed; innervates
contralateral SO muscle
 Very long and slender
PATHWAY OF TROCHLEAR NERVE

NUCLEUS
 Midbrain at
inferior
colliculus
CAVERNOUS
SINUS
 Below CN III,
above CN V1
CLINICAL FEATURES
 Hyperdeviation
 Diplopia
 PARKS-BIELCHOWSKY 3-STEP TESTING
 Step 1:
 Hypertropic in primary
position?
 Step 2:
 Hypertropia greater in R gaze
or L gaze?
 WOOG (Worse on Opposite
Gaze)
 Step 3:
 Head tilt
 BOOT (Better on Opposite
Tilt)
 ABDUCENS NERVE
 Anatomy
 Clinical Features
COURSE OF ABDUCENS NERVE
CLINICAL FEATURES
 Ocular deviation (esotropia)
 Limited abduction
 Diplopia
 Head posturing
 Head turned toward the side of the lesion
HIGH YIELD FACTS
CN3: The eyes are “down and out” with a droopy eyelid.
aneurym if the pupil is blown

CN4: Patient tilts their head away from the lesion.

trauma
CN6: The patient looks “cross-eyed.”
increased intracranial pressure
MUST KNOW: THE BASICS
 EOM actions, innervations
 RAd Sin
 SO↓ IO↑
 SO4 LR6 (LA SOT)

Muscle Primary Secondary Tertiary

Medial rectus Adduction - -
Lateral rectus Abduction - -
Inferior rectus Depression Extorsion Adduction
Superior rectus Elevation Intorsion Adduction
Inferior oblique Extorsion Elevation Abduction
Superior oblique Intorsion Depression Abduction
 VISUAL FIELD
 Extent of Visual field- 90° temporally
60° nasally
70° superior/inferior
 VISUAL FIELDS

 “Hill of vision”-sensitivity of the visual field

ASSESSING FOR VISUAL FIELD DEFECTS
CAN BE VIA
 Screening tests:
 Confrontational visual field testing
 Amsler grid (assesses the central 10° the visual field ) .
ASSESSING FOR VISUAL FIELD DEFECTS
CAN BE VIA
 Quantitative measurements
 Perimetry
 Static testing
 Kinetic testing

 Tangentscreen
 Goldman Bowl perimetry
 Automated Static perimetry
 PEARLS
 Lesions in optic disc, RNFL, follows the nerve fiber
arrangement
 Lesions in the central body of chiasm cause (bitemporal)
field defects that is assymetrical
 Optic nerve related visual field defect in one eye and a
contralateral superior temporal field suggests lesion at the
junction of O.N. and chiasm(junctional scotoma)
 PEARLS
 Optic tract and posterior visual pathway lesions
contralateral homonymous visual field defects
 Temporal lobe lesions homonymous field defects
denser superiorly
 Parietal lobe lesionsdenser inferiorly

 The more posterior the lesion from the chiasm (closer

to occipital lobe), the more congruous the lesion
 THE END

THANK YOU 