Neuroophthalmology

BY
ABDELRAHMAN AHMAD.
MSc.

AGENDA
 Short notes about Anatomy & physiology
I. Eye
II. Vision
III. reflexes
 Evaluation and examination of the eye

Anatomy
A.Eyelids
 Three muscles control lid position
1. Levator palpebrae superioris
2. Muller’s muscle
3. Orbicularis oculi

Anatomy
C. Nervous control of eye movement
1. Oculomotor nerve.
2. Trochlear nerve.
3. Abducens nerve.

Types of Eye Movements
1. Saccades: Quick, (darting = jumping), conjugate
movements which direct the eyes to a new target.

2. Smooth pursuit: A slower conjugate movement
which allows for tracking of a moving object, or of a
stationary object while we are moving.

3. Convergence: A dysconjugate movement of both
eyes toward the midline to allow for focusing on a
near object by adjusting the angle between the eyes.

Anatomy
 eye muscles control gaze by
1. Occulomotor system
2. Optokinetic response

Occulomotor system

1. Vestibulo-ocular response system
Three semicircular canals, Resting firing rate increased by
acceleration/rotation of the head .
Canal function is initiated by head rotation toward it
 Generate compensatory eye movements in the direction
opposite the head motion to keep the eye stable
2-Otoliths
Also component of the vestibular system
Saccule and utricle, Detect linear accelerations of the head

Optokinetic Reflex
 Combination of saccades and
smooth pursuit that allow tracking of
targets in turn (e.g. counting sheep
as they jump over a fence).

 smoothly follow one target, then
saccade in the opposite direction to
pick up the next target

 parieto-temporal junction (smooth
pursuit area) projects down to
ipsilateral vestibular nucleus,
inhibits it allowing ipsilateral
smooth pursuit

 then, the FEF of the same
hemisphere generates a saccade back
to the next target

Anatomy
D. Pupillary anatomy
1. Parasympathetic
pathway
2. Sympathetic pathway

Anatomy
Parasympathatic supply
a. Muscles innervated
i. Iris sphincter: for pupillary constriction
ii. Ciliary muscle: for accommodation
b. CN III
i. Innervation of intraocular muscles
ii. Pupillomotor fibers are located on the outside (susceptible to
compression)
iii. Within the orbit, the parasympathetic fibers synapse in the
ciliary ganglion and postganglionic parasympathetic fibers
proceed anteriorly as short ciliary nerves to innervate the iris
sphincter and ciliary muscles

Anatomy
 Sympathetic pathway
 First-order neurons: originate in the posterolateral
hypothalamus and synapse within the intermediolateral
gray matter column of the lower cervical and upper
thoracic spinal cord
 Second-order neurons: arise from the ciliospinal center
and exit the spinal cord through the ventral roots of C8–
T2 to synapse in the superior cervical ganglion
 Third-order (postganglionic) neurons: originate from the
superior cervical ganglion and travel as a plexus along the
internal carotid artery

Anatomy
E. Retina:
light first enters the innermost layer of the retina through
the ganglion cell layer
 Rods: use rhodopsin pigment; mediate light perception
 Cones: use iodopsin pigment; mediate color vision

Anatomy
 The medial longitudinal fasciculus (MLF) is a pair of
crossed fiber tracts, one on each side of the brainstem,
situated near the midline and are composed of both
ascending and descending fibers

Anatomy
 The Medial Longitudinal Fasciculus carries information
about the direction that the eyes should move.
 It connect the cranial nerve nuclei III , IV and, VI together, and
integrates movements directed by the gaze centers (frontal eye
field) and information about head movement (from cranial
nerve VIII, Vestibulocochlear nerve).
 It also carries the descending tectospinal tract and medial
vestibulospinal tracts into the cervical spinal cord, and
innervates some muscles of the neck and upper limbs

Anatomy
 Input of MLB
1. the 8th cranial nerve
about head movements,
2. from the flocculus of
the cerebellum,
3. head and neck propioce-
ptors and foot and ankle
muscle spindle, via
the fastigial nucleus

Important reflexes
Light reflex

Anatomy
 Accomodation
reflex

II. Clinical Assessment

1. Ocular
a. Loss of vision in one eye vs. both eyes
b. Homonymous hemianopia may be misinterpreted by
patient as monocular vision loss
2. Retro-ocular
a. Hemianopia vs. quadrantanopia
b. Peripheral visual fields vs. central visual field

II. Clinical Assessment
3. Time
a. Duration: transient vs. permanent
b. Time of onset (acute, subacute, chronic)
c. Prior events
4. Associated phenomenology
a. Positive (hallucinations, scotoma, diplopia, etc.)
b. Negative (vision loss with darkness; complete vs. partial)
c. Associated symptomatology (eye pain, headache, focal
weakness)

EYE EXAMINATION
a. Eyelids
b. Conjunctiva
c. Visual acuity:
d. Visual fields
e. Extra ocular movement
f. Pupillary reactivity
g. Ophthalmoscopic examination

EYE LED EXAMINATION
 Periorbital edema
a. Ocular inflammation
b. Cavernous sinus disease
c. Thyroid ophthalmopathy
d. Renal impairement

EYE LED EXAMINATION
 Ptosis
 CN III palsy
 Horner’s syndrome
 Neuromuscular junction (MG, botulism)
 Myopathic (occulopharyngeal myopathy)
 Congenital
 Progressive external ophthalmoplegia
 Endocrine (thyroid)
 Trauma

EYE LED EXAMINATION
 Blepharospasm
a. Abnormally low and upper lid position that results from
excessive contraction of the orbicularis oculi

EYE LED EXAMINATION
 CAUSES OF BELPHAROSPASM
i. Isolated
ii. Associated with other facial dystonias: Meige’s syndrome
iii. Part of a generalized dystonia
iv. Occurs with parkinsonian syndromes
v. Medications (levodopa or the neuroleptics)
vi. Focal brain stem or basal ganglia lesions

Conjunctiva EXAMINATION

i. Transparent with only a few visible blood vessels
ii. Tortuous conjunctival vessels—carotid cavernous fistula
iii. Halo of redness at the limbus—uveitis or acute glaucoma
iv. Palpebral redness—keratopathy or dry eye syndrome
v. Diffuse eye injection—viral conjunctivitis

Visual acuity examination
 Snellen visual acuity test
Pseudoisochromatic color plates assessment of color
discrimination

Visual field examination
 Visual field testing: confrontation methods—comparisons
between hemifields and quadrants; Goldmann perimetry—
standardized visual field testing

Eye movement examination
1- myopathic disorder
a. Congenital myopathy (Myotubular ,Central core )
b. Muscular dystrophy ( Oculopharyngeal dystrophy)
c. Myotonic disorders ( Paramyotonia congenita ,
Hyperkalemic and hypokalemic periodic paralyses)
d. Mitochondrial myopathy
i. Progressive external ophthalmoplegia/Kearns-
Sayre syndrome
ii. MELAS
e. Metabolic myopathy: abetalipoproteinemia

f. Endocrine myopathy
i. Thyroid (Graves’) ophthalmopathy: characteristic feature
is lid retraction
ii. Steroid myopathy

2-Neuromuscular disorders
a. MG
i. Symptoms more likely as day progresses or with significant
motor activity
ii. Ptosis that increases throughout the day, ptosis that worsens
with repeated eye opening
iv. Diplopia with extraocular muscle involvement
b. Lambert-Eaton myasthenic syndrome: ocular signs are rare
c. Toxins
i. Organophosphate insecticides
ii. Botulism
iii. Venom (cobras, kraits, coral snakes, and sea snakes)

3. Neuropathic disorders
 Etiologies
i. Ischemic (atherosclerotic, diabetes mellitus)
ii. Hemorrhagic
iii. Increase ICT (tumor, aneurysm)
iv. Trauma
v. Acute inflammatory demyelinating polyradiculopathy
(Miller-Fisher variant)
vi. Cavernous sinus problem

Oculomotor (CN III) palsy
 Idiopathic (30–35%)
 Vascular (25%)
 Trauma (15%)
 Tumor (10%)
 Inflammatory/infectious (5–10%)

 Clinical
 Diplopia
 Ptosis
 Blurred near vision
Complete CN III palsy
 Eye in primary position is down and out
 Cannot elevate or adduct
 Full abduction
 Ptosis is severe
 Accommodation impaired
 Pupil is large and does not constrict to light or on convergence
(C) Pupil rule
 pupil involved in >90% in PCA Aneurysm

 In nuclear occulomotor lesion there is
 Ophthalmoplegai with bilateral ptosis and contralateral
superior rectus palsy

Trochlear (CN IV) palsy
 Trauma (30%)
 Idiopathic (20–25%)
 Ischemic (15%)
 Congenital (10%)
 Tumor (5–10%)

Clinical
 Compensatory lateral head tilt away from the side of the
lesion to minimize
 diplopia
 It is impossible to differentiate clinically between
trochlear lesion and nuclear lesion

Differential diagnosis of vertical diplopia
(1) Ocular MG
(2) Thyroid ophthalmoplegia
(3) Orbital lesion (i.e., tumor)
(4) CN III palsy
(5) CN IV palsy

Abducens (CN VI) palsy
 Idiopathic (25%)
 Tumor (20%)
 Trauma (15%)
 Ischemia (15%)

 Clinical
 Horizontal diplopia that is uncrossed, meaning that the
ipsilateral image belongs to the ipsilateral eye and is more
noticeable for distant targets

Rules for Evaluation for Diplopia
 Head tilt: When the weak extraocular muscle is unable
to move the eye, the head moves the eye. Therefore, the
head tilts or turns, or both, in the direction of action of
the weak muscle
 The image from the nonfixating eye is the false image
and is displaced in the direction opposite the deviation;
thus, when the patient fixates with the nonparetic eye,
the false image is displaced in the direction of action of
the paretic muscle

 The false image is the most peripheral image and is
displaced in the direction of action of the weak muscle,
except when the patient fixes with the paretic eye.
When the lateral rectus is paralyzed, the eyes are
esotropic (crossed), but the images are uncrossed. The
diplopia is worse at a distance and on looking to the
side of the weak muscle. When the medial rectus is
paralyzed, the eyes are exotropic ,but the images are
crossed . The diplopia is worse at near and on looking
to the opposite side.

 The images are most widely separated when an attempt is
made to look in the direction of the paretic muscle.
 Secondary deviation (the angle of ocular misalignment when
the paretic eye is fixating) is always greater than primary
deviation (when the good eye is fixating). Patients who
fixate with the paretic eye may appear to have intracranial
disease.
 Comitance: With a comitant strabismus, the angle of ocular
misalignment is relatively constant in all directions of gaze.
With a noncomitant (paralytic) strabismus, the angle of
misalignment varies with the direction of gaze.

Cavernous sinus syndromes
Etiologies
 Tumors (70%)
 Nasopharyngeal carcinoma (most common cause)
 Pituitary Adenoma
 Meningioma
 Craniopharyngioma
 Chondroma
 Metastatic (breast, lung, and prostate) carcinoma
 Aneurysms (20%)
 Infection

Tolosa-Hunt syndrome
 idiopathic noncaseating granulomatous inflammation in the cavernous sinus
 Diagnosis of exclusion
Clinical
 Acute painful ophthalmoplegia
 Progression over days to weeks
 Most commonly, CNs III and VI involved
 CN IV and CN V-1 in one-third of cases
 Optic nerve is affected in 20%
 CN V-2 sensory loss in 10%
 Horner’s syndrome, CN V-3 sensory loss, and CN VII palsy are unusual
 May have elevated erythrocyte sedimentation rate and positive systemic
lupus erythematosus preparation
 May have recurring attacks over months to years

35-year-old woman with Tolosa-Hunt syndrome presenting with painful
ophthalmoplegia. Extension of enhancing tissue into left orbital apex
(arrow) is seen on contrast-enhanced axial T1-weighted image.

 Pituitary apoplexy
a. Multiple oculomotor palsies
b. Severe headache
c. Bilateral vision loss

Internuclear ophthalmoplegia Etiologies
a. Lesion of the medial longitudinal i. Brain stem ischemia (usually
fasciculus (MLF) blocks information unilateral)
from the contralateral ii. MS (usually bilateral)
CN VI to the ipsilateral CN III iii. Brain stem encephalitis
b. Internuclear ophthalmoplegia named iv. Behcet’s disease
after ipsilateral MLF lesion v. Cryptococcosis
c. Clinical vi. Guillain-Barré syndrome
i. Impaired adduction during conjugate
gaze away from the side of the MLF
lesion
ii. Nystagmus of the abducting during
conjugate version movements
iii. Slowed adducting saccades with lag in
the adducting eye compared with the
abducting eye

One-and-a-half syndrome
a. Combined damage to
i. ipsilateral paramedian pontine reticular formation
ii. MLF and ipsilateral CN VI nucleus
b. Clinical
characterized by "a conjugate horizontal gaze palsy in one
direction and an internuclear ophthalmoplegia in the other

Nystagmus
 Nystagmus is an involuntary biphasic rhythmic ocular
oscillation in which one or both phases are slow .
 The slow phase of jerk nystagmus is responsible for the
initiation and generation of the nystagmus, whereas the
fast (saccadic) phase is a corrective movement bringing
the fovea back on target.

 Nystagmus may result from dysfunction of the vestibular
end organ, vestibular nerve, brainstem, cerebellum, or
cerebral centers for ocular pursuit
 Pendular nystagmus is central (brainstem or cerebellum)
in origin
 Jerk nystagmus with a linear slow phase is caused by
peripheral vestibular dysfunction.

Nystagmus syndromes LOCALIZATION

Downbeat nystagmus Bilateral cervicomedullary junction (flocculus)
Floor of the fourth ventricle
NUSTAGMUS SYNDROMES
Periodic alternating nystagmus Cervicomedullary junction

Upbeat nystagmus Bilateral pontomesencephalic junction
Bilateral pontomedullary junction
Cerebellar vermis

Pendular nystagmus Deep cerebellar (fastigial) nuclei

Seesaw nystagmus Mesodiencephalic junction, chiasm,
disorders that disrupt central vision
Hemi-jerk SSN Unilateral mesodiencephalic (upper poles
of the eyes jerk toward side of lesion)
Lateral medullary lesions (upper poles of
the eyes jerk away from side of lesion

Alternating hemi-SSN with vertical gaze Middle cerebellar peduncle

Optokinetic nystagmus
 Normal physiologic response to a series of objects moving
in the same direction across the visual field.
 It is a reflex phenomenon depends on the integrity of the
cortical visual pathways.
 May be absent with deep parietal lesions.

Physiologic nystagmus
 It is jerk nystagmus.
 Appear on extreme gaze; lateral or upward.
 Distinuished from pathological nystagmus:
 Neurological features
 Occurs with gaze angle less than 30

Nystagmus
Pendular nystagmus
Due to
i. MS (most common)
ii. Strokes
iii. Encephalitis
iv. Brain stem vascular

Nystagmus
Spasmus nutans
a. Disorder of young children, with age at onset usually 6–
12 months and resolves by age 3 years
b. Clinical triad
i. Ocular oscillations
ii. Head nodding
iii. Head turn

Nystagmus
Seesaw nystagmus
Present in all gaze positions
Etiologies
i. Tumor
Pituitary adenoma, Craniopharyngioma
ii. Stroke
Pontomedullary infarct, Midbrain/thalamic infarct
iii. Trauma
iv. Congenital
v. Vision loss

nystagmus
Downbeat nystagmus
i. Clinical
(A) Associated signs/symptoms
(1) Ataxia
(2) Blurred vision
(3) Oscillopsia
ii. Etiologies
(A) Arnold-Chiari syndrome (20–25%)
(B) Idiopathic (20%)
(C) Spinocerebellar degeneration (20%)
(D) Brain stem stroke (10%)
(E) MS (5–10%)
(F) Tumor
(G) Medication (lithium, antiepileptic drugs)/alcohol
(H) Trauma

Nystagmus
 Mechanism:
 Interruption of the posterior semicircular canal projections,
which are responsible for the downward vestibulo-ocular
reflex.
 Impaired cerebellar inhibition of the vestibular circuits for
upward eye movements.

nystagmus
Upbeat nystagmus
i. Associated with
(A) Oscillopsia
(B) Ataxia
ii. Etiologies
(A) Spinocerebellar degeneration (20–25%)
(B) Brain stem stroke/vascular malformation (20%)
(C) MS/inflammatory (10–15%)
(D) Tumor (10%)
(E) Infection
(F) Medication/alcohol
(G) Trauma

nystagmus
Torsional nystagmus
Usually attributed to dysfunction of vertical semicircular canal
inputs ,The fast phase changes with direction;
Toward the side of the lesion on downward gaze
Away from the side of the lesion on upward gaze
Etiologies
(A) Stroke
(B) MS
(C) Vascular malformation
(D) Arnold-Chiari syndrome
(E) Tumor
(F) Encephalitis
(G) Trauma

Gaze-evoked nystagmus
a. Most common nystagmus
b. Dysfunction of cerebellar flocculus in conjunction with the
lateral medulla for horizontal gaze and the midbrain for vertical
gaze
c. Differential diagnosis/etiologies
i. Medications
(A) Antiepileptic agents
(B) Sedative hypnotics, alcohol
ii. Bilateral brain stem lesion
iii. Cerebellar lesion
iv. MG

Vestibular nystagmus
 The most common form of jerk nystagmus, mostly rotatory.
 Result from damage of the labyrinth, vestibular nerve,
vestibular nucei, or their connections in the brainstem or
cerebellum also, in Meniere disease.
 No change in intensity with removal of fixation (using Frenzel
goggles).
 Central or peripheral:
 Peripheral type is associated with vertigo, nausea and vomiting.
 While in the central type it is less common but associated with
neurological findings.

Vestibular nystagmus
 Normally occurs with:
 Caloric irrigation
 Galvanic stimulation of the labyrinth or vestibular nerve.

Brun's Nystagmus
 It is bilateral and asymmetrical.
 It occurs in:
 large cerebellopontine angle tumors.
 AICA territory stroke.
 It is of large-amplitude and low frequency on gaze toward
the side of the lesion but small-amplitude, high-frequency
on gaze to the other side.

Ictal Nystagmus
 It may accompanies adversive seizures.
 Rarely is the only motor manifestation of a seizure.
 Nystagmus in comatose patients may be a manifestation
of a seizure.

Periodic Alternating Nystagmus
 It is a jerk nystagmus.
 Its fast phase beats in one direction and then damps or stops for
a few seconds before changing direction to the opposite side.
 A complete cycle takes approximately 1½ - 3 minutes.
 Causes:
 Congenital
 Craniocervical junction lesion e.g. MS, Chiari malformations
 Creutzfeldt-Jakob disease.

Monocular nystagmus
 Causes:
 Monocular blindness (in blind eye)
 Amblyopia
 Spasmus nutans
 Brainstem infarction
 Internuclear ophthalmoplegia
 Multiple sclerosis

Opsoclonus

1. Pathophysiology: dentate nucleus lesion
2. Clinical
a. Involuntary bursts of spontaneous saccades in all directions
b. Classic triad
i. Opsoclonus
ii. Myoclonus
iii. Ataxia (trunk and gait)
3. Etiologies
a. Neuroblastoma (childhood)
b. Infection (young adults)
i. Enterovirus
ii. Coxsackie virus B3, B2
iii. St. Louis encephalitis

Opsoclonus

iv. Rickettsia
v. Salmonella
vi. Rubella
vii. Epstein-Barr virus
viii. Mumps
c. Paraneoplastic
i. Breast
ii. Lung
iii. Uterine/ovarian
d. Brain stem stroke
e. Head trauma
f. MS
g. Midbrain tumor

Ocular bobbing

1. Clinical: rapid downward jerk with slow return to primary
gaze
2. Causes
a. Pontine lesion
b. Subarachnoid hemorrhage
c. Head trauma
d. Leigh disease
e. Cerebellar hemorrhage

Oculogyric crisis

1. Temporary period of frequent spasms of eye deviation, often
upward, Lasts for seconds to hours
2. Etiology
a. Medication
i. Neuroleptics
ii. Carbamazepine
iii. Tetrabenazine
iv. Lithium toxicity
b. Brain stem encephalitis
c. Rett’s syndrome
d. Tourette’s syndrome

Disorders of the visual
system and pathways
1. Optic disc edema
Causes of optic disc edema
i. Papilledema (elevated intracranial pressure)
ii. Optic neuritis
iii. Anterior ischemic optic neuropathy (AION)
iv. Giant cell arteritis
v. Diabetic papillitis

system and pathways
1-Optic neuritis
a. inflammation of the optic nerve
b. Pain in the involved eye worsened with eye movement
followed by monocular vision loss
c. Usually young adults
d. 5 females:1 male
e. Visual acuity is usually affected with central scotoma as the
classic finding
f. Relative afferent pupillary defect may persist even after the
visual function improves
g. Visual-evoked potential: prolonged P100

system and pathways
2-AION
a. Pathophysiology: ischemic infarct of the optic disc due to
atherosclerotic disease (nonarteritic AION), or from
vasculitis, most commonly giant cell arteritis (arteritic
AION)
b. Clinical
i. NB: Sudden painless vision loss associated with
unilateral optic disc swelling
ii. Usually >45 y/o

system and pathways
3-Papilledema
a. Associated with bilateral optic disc edema due to elevated
intracranial pressure
b. Secondarily, compression of the venous structures within the nerve
head that causes venous engorgement and tortuosity, capillary
dilation, and splinter hemorrhage
c. Etiologies
i. Intracranial mass lesion
ii. Pseudotumor cerebri
iii. Hydrocephalus
iv. Intracranial hemorrhage
v. Venous thrombosis/obstruction
vi. Meningitis

system and pathways
4-Tumors affecting the anterior visual system, as
Optic nerve sheath meningiomas , gliomas

system and pathways
5-Toxic/nutritional optic neuropathies
a. Nutritional deficiencies
i. Pyridoxine
ii. B12
iii. Folate
iv. Niacin
v. Riboflavin
vi. Thiamine
b. Toxic
i. Ethambutol
ii. Ethanol with tobacco
iii. Methanol
iv. Ethylene glycol
v. Amiodarone
vi. Isoniazid
vii. Chloramphenicol
viii. Chemotherapy
c. Toxic amblyopia
i. Typically affects heavy drinkers and pipe smokers

system and pathways
6-Hereditary optic neuropathies
Leber’s optic neuropathy
i. Pathophysiology: maternal mitochondrial DNA point mutation
ii. Clinical
(A) Optic neuropathy: upper limb, acute, painless optic neuritis
(B) Asymptomatic cardiac anomalies including accessory cardiac
atrioventricular conduction pathways (Wolff-Parkinson-White)
(C) Adolescent males

Disorders associated with the optic
chiasm

1. Clinical: classic pattern is bitemporal visual field defects
2. Etiologies
a. Sella tumors
i. Pituitary macroadenomas (may have associated endocrine
abnormalities): pituitary
apoplexy—acute enlargement of a pituitary adenoma due to necrotic
hemorrhage
or postpartum (Sheehan’s syndrome)
ii. Craniopharyngiomas
iii. Gliomas
b. MS
c. Aneurysm
d. Trauma

Anterior chiasm lesion
(Willebrand’s knee)
a. Nasal retinal fibers cross anterior in the chiasm before
joining the contralateral temporal fibers
b. Signs/symptoms
i. Ipsilateral monocular central scotoma
ii. Contralateral upper temporal field cut

Retrochiasmal visual pathways
 Disorders of the optic tract
 Disorders involving the lateral geniculate nucleus
 Optic radiations
 Occipital lobe
Most common causes
Stroke, SOL

Disorders of pupillary
function
 Pupil should be Regular ,Rounded, Equal in size
Topical cholinergic agents that influence pupil size
a. Cholinergic agonists that produce miosis
i. Pilocarpine , Carbachol , Methacholine , Physostigmine ,
Organophosphate insecticides
b. Cholinergic antagonists that produce mydriasis
i. Atropine
ii. Scopolamine

function
Adrenergic agonists that produce mydriasis
Epinephrine , Phenylephrine, Cocaine
,Hydroxyamphetamine Ephedrine,
b. Adrenergic antagonists that produce miosis
Guanethidine
Reserpine
Thymoxamin

function
(Marcus Gunn pupil)
a. Diagnosis via swinging flashlight test
b. Etiologies
i. Amblyopia
ii. Retinopathies
iii. Maculopathies
iv. Optic neuropathies
v. Optic chiasm lesions
vi. Optic tract lesions
vii. Midbrain lesion involving the pretectal nucleus or the
brachium of the superior colliculus
viii. Lateral geniculate nucleus

function
Large and poorly reactive pupil
i. Unilateral
(A) Adie’s tonic pupil
(B) Pharmacologic (anticholinergic agent, jimson weed, adrenergic
agonist)
(C) Trauma/surgery
(D) Ischemia (carotid artery insufficiency, giant cell arteritis, carotid
cavernous fistula)
(E) Iridocyclitis
(F) Complication of infection (e.g., herpes zoster)
(G) CN III palsy
(H) Tonic pupil associated with peripheral neuropathy or systemic
dysautonomia

function
Bilateral
(A) Adie’s tonic pupils
(B) Pharmacologic (anticholinergic agent, jimson weed,
adrenergic agonist)
(C) Parinaud syndrome
(D) Argyll-Robertson pupils
(E) CN III palsy
(F) Carcinomatous meningitis
(G) Chronic basilar meningitis
(H) Guillain-Barré syndrome
(I) Eaton-Lambert syndrome
(J) Botulism

function
Argyll-Robertson syndrome
Miotic irregular pupils
Light-near dissociation
(A) Absence of light response associated with normal
anterior visual pathway function
(B) Brisk pupillary constriction to near object
iii. Normal visual acuity
iv. Diminished pupillary dilatation, particularly in dark
v. Usually bilateral

function
Etiology
i. Neurosyphilis
ii. Muscular dystrophy
iii. MS
iv. Chronic alcoholism
v. Sarcoidosis

function
Horner’s syndrome
i. Miosis
ii. Ptosis (denervation of Müller’s muscle)
iii. Anhidrosis (ipsilateral facial)

function
(A) Brain stem (Wallenberg’s) or thalamic stroke
(B) Intra-axial tumor involving the thalamus, brain stem, or
cervical spinal cord
(C) Demyelination or inflammatory process involving the
brain stem or cervical
spinal cord
(D) Syringomyelia
(E) Neck trauma

function
(A) Tumors involving the pulmonary apex, mediastinum,
cervical paravertebral
region, or C8–T2 nerve roots
(B) Lower brachial plexus injury
(C) Subclavian or internal jugular vein catheter placement
(D) Stellate or superior cervical ganglion blocks
(E) Carotid dissection below the superior cervical ganglion

function
(A) Internal carotid artery dissection
(B) Cluster headache
(C) Skull base or orbital trauma or tumors
(D) Intracavernous carotid artery aneurysm
(E) Carotid endarterectomy
(F) Herpes zoster ophthalmicus
(G) Complicated otitis media

function
Opiate overdose
a. Bilateral pinpoint pupils
b. Also seen in pontine dysfunction

Fundus examination
Adjust the diopter dial to bring the retina into focus.
*Find a blood vessel and follow it to the optic disc.
*Inspect outward from the optic disk in at least four quadrants
and note any abnormalities.
* Move nasally from the disk to observe the macula

Why it is performed
 Fundus examination is one of the most valuable tests
conducted during an eye examination because it can detect
some signs and physiological effects of various circulatory,
metabolic and neurological disorders.
 Fundus examination is routinely used to assess and
diagnose vitro-retinal diseases (such as diabetic retinopathy,
retinal tear and detachment, macular hole, retinal
haemorrhage, retinal artery and vein occlusion, choroidal
tumor, or macular edema), optic nerve defects, and
hereditary diseases

Stages
Early papilledema I

 Earliest change is disc hyperemia and dilated capillaries.
 Blurring of disc margins,
 Spontaneous venous pulsation is absent
 Splinter hemorrhages at or just off the disc-margin.

. An optic nerve with mild swelling (papilledema).
Note the pathologic"C"-shaped halo of edema surrounding the optic disk (Grade I
papilledema).

stageII
Established papilledema:
 Disc margins become indistinct and central
cup is obliterated.
Disc surface is elevated above the retinal plane (more than + 3D
(1mm) with direct ophthalmoscope).
 Peripapillary oedema.
 Venous engorgement . Flame-shaped
 hemorrhages and 'cotton-wool' spots around
 the disc. Hard exudates in radiating pattern
around the macula, [macular star]

Grade II papilledema. The halo of edema now surrounds the optic disc

Stage III
Chronic papilledema or Vintage papilledema:
 Disc edema resolves, but margins are blurred
 Hemorrhagic and exudative components
 gradually resolve.
 Optic disc appears pale like a champagne cork.

Stage IV
Atrophic papilledema
 Peripapillary retinal vessels are attenuated and heathed.
Dirty-white appearance of the optic disc, due to reactive gliosis
– leading to secondary optic atrophy.

 Grade IV papillededema. With more severe swelling in addition to a circumferential halo, the edema
covers major blood vessels as they leave the optic disk (grade III) and vessels on the disk (grade IV).

Neuroophthalmology

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