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Diplo Pia
Diplo Pia
TO SWIM OR TO SINK
By
AHMED MAHMOUD AMIN
MD,FRCS(Glasgow)
Orbital fellow , AMC , Amsterdam , Netherlands
Lecturer of Ophthalmology, Al Azhar University, Cairo
AKNOWLEDGEMENT
OUTLINE
INTRODUCTION
HISTORY
EXAMINATION:
- Individual tests
- Sequence of examination
INVESTIGATIONS
POSSIBLE SCENARIOS
THE 1-2-3 OF NEURO-OPHTHALMIC
EXAMINATION
1- The afferent visual pathways:
Visual acuity
Visual fields
Color vision
Ocular fundus examination.
2- The efferent pathways of ocular motility:
Cover–uncover testing
Saccade
Smooth pursuit
Vergence
Vestibulo-ocular and optokinetic testing
Red glass or even better the Maddox rod to characterize diplopia.
3- The afferent and efferent limbs of the pupil
Sensory
Motor
Adaptive
PSEUDO
TRUE
= APPARENT
LATENT MANIFEST
CONCOMITANT INCOMITANT
RESTRICTIVE PARALYTIC
Static (Alignment)
Tendency to deviate
Kinetic (Motility)
AN
APPROACH
TO
EXAMINING
OCULAR
MOTILITY
■ Measure VA and record refraction.
■ Observe any abnormal head posture (AHP).
■ Using a pen torch at 33 cm, observe the corneal reflections(CRs).
Look for symmetry or asymmetry.
■ Perform cover test (CT) at near (33 cm) to a light and then accommodative target (e.g.
reduced Snellen letter at VA of worst eye, or pictures/toys for children).
CT involves two manoeuvres.
1. Cover-uncover test: to detect manifest strabismus. Cover one eye and look at the non covered
eye. Movement inward to take up fixation indicates an exotropia. Movement outward indicates
an esotropia. If the eye is slow to fix the target, this may indicate poor VA or amblyopia. Note
any manifest or manifest latent nystagmus (MLN) – horizontal jerky, often very fine nystagmus
with fast phase towards the uncovered eye. Note any movement of the covered eye, particularly
dissociated vertical deviation (DVD) associated with infantile esotropia.
2. Alternating cover test: to detect latent strabismus.
Alternately occlude left and right eye for 1–2 seconds each. Do not allow both eyes to view in
between covering as fusion may then take place. A latent deviation sometimes becomes
temporarily manifest after fusion is disrupted by testing. Note how fast the eyes resume
binocular single vision (BSV) once testing is complete (rapid or slow recovery) indicating how
well the deviation is compensated.
■ Move the target occasionally to check fixation.
■ Perform CT at distance to a suitably sized chart letter or picture/toy.
■ Repeat CT with/without glasses, and then with/without AHP.
Eye movements (cranial nerves III, IV, VI)
■ If suggested by the history, check for monocular diplopia by occluding each eye separately.
Note VA. If not already known, clarify if diplopia is horizontal, vertical, or tilted.
■ Observe any head tilt, proptosis , ptosis, or lid retraction.
■ Ask the patient to follow a light held at 50 cm and report if they see diplopia.
Go from primary position and back again in the other 8 cardinal positions of gaze. Ensure the
CRs are always visible; the patient or examiner may need to lift the lids, particularly in down
gaze. Check for lid-lag on downward smooth pursuit and any narrowing (Duane’s syndrome) or
widening (aberrant 3rd nerve regeneration or Brown’s syndrome) of the palpebral aperture on
adduction; observe any pupillary changes, e.g. constriction of the pupil in adduction or other
gaze position may occur with aberrant 3rd nerve regeneration.
■ If diplopia occurs in any position, check which image disappears when an eye is covered; the
more peripheral image comes from the eye with the paretic muscle(s).
■ If CT shows a hypertropia/hyperphoria in the primary position (step 1) then do a CT in right
and left gaze to see where the height is greatest (step 2). If greater in right gaze then repeat
the CT up and down to the right. If the deviation is greater down to the right, a left 4th nerve
palsy is suspected. Finally, compare CT (eyes in primary position, fixing at 3 meters) with the
head tilted right and left, to see if the height differs (step 3). If the deviation is greater on head
tilt left, a left 4th nerve palsy is likely. However, the head tilt test is not always reliable and other
causes of hypertropia should not be ignored, e.g. thyroid eye disease. Park’s three-step test
refers to steps 1, 2, and 3 combined. Step 3 is also called the Bielschowsky headtilt test.
However, the diagnostic importance of testing in all 9 positions cannot be overemphasized.
Vertical deviations can be associated with bilateral (often asymmetrical) muscle under- or
overactions.
■ Examine saccades in suspected supranuclear lesions to help differentiate newly acquired
palsies from mechanical strabismus (normal in the latter). Position a target to the right and left
of the patient’s eyes, within the visual field; instruct the patient to look from one target to the
other as quickly as possible, without moving the head. Repeat the test in the vertical plane.
Compare the vertical and horizontal velocity of the excursion, as well as the velocity in each eye;
e.g. a reduced excursion of the adducting eye on horizontal saccades may indicate an inter
nuclear ophthalmoplegia (same side).
Cerebellar disease and MS may produce hypermetric saccades (eyes overshoot the target).
Myasthenia gravis and Parkinson’s disease may produce hypometric saccades (eyes undershoot
the target).
■ Test convergence to a detailed target, and observe normal pupillary constriction.
■ If required perform Doll’s head maneuver to differentiate supranuclear from nonsupranuclear
lesions (e.g. Steele Richardson Olszewski Syndrome). Ask the patient to fixate a target in the
distance. Inform the patient that you are going to gently move the head right, left, up and down.
Observe the extent of ocular rotations. Doll’s head movements may be absent in supranuclear
lesions.
■ Test optokinetic nystagmus with an OKN drum rotated slowly in front of the patient, both
horizontally and vertically, and in both directions. Horizontal asymmetry may indicate a parietal
lesion. Convergence retraction nystagmus with a downward moving drum (producing upward
refixation saccades) suggests Parinaud’s syndrome.
AS ANY MUSCLE
Posture
Tone (passive)
Power (active)
Coordination
OCULAR SYSTEMIC
-Diplopia chart -Laboratorial
-Hess screen -Radiological
-EMG
-Instrumental
DIPLOPIA CHART
HESS SCREEN
DIFFERENTIAL DIAGNOSIS OF ENLARGED EOMs
COMMON CAUSES OF EOM ENLARGEMENT
EOMs IN TED
Smooth
Spindle shaped
Sparing the tendons
Solitary (? IR)
Special Sequence of involvement
Symmetrical if bilateral
I’M Slow or (I’M So Late)
(Inferior, Medial, Superior, & Lateral rectus)
Single EOM
Group of EOMs → Single cranial nerve (3rd)
Multiple cranial nerves → Syndrome
( 3 motor cranial nerves & 3 syndromes)
If not → think of mimickers
(LR6 SO4)3
The ocular motility examination consists of the following:
● Observation in primary gaze
● Ductions (monocular eye movements)
● Vergence (binocular dysconjugate movements)
● Versions (binocular conjugate eye movements)
○ Saccades
○ Pursuit
○ Oculocephalic responses and vestibulo-ocular reflex
(VOR)
○ Optokinetic nystagmus
● Detection and measurement (with prisms) of ocular
misalignment (strabismus)
● Detection of nystagmus
Saccade is a fast eye movement used to acquire a
target by placing the image of the target on the fovea.
Smooth pursuit is a slow eye movement used to track a
target as it moves by keeping the target on the fovea.
The vestibular ocular movement is used to keep the
eyes on a target during brief head movements.
The optokinetic eye movement is a combination of
saccadic and slow eye movements that keeps a full-field
image stable on the retina during sustained head
rotation.
Each of these movements is a conjugate eye
movement, that is, movements of both eyes together
driven by a common neural source.
Vergence movement is a non-conjugate eye movement
allowing the eyes to track targets as they come closer or
farther away.
NPC
A: METHOD FOR EXAMINING AND RECORDING OCULAR MOTILITY.
B: RECORD OF SIXTH NERVE PALSY OF RIGHT EYE.
C: RECORD OF RIGHT ORBITAL BLOW-OUT FRACTURE AND LIMITED
UPGAZE.
The direction of the caloric response is named after the FA ST phase
Trauma
Thyroid
Tensilon ( Myasthenia)
Thiamine deficiency
Toxins
Turkey
PROGRESSIVE
OPHTHALMOPLEGIA
Rapidly progressive ophthalmoplegia should
suggest myasthenia, the Miller Fisher variant
of Guillain-Barre´ disease, or botulism; prognosis
in these disorders depends on respiratory
involvement, and early symptoms of
dyspnea should be carefully sought.
MYASTHENIA GRAVIS
(Look for an eyelid that won’t stay open or closed)
Diurnal variation
Descending march course
- Drooping of upper lid
- Diplopia
- Dysphagia
- Dysarthria
- Dyspnea
Decremental response on EMG
Dysthyroid ophthalmopathy ( 5–10%).
CASCADE OF EVENTS IN
MYASTHENIA GRAVIS
1- Thymus
Thymus imaging
Thymectomy if indicated
2- Antibodies
Acetyl choline receptor antibodies assay
Plasmapheresis to wash these Antibodies
3- Antigen / Antibody reaction
Steroids
Cytotoxic drugs
4- Acetyl choline as if depleted
Tensilone test (diagnostic)
Anticholine estrases as Mestinon (therapeutic)
5- Muscle dysfunction
EMG & preferably single muscle fiber EMG
AAO
ATAXIA
AREFLEXIA
OPHTHALMOPLEGIA
Third nerve palsies may reveal a neurosurgical emergency such as
intracranial aneurysm or pituitary apoplexy, especially when the
pupil is involved.
Be particularly aware of the possibility of aneurysm when the third
nerve palsy is partial, even when the pupil is spared .
The ‘‘rule of the pupil’’ applies only if the patient has a complete
third nerve palsy (i.e., all muscles innervated by the third nerve are
involved, with minimal remaining function).
A patient with pupil sparing complete third nerve palsy must be
seen in follow-up to verify that the pupil remains normal, because
mydriasis may be delayed for a few days in patients with
compressive third nerve palsy.
3rd NERVE PALSY
FOUR CLINICAL FEATURES FOUR COMMON LESIONS
WHERE IS THE LESION?
WHAT IS THE LESION?
PUPIL INVOLVEMENT?
التاريخ و الجغرافيا
PAINFUL DIPLOPIA
RED FLAGS
Except for infectious orbital cellulitis and some
forms of orbital pseudotumor, diseases
involving the extraocular muscles rarely
represent an emergency.
Ocular myasthenia gravis is not an emergency
unless the patient has systemic symptoms
such as respiratory distress or dysphagia.
Isolated fourth nerve palsy is rarely an
emergency.
STRUCTURES PASSING
THROUGH THE SUPERIOR
ORBITAL FISSURE
7 PASSENGERS (SHIPS)
1- 3rd
2- 4th
3- 6th
4- 1st division of 5th
5- 2nd division of 5th
6- Sympathetic fibers
7- ICA
CCF
Direct or indirect
High flow or low flow
Spontaneous or traumatic
CCF
Enlargement of :
Superior ophthalmic vein
EOMs
Cavernous sinus
BARROW CLASSIFICATION
COMPARISON OF DIRECT & INDIRECT CCF
CCF
BLOOD IS SHIFTED AWAY
FROM THE ARTERY RESULTING
IN ISCHAEMIA
NULL POINT
OCULAR
NYSTAGMUS VERSUS NYSTAGMUS BLOCKAGE PRISM
VESTIBULAR
NYSTAGMOID SYNDROME SURGERY
CNS
TORTICOLLIS
EARLY ONSET NYSTAGMUS
LATENT NYSTAGMUS
(A) WITH BOTH EYES OPEN ,NO ABNORMAL EYE MOVEMENTS MAY BE
EVIDENT.
(B) WHEN ONE EYE IS COVERED, BOTH EYES DEVELOP A JERK
NYSTAGMUS WITH A FAST PHASE TOWARDS THE UNCOVERED EYE.
Associations
PUPIL EXAMINATION
QUALITATIVE & QUANTITATIVE
Pupil size in mm
Grading of RAPD with neutral density filters
RAPD
ARP
وطفئ الىور والمية تكدب الغطاس
Scotopic conditions aggravate the difference ..Sympathetic lesion..? Smaller pupil is abnormal
EFFERENT PUPILLARY
DEFECTS
3RD NERVE PALSY
Isolated or as a part of …syndrome
Pupil involving or sparing or delayed
Partial or complete
Signs of aberrant regeneration
DORSAL MIDBRAIN SYNDROME
Abnormal pupil
Light-near dissociation
Pupils usually large
Slightly unequal
Often oval in shape
ARGYLL ROBERTSON PUPIL
(ARP)
ARP: Accomodation Reflex Present
PRA : Pupillary Reflex Absent
SYPHILIS ??
ADIE’S
DENERVATION
ABERRANT REINNERVATION
DENERVATION SUPERSENSITIVITY
LIGHT–NEAR DISSOCIATION
?? TONIC
?? SYNDROME
Acute ADIE’S
LITTLE OLD ADIE’S
Iritis
PUPIL
Trauma Drugs
TRAUMA (the 7 rings)
IRITS (Posterior synechiae)
Small difference
Same in bright or dim light
Sound pupil
LIGHT NEAR DISSOCIATION
HIPPUS