CHAPTER 1

BACKGROUND

Diplopia is the subjective complaint of seeing two images instead

of one and is often referred to as double-vision in lay parlance. The term
diplopia is derived from two Greek words: diplous, meaning double,
and ops, meaning eye. Diplopia or double vision is a common subjective
complaint, or diplopia may be elicited during the course of an eye
examination. Diplopia is often the first manifestation of many systemic
disorders, especially muscular or neurologic processes. 1 An accurate, clear
description of the symptoms (eg, constant or intermittent; variable or
unchanging; at near or at far; with one eye [monocular] or with both eyes
[binocular]; horizontal, vertical, or oblique) is critical to appropriate
diagnosis and management.2,3
Binocular diplopia can be corrected by covering either eye and
monocular diplopia persists in one eye despite covering the other eye.
Physiologic diplopia is a normal phenomenon depending on the alignment
of the ocular axes with the objects of regard (eg, focusing on a finger held
close results in distant objects being blurry but double).3
A review of patients presenting at a hospital casualty department
complaining of diplopia found that 25% presented with monocular
diplopia. Of the remainder with binocular diplopia, 39% were due to
infranuclear palsies, 26% were due to mechanical anomalies (muscular or
traumatic),

14%

were

longstanding

concomitant

deviations

or

convergence/accommodation deficits, 8% were due to supranuclear

palsies, 3% were due to spectacle intolerance, and in 10% of cases a
cause could not be established. This paper emphasised the importance of
not jumping to the conclusion that every patient complaining of diplopia
has an underlying sinister pathology. In addition, as less than half the
incomitancies were due to a single muscle infranuclear palsy, caution

should be exercised when trying to describe an ocular motility pattern in

terms of a single muscle defect. 4
Any patient presenting with diplopia should be examined carefully
to exclude the possibility of sinister etiology. Neurological disease
affecting the ocular motor system most commonly results in an
incomitancy, but can present as a concomitant deviation below is a
diagnostic routine and methodology that can be used in the event of a
patient presenting with diplopia. Particular emphasis is placed on
techniques that can be used for differential diagnosis. This is followed by a
summary of many of the different classes of defect that can lead to
diplopia, and their specific differential characteristics.5
CHAPTER 2
DISCUSSION

2.1 Epidemiology
A recent literature search for evidence-based data on diplopia
in the emergency department yielded one article (Morris), and that
from an ophthalmologic hospital in London. The incidence of diplopia
as a chief complaint in EDs must be low but is unknown. In this eyeonly facility, diplopia accounted for 1.4% of the chief complaints.6
From the report of Morris, we can extract some of the relative
frequencies of the different causes of diplopia as a presenting
complaint. Monocular diplopia, that is the double images from only
one eye, was surprisingly high accounting for 25% of the cases. This
seems high, particularly with one old clinical axiom that states that
monocular diplopia is often psychogenic, and must reflect the large
number of patients with refractive errors seen at that facility.
Binocular diplopia accounted for the majority of cases with isolated
2

cranial nerve palsies accounting for the largest portion of binocular

diplopia.7

2.2 Pathophysiology
The two most common mechanisms for diplopia are ocular
misalignment and ophthalmic aberrations (ie. Defects of the cornea,
lens, iris or retina). The most important clue to the identification of
the mechansm is whether the patient has monocular or binocular
diplopia. Ocular misalignment in a patient with normal binocular
vision results in binocular diplopia. Defined as diplopia that resolves
when either eye is occluded. If the image of an object that is being
viewed does not fall on the fovea of both retinas, then the image
appears to be in two different spatial locations and diplopia occurs.8
Monocular diplopia is defined as double vision that is present
in the affected eye while the other eye is occluded.In nearly all
circumstances, monocular diplopia is the result of a local ocular
aberration of the cornea, iris, lens, or rarely, the retina. Monocular
diplopia is never caused by misalignment of the eyes.
A third rare mechanism of diplopia is dysfunction of the
primary or secondary visual cortex. This results in bilateral monocular
diplopia and should be considered in the appropriate setting when
the patient has no ocular aberration.
Finally, diplopia that occurs without any pathologic cause may
be termed functional, patient whose diplopia is functional often
complain of multiple other somatic or neurologic symptoms in
addition to double vision. Historical clues should be gathered to help
define one of there four mechanisms before embarking on the
examination.9

2.3 Clinical Presentation

Every effort should be made to ascertain whether the diplopia
is monocular or binocular becaus this is critical in determining the
mechanism and cause. For patients with binocular diplopia, the
examiner can evaluate for causes of ocular misalignment due to
neurologic or orbital disease, whereas for patients with monocular
diplopia, the examiner can focus on disoreders of the eyes. If a
patient is uncertainty whether the diplopia is monocular or binocular,
he or she should be asked during the history to look at an object in
the examining room that appears double and determine whether the
double vision remains if the right eye is occluded. Note that
monocular diplopia can occur in both eyes simultaneously.10
The history elicited should include elements to aid in the
localizing the source of the problem. As is customary, the examiner
should gather information regarding onset, duration, frequency,
associated symptoms and exacerbating or relieving factors. Patients
should be asked specifically about vision loss, trauma, childhood
strabismus, amblyopia, and prior ocular or strabismus surgery. It is
essential to perform a full neurologic and ophtalmic review system.11

2.3.1 Monocular diplopia

a. Opthalmic cause
The most common ophthalmic causes of monocular
diplopia are uncorected refractice error and other defects of the
cornea. Certain descriptions of the diplopia can help the
examiner determine the cause. Patients with corneal defects
often experience double vision as a shadow image or a second

image that surrounds an object, they also may complain of a

haze or blur to their vision. Common cornea problems in the
otherwise healthy patients include irregular astigmatism, corneal
scars, and corneal defects induced by laser eye surgery. Cataract
formation usually results in loss of visual acuity and glare, but
occasionally, patients report diplopia due to a ghost image that
is much lighter and less defined. Retinal defects involving the
macula result in distortions of images that appear to be bent or
warped. Some macular defects result in diplopia that typically is
monucular but can be binocular. Skilled ophthalmoscopy allows
one to easily recognize macular disease and should be
performed

when

retinal

disease

is

suspected.

Prior

the

examination, the patient can be asked to draw and describe

what he or she sees and the characteristic distortions of macular
disease might become apparent.12

Figure 1. Drawing by a patient with diplopia due to macular

disease.

12

b. Neurologic causes
A rare manifestation of disease involving the primary and
secondary visual cortex is the visual perception of multiple
images, which is a bilateral monocular phenomenom beacause it
is present with either eye closed. Cerebral diplopia are rare
presentation of cortical disease.

13

c. Nonpathologic cause
Patient

whose

diplopia

is

functional

generally

have

numerous other vague complaints about their vision. Patients

shoud never be labeled as a functional unless comprehensve
ophtalmologic and neurologic examinations and work up indicate
no pathologic cause. A second visit may be necessary thing
course is not the origin of the diplopia.13

2.3.2

Binocular Diplopia
From the eye to the brain, following 7 mechanisms and
their associated locations shoud be kept in mind while gathering
historical information regarding binocular diplopia14.
-

Orbital or ocular displacement

extraocular muscle restriction,

extraocular muscle weakness,

neuromuscular junction dysfunction,

dysfunction of the third, fourth or sixth cranial nerves,

cranial nerve nuclear dysfunction in the brain stem,

supranuclear dysfunction involving the pathways to and

between the nuclei of the third, fourth or sixth cranial
nerves.
Patients should routinely be asked if the diplopia is

horizontal, vertical or oblique. Horizontal diplopia is related to

the control and movement of the medial rectus muscle, the
lateral rectus muscle, or both. Vertical diplopia is related to the
6

control and movement the inferior rectus muscle, the superior

rectus muscle, the inferior oblique muscle, the superior oblique
muscle or a combination of these muscles.13,14
These direction of gaze that results in diplopia or in
creasethe separation of the images can help determine which
structures are involved in the cause of diplopia. For instances, if
a horizontal, binocular diplopia is worse in left gaze, then either
the left eye cannot fully abduct (lect sixth nerve palsy) or the
right

eye

cannot

ophthalmoplegia).

fully

adduct

right

intranuclear

15

Table 1
Common Terms used in Describong Ocular Movementn and
Misalignment15

Figure 2. Extraocular muscle

15

a. Orbital disease or Extraocular muscle retriction

Most patients with orbital disease or extraocular muscle
restrictive processess will have conspicuous signs or periorbital
or orbital abnormalities on examination. Nonetheless, patient
must be questioned about changes can be subtle and difficult to
detect by the examiner. For example signs such as eyelid
retraction and periorbital edema fluctuate in disease such as
thyroid-assosiated ophthalmopathy and can be less evident in
early or mild stages of disease. Old photographs or drivers
license photo are extremely useful for detection of subtle
changes. Patients also shoud be asked about recent ocular
surgery, trauma and eye paint. Orbital processes such as
cellulitis mass lesions and inflammatory disorders of orbital
tissues can begin with eye pain and diplopia.16

Figure 3. Actions of extraocular muscles and cranial nerve control

from the examiners view. The wide arrows represent the primary
action by the muscle and the narrow arrows represent the
secondary action. Of note, the superior rectus and the superior
oblique muscle intort the eye, and the inferior rectus and the
inferior oblique muscles extort the eye, this is represented by
curved arrows. CN = cranial nerve, IO = inferior oblique muscle,
IR = Inferior rectus muscle, LR = lateral rectus muscle, MR =
Medial rectus muscle, SO = Superior oblique muscle, SR =
Superior rectus muscle.17

b. Extraocular myopathic weakness.

Mitochondrial myopathies, some congenital myopathies,
and muscular dystrophies such as oculopharyngeal dystrophy,
can present with diplopia due to significant extraocular muscle
weakness.

Of

note,

inflammatory

myopathis,

such

as

dematomyositis, polymiositis and steroid-induced myopathies,

arguably never involve weakness of the extraocular muscles.
Alternative explanations for diplopia in these disorders should be
sought.18
c. Neuromuscular junction dysfunction

Fluctuating

weakness

is

the historical hallmark

of

neuromuscular junction dysfunction, and patients with diplopia

should be routinely questioned about diurnal variation of
diplopia. More than 50 % of patients with myasthenia gravis,
which is the most common disorder of the neuromuscular
juntion, present with ptosis (eyelid drooping) and diplopia
without any symptoms or signs of weakness.19
d. Third, fourth, and sixth cranial nerve palsy
Historical

information

is

best

gathered

with

clear

understanding of the pathways of the third, fourth, and sixth

cranial nerves as they transverse from the brain stem to the
orbit. The cranial nerves that innervate the extraocular muscles
can be injured in the following locations from the eye to the brain
: orbit, superior orbital fissure, cavernosus sinus, subarachnoid
space and brain stem. Characterization of associated historical
and examination features are vital to localizing the site of injury,
and localzation leads to an accurate differential diagnosis.19
When cranial nerve palsies occur in isolation, patients
should be questioned about vascular risk factors the third,
fourth, or sixth cranial nerve can occur. Systemic vasculitides,
such as temporal arteritis, can present with a cranial nerve
palsy,

symptoms

of

jaw

claudication,

headache,

scalp

tenderness, and arthralgias should be inquired about in older

patients with diplopia due to a cranial nerve palsy.
A third cranial nerve palsy typically presents with vertical
and horizontal diplopia that improves when the affected eye is
abducted because the lateral rectus muscle and sixth cranial
nerve abduct the eye. Fourth cranial nerve palsies result in
vertical diplopia thatis worse or only present with near vision and
downward gaze in the opposite direction of the affected eye.
10

Because the superior oblique muscle intorts the eye, patients

with fourth nerve palsies also may report that one of the images
it tilted. Patients with a sixth nerve palsy experience horizontal
double vision that is worse when affected ye is abducted or when
viewing objects at distance, because the eyes must diverge.18,19

Tabel 2. Localization of third, fourth, and sixth Cranial Nerve

Palsies19

e. Brain stem injury

Injury within the brain stem to the supranuclear pathways,
the cranial nerve nuclei, or the cranial nerve fascicles rarely
result in isolated diplopia. Instead, most patients experience
diplopia

associated

with

additional

neurologic

symptoms

because the anatomic structures that control sensory, motor,

coordination, gait functions are in close proximity to the
11

structures that control eye movements. Familiarity with the

structures within the midbrain, pons, and medulla is neccessary
to localize the lesion using historical information. Patients should
be asked about facial numbness or weakness, hearing loss,
dysphagia, dysarthria, vertigo, and imbalance, as well as
incoordination, numbness, or weakness of the extremeties.20

f. Supranuclear pathways
Supranuclear pathways make connections to and between
the cranial nerve nuclei and originate in the cortex, brain stem,
cerebellum,
Supranuclear

and

the

peripheral

vestibular

can

in

dysfunction

result

structure.

conjugate

or

dysconjugate gaze abnormalities. If both eyes are equally paretic

in the same direction of gaze due to a supranuclear lesion, then
the deficit is conjugate and patients will not have diplopia.
Deficit can be congenital or aquired.21

Table 3. Supranuclear gaze palsies

12

20

Supranuclear gaze palsies can be either horizontal or

vertical. In most case, conjugate horizontal gaze palsies localize
to the pons or frontal cortex and conjugate vertical gaze palsies
localize to the midbrain. Dysconjugate gaze palsieshave various
localizations.

22

As with injury to the cranial nerves and their nuclei,

supranuclear pathway injuries are often accompanied by other
neurologic sign and symptoms. The numerous structures and
etiologies that are commonly associated with lesions of the
supranuclear pathways are shown in table 3. Patients should be
asked about symptoms of weakness, numbness, cognitive
impairment, imbalance, incoordination, dysphagia, dysarthria,
vertigo, nausea, adn vomiting.21

2.4 Examination for Anatomic Localization

Examination of all basic visual sensory and ocular motor
functions is necessary in the evaluation of diplopia. Best-corrected
visual acuity, visual fields to confrontation, pupil appearence and
reaction to loght, and posterior fundi should be examined in every
patient. In addition, if the pupil light response is abnormal for either
eye, then the pupil response to viewing a near terget should be
recorded (ie,part of the accommodation reflex). Alignment should be
noted while the patient is fixating on distant and near targets in all
directions of gaze, and evaluation of ductions, versions, saccades,
and pursuits should be performed. An invaluable tool for measuring
visual acuity is a handheld pinhole device that allows a patient to
have a monocular view of an eye chart through small holes. Pinholes
can eliminate refractive error and eliminate monocular diplopia
caused by many types of refractive error.23
13

Table 4. Pertient Questions to Establish Cause of Binocular Diplopia

2.4.1

23

Examination for monocular diplopia

To determine the specific ocular cause of monocular
diplopia, a complete ophtalmologic examination, including a slit
lamp examination, is necessary. If expertise or equipment is
inadequate, a formal ophthalmologic consultation should be
obtained for refraction and examination of the cornea, iris, lens,
ocular media, and retina for every patient who complains of
monocular diplopia. If pinholes correct the diplopia, then the
cause likely involves the cornea of lens. Macular disorcause likely
involves the cornea of lens. Macular disorders of the retina do not
improve with pinholes. An amsler chart can be used to identify
macular

disease,

which

should

be

verified

by

direct

ophtahlmiscopy.24
2.4.2

Examination for Binocular Diplopia

The examinationn of a patient with ocular misalignment
involves more than the evaluation of the movement of the eyes.
The examiner should measure or note ocular alignment in various
directions of gaze, periorbital swelling, orbital abnormalities such
as

forward

of

backward

displacement

of

the

globe

(ie,exophthalmos/proptosis or enophthalmos) injection of the

ocular conjunctiva or sclera, eyelid position, and fatigable
weakness of the extraocular muscles or levator palpebrae

14

muscles

of

the

eyelids.

examination also is neccessary.

complete

general

neurologic

25

Figure 4 . Example of an Amsler grid chart to test central

vision.

2.4.3

25

Globe, orbit, and eyelid examination

An exopththalmometer is used to detect and measure
proptosis or enopthalmos, and readings greater than 21 mm for
either eye or differences greater than 2 mm between each eye
indicatesproptosis or enopthalmus. Some people have shalow
orbits and readings that range from 23 mm to 25 mm can be
normal. If an exopthalmometer is not available, one should view
the eyes in a side profile or from above the patient to evaluate for
asymmetry.26
Eyelid function and eyelid position should be examined.
The upper eyelid position should be just slightly below the top of
the iris. When the upper eyelid is above the iris and sclera is
showing lid retraction si diagnosed, and if the eyelid lags behind
the eye with downward eye pursuits, then lid lag is present. These
two signs are very common in patients with thyroid-associated
ophthalmopathy. Dorsal midbrain disease can result in eyelid
retraction but not lid lag. Ptosis is present if there is less than 4
mm between the corneal light reflex on the center of the pupil
15

and the upper eyelid. Neurologic cause of ptosis result from

dysfunction of the levator palpebrae muscle, controlled by the
third cranial nerve, or from dysfunction of Mullers musclem which
is controlled by sympatheticinnervation. Ptosis from Mullers
muscle weakness caused by Horners syndrom is always minimal
and often the lower lid is slightly elevated. Old photographs help
to diifferentiate acute versus chronic processes involving the
globe, orbit, and eyelids.26

Figure 5. Photo of a patient with thyroid- associated

ophthalmopathy demonstrating bilateral eyelid retraction with
the lids above the iris with sclera showing (arrow)

2.4.4

27

Extraocular muscle movement examination

The cardinal positions of gaze are examined by asking the
patient to follow a target or the examiners finger held at
approximately 12 to 14 inches away from the patients eyes. If
ductions or versions are limited, one must determine whether the
limitation is caused by a restrictive process, muscle weakness,
neuromuscular junction dysfunction, cranial nerve palsy, or a
supranuclear process. Forced duction testing is useful to detect
mechanical limitation for patients with substantial extraocular
muscle limitation. Following topical anesthesia of the cornea and
conjungtiva, the tip of a cotton swab applicator or fine-toothed
forceps is used to attempt to move or force the eye into the
direction of limitation. If no restance is encountered mechanical
restriction is not present.28
16

The gross examination may be insensitive to the cause of

binocular diplopia, especially when dealing with a partial third or
fourth nerve palsy. A Maddoxrod-a red lens with ridges or a red
lens without ridges can be used to determine the presence and
degree of ocular misalignment. The red lens is held over the right
eye (by convention) while the patient views a pinpoint white light
from a transilluminator on the body of an ophthalmoscopeor
another light source held by the examiner. The location of the red
bar seen by the patient using a red lens without ridges, in relation
to the white light indicates how the eyes are misaligned. Ocular
torsion can be measured with use of a double Maddox rod.28

2.4.5

Neuromuscular junction examination

Evaluation for signs of fatigable extraocular muscle and
fatigable

eyelid

accomplished

weakness

with

with

techniques

recovery

such

as

of

strength

sustained

gaze

is
or

repetititve eye closure. Extraocular muscle fatigue is somewhat

difficult to observe but an attempt at maintaining eccentric
positions of gaze by a patient with neuromuscular junction
dysfunction might reveal in creasing strabismus, even in patients
without

initial

evidence

of

ocular

misalignment.

Repeat

extraocular muscle duction and version testing if no rest or

recovert is allowed after sustained gaze might reveal in creased
ophtalmoplegia from baseline. Weakness of the levator palpebrae
muscle results in ptosis. Ptosis that is characterized by recovert
after reat is referred to as cogans lid twitch. It is observed by
having the patient maintain fixation in downgaze for 10 to 20
seconds; the patient then should refixate with a saccade (ie, a
fast eye movement) on a target in primary (straight ahead) gaze.
If upon return to primary gaze, the ptotic lid rises and then falls
quickly, cogans lid twitch is present. The triad of fatigable ptosis,
17

fatigable extaocular muscle weakness, and weakness of the

orbicularis oculi muscles is highly suspicious for myasthenia.29

Figure 6. Maddox rod assessment of ocular misalignmet29

2.4.6

Third, fourth, and sixth cranial nerve examination

Examination

of

the

range

of

extraoculae

muscle

movement as well as the determination of the degree of

horizontal or vertical misalignment in all positions of gaze, and
with a right or left head tilt, allows one to diagnose whether a
cranial

nerve

is

responsible

for

the

deficit.

The

greatest

misalgnment of the eyes will occur in the direction of the action of

the weak muscle.
The third cranial nerve innervates the superior, inferior,
and medial recti muscles; the inferior oblique muscle; the
pupillary sphincter muscle; and the levator palppebrae superioris
muscle of the eyelid. Injury to the third nerve results in the
following signs: limited supraduction, infraduction, and adduction;
pupil mydriasis and partial or complete pupil paralysis to light;
and partial or compete ptosis of the affected eye. When the
18

unaffected eye is fixating on a sistant target in primary gaze, the

affected eye usually is positioned down and out

because of the

unopposed action of the superior oblique and lateral rectus muscles,

which

are

innervated

by

the

fourth

and

sixth

cranial

nerves,

respectively. Complete paralysis of the extraocular muscle and eyelid

without involvement of the pupil (ie, complete pupil-sparing third nerve
palsy) is most often due to ischemia of the third nerve. In cases of
partial third

nerve palsies, a maddox rod or red glass test often is

needed to verify the diagnosis. The maddox rod typically reveals a

hyperdeviotion of the affected eye in downgaze and a hyperdeviation
of the unaffected eye in upgaze, referred to as an alternating
hyprerdeviation. There also will be an exodeviation that

worsens when

the affecteed eye is adducted.30

The fourth cranial nerve innervates the superior oblique

muscle, which infraducts and intorts the eye. When the unnaffected eye
is fixating on a distant target in primary gaze, a misalignment may not
be present; for this reason, and because limitations in down gaze can
be difficult to directly lu observe, fourth nerve palsies often are poorly
recognized. If no limitation with inftaduction and adduction is obvious to
the examiner, the patient can be asked to view a straight line on paper
place near and below the eyes to the right and left. If double-vision
present, the patient can draw the false second image. the false image
should be below the line and tilted in cases of fourth nerve palsies such
19

that it forms an arrow that points to the side of the palsy. Due to the
intorsion action of the superior oblique muscle, the separation of the

doubled images increases when the head is tilted toward the side
of the fourth nerve palsy and the deficit improves when the head
is tilted to he side opposite the fourth nerve palsy. Thus, a right
fourth nerve palsy is made worse by a right head tilt. For this
reason, patients may unconsciously hold their head slightly tilted
the opposite side of the fourth nerve palsy. A maddox rod test will
show hyperdeviation of the affected eye when itu is infraducted
while in adduction.31
The sixth cranial nerve innervates the lateral rectus
muscle, which abducts the eye. When unaffected eye is fixating
on a distant target in primary gaze, the affected eye is often
deviated in ward (esotropia). The Maddox rod will reaveal an
esotropia that is greatest when the affected eye is abducted.

2.4.7

Brain stem examination

In order to assess brain stem function, the third, fourth,
and sixth cranial nerves as wel as all other cranial nerves must be
tested. Testing of facial strength and sensation, corneal sensation,
maseter strength, hearing, elevation of the palate and the uvula,
sternocleidomastoid and trapezius muscle strength, gag reflex,
and position and strength of the tongue will complete the cranial
nerve examination. Characteristic stroke syndromes within the
brain stem are defined and can be recognized by the combination
of signs and symptoms that result because of distinctive vascular
territories of penetrating small vessels.32

2.4.8 Supranuclear pathway examination

20

The

most

important

examination

feature

of

supranuclear motility deficit is the ability to overcome the ocular

motility limitation with an oculocephalic maneuver. In cases of
supranuclear injury, the nuclei that control the third, fourth, and
sixth cranial nerves are still intact and the cranial nerve fascicles
are functioning normally. Therefore, stimulation of the nuclei with
head movements shoud result in full ocular ductions. To perform
the oculocephalic maneuver, the patient should fixate on an
object 14 to 16 inches away, such as the patient;s thumb or the
examiners nose. Then while the patient continues to fixate, the
patients head is turned slowly to the right and left and up and
down. This head movement during fixation should overcome any
limitation of ductions or versions due to supranuclear pathway
dysfunction.32

2.5 Physical Test

1. Tensilon test is performed to exclude myasthenia gravis.
Intravenous injection of a short-acting anticholinesterase
(ie, 10 mg/mL edrophonium chloride [Tensilon]) should be part of
the initial workup of a patient with diplopia. Draw up 1 mL, and
establish venous access. Then, inject a test dose of 1 mg
intravenously to exclude possible hypersensitivity; if no adverse
effect is evident, inject the remaining 9 mg.33
The expected (normal) cholinergic response includes
salivation; lacrimation; flushing; and a brief, but often quite
dramatic, reversal of muscle weakness with temporary correction
of diplopia and/or ptosis. Occasionally, an excessive cholinergic
response may result in increased vagal tone with serious
bradyarrhythmias; atropine (0.5 mg) should be available as an
antidote.
21

Other

myopathies

ophthalmoplegia,

myotonia)

(eg,
do

progressive
not

external

respond

to

anticholinesterases.
2. Forced duction test
If a lack of movement of one eye occurs in a given direction,
excluding a tethered (or fibrotic) muscle may be helpful. Evaluate
whether the globe can be passively moved toward the affected
area. Traditionally, a forceps is used (after topical anesthesia) to
grasp the limbus, and then the eye can be gently tugged in the
desired direction. It may be possible to achieve the same result
less traumatically by using a cotton wool bud (soaked in topical
anesthetic) to "push" on the limbus in the desired direction.
3. Lee or Hess screen
This highly specialized test separates the field of vision of the 2
eyes. With one eye, the subject fixates on the corners of a
rectangle. The other eye is used to visualize the placement of a
marker on the same location. Any overaction or underaction will
become evident; when one eye has a weak muscle, it will not
move as much as the other eye. However, if that eye is used to
fixate, the excessive stimulation required will result in an
overshoot of the normal yoke muscle in the opposite eye.
4. Park three-step test
The Park three-step test can help elucidate which of the 4
extraocular muscles responsible for vertical eye movements are
responsible for a vertical diplopia. Although first appearing
impossibly complex, this test follows a logical progression to
progressively eliminate groups of muscles from the 4 pairs.

22

First, determine which eye appears higher with the head in a

normal position. Then, determine which eye is higher with gaze to
the left or to the right (ie, with the head turned to the right and
then turned to the left). Lastly, determine which eye is higher with
the head tilted left and tilted right. (The patient can also help by
commenting about when the diplopia is worse.) Then, answer the
questions in the following steps:

Step 1: Is the left eye or the right eye higher in primary gaze?
This reduces the possibilities of muscles from 4 pairs to 2
pairs. For example, if the right eye is higher, the weakness
resides either in the muscles depressing the right eye (right
superior oblique muscle and right inferior rectus muscle) or in
the elevators of the left eye (left superior rectus muscle and
left inferior oblique muscle).

Step 2: Is the deviation greater with left head turn or with right
head turn? This step reduces the alternatives to only one pair
of muscles. If the right eye deviates most when the head is
turned to the right (both eyes are turning to the left), then
only the right superior oblique muscle or the left superior
rectus muscle remains.

Step 3: Is the deviation greatest with tilting the head to the

left or to the right? Called the Bielschowsky head tilt, it relies
on the torsional balancing reflexes provoked by head tilt. The
higher eye extorts (because of the inferior oblique muscle),
while the lower eye intorts (because of the superior oblique
muscle).
By combining steps 1-3, only one muscle remains as the

culprit. This test requires a logical analysis and the exclusion of

alternative possibilities. However, the astute clinician can greatly
simplify this process by recognizing that the superior oblique
muscle is by far most likely to be responsible for a vertical

23

diplopia. A head tilt to the same side as the involved muscle

exacerbates the problem. A very simple rule of thumb is that "the
eye that is highest in adduction looks at the affected muscle."
The severity of the diplopia can be quantified by plotting
the field of single binocular vision on a Goldmann perimeter
(when available) or by using either a device to standardize the
head position or a questionnaire.
The Cervical Range of Motion (CROM) device uses a headmounted device with direction indicators to reproduce specific
gaze positions (10 degrees and 30 degrees up; down, left, right,
straight ahead, and reading position).
The questionnaire assigns a score of 6 if the diplopia is
always present straight ahead, a score of 4 if the diplopia is
present in the down, right, left, and reading position, and a score
of 2 if the diplopia is present in upgaze. The scores are halved if
the diplopia is sometimes present in these gaze directions.34

2.6 Imaging Studies

Evaluate old photographs to determine if a head posture (if
present) is long-standing. Commonly, a congenitally weak superior
oblique

muscle

can

be

compensated

for

by

head

tilt,

but

osteoarthritis of the neck or other mechanism can result in

decompensation and sudden symptoms of a chronic subclinical
condition.35
Order CT scan or MRI (with contrast) of the skull and orbits to
rule out intracranial masses or other pathologic processes, such as
the following :
A blow-out fracture requires imaging of the orbital floor.
24

 Enlarged muscles from thyroid ophthalmopathy help explain a

vertical diplopia.
Tumor of orbit
Tumor a long cranial nerve pathway
Increased intracranial pressure can account for bilateral
abducens palsy.
Aneurysm of intracranial carotid artery
Carotid cavernous fistula: Angiography may be required to
confirm the presence of a low-flow fistula.
Disease of sinuses (eg, infection, tumor) or bony disorders (eg,
dysostoses, encephalocele) can account for displacement of
the eye.
Traditional guidelines for imaging patients with new-onset
diplopia include imaging all patients younger than 50 years with
other neurologic findings, with a progressive course of diplopia, or
with a history of cancer. For patients older than 50 years, imaging is
not always necessary during the initial evaluation. Physicians should
conduct a careful review of the patients history to determine if
imaging is medically indicated.36

2.7 Work up and Treatment

Work up and treatment depends on the suspected cause of he
diplopia. In case of monocular diplopia, refraction may be all that is
needed. For orbital disorders, a computed tomography scan or
magnetic resonance imaging scan of the orbits is indicated. In case of
chronic, binocular diplopia, magnetic resonance imaging of the brain
25

is indicated unless the etiology is well understood. If myasthenia

gravis is suspected, anti acetylcholine receptor antibodies and
electromyography

should

be

performed.

Surgical

or

medical

treatment or the use of prism lenses can be relieve symptoms of

diplopia once the cause has been determined and the patient has a
stable deficit.

36

Table 5 . Sugested Treatments for Diplopia

36

CHAPTER III
CONCLUSION

Diplopia is the perception of two images of a single object. Often, we ask patients
if they have double vision and it is all too common for us to receive a positive response.
However, a patients perception of diplopia is often not the same as the conditions definition.
It is therefore important to ask patients what they mean by double vision and to have them
describe what they actually see. Responses may include decreased or loss of vision,
hemianopia or other visual field defects, as well as after images, image distortion or aching
26

eyes, all of which can be misconstrued as diplopia. It is also important to rule out both
monocular and physiologic diplopia.
Monocular diplopia persists in the affected eye despite covering the other eye.
Monocular diplopia rarely represents serious pathology, its most common causes being
uncorrected refractive error (usually astigmatism) and cataract. Other causes of monocular
diplopia are corneal surface irregularities (scarring or dryness), keratoconus or, rarely,
vitreous opacities and retinal conditions. A quick and easy method for evaluating monocular
diplopia is to have the patient look through a pinhole with the affected eye while the other eye
is occluded. If the monocular diplopia resolves during this test, then one can be fairly
comfortable in attributing the problem to an optical cause, which can be treated with glasses,
contact lenses, artificial tears (for dry eyes) or cataract surgery. Physiologic diplopia is noted
when an individual is focusing on a target, but the objects both in front and behind the point
of focus appear as double. Although its presentation is more common in children, physiologic
diplopia may not be discovered until later in life. This is a normal phenomenon that simply
requires the physician to reassure the patient that there is no serious underlying neurological
disorder.
Binocular diplopia, however, indicates a breakdown of the fusional capacity of the
binocular system, making its verification particularly important. When confronted with a
patient complaining of binocular diplopia, further information is required to try to determine
a cause. Comitant ocular deviations are the same in all gaze positions, whereas incomitant
deviations vary with different gaze positions. Patients who have comitant deviations usually
do not complain of diplopia because of the cortical ability to suppress one image (suppression
scotoma). This suppression is associated with congenital strabismus which, on occasion, can
break down or change, causing diplopia. Comitant deviations are frequently referred to as
decompensated deviations or phorias.Patients who have incomitant deviations usually
complain of diplopia and the most common causes are acquired. The deviations are typically
due to restriction or weakness of one or more of the extraocular muscles. Avariety of
etiologies is possible, but the more common conditions that affect the elderly and result in
double vision are discussed here in detail.
Evaluation

of

diplopia

can

be

dauting

without

basic

understanding of the mechanism and anatomy involved in ocular motility.

27

A systematic approach is necessary to uncover the mechanism of diplopia

and to appropriately direct the work up and management. With an
understanding of the important historical clues that help one guide and
execute the examination, the challege of evaluating diplopia can be
uncomplicated and rewarding.

28

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