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Transcript of Diplopia
Beginner's guide to diplopia;
Clinical evaluation with differential diagnosis
Figuring out diplopia can be a very challenging task. Just like the appearance of this iceberg's peak, your patient could present with double vision or visual blurriness that may appear benign, but...
- These results suggests
due to refractive error or a local eye disease
- It is unlikely to be of neurological etiology
may occur due to ocular misalignment. This is why when the patient covered one eye, the diplopia was eliminated.
- This means that the next things for us to note is the movement of the patient's eyes.
Abnormalities of refractive media
Looks like your patient's diplopia is due
which can be corrected with glasses/lenses or surgically .
Nice work figuring this out!
Refractive errors happen when the shape of the eye keeps us from focusing well. The cause could be the length of the eyeball (longer or shorter), changes in the shape of the cornea, or aging of the lens.
Your patient may be experiencing other symptoms such as headaches, glare, eye strain and eye squinting
Have the patient look through a
Is the diplopia resolved?
To avoid getting yourself confused when provided with overwhelming amount of detail, we've compiled a series of assessment tests that if performed correctly and in the right order, can provide you with a simpler and practical framework to navigate your way towards making the correct diagnosis. Let's begin.
A. Forced duction test
Next, let's figure out how to distinguish between
Conduct one of the following tests:
B. Intraocular pressure - test in primary & eccentric gaze
Were you able to easily move the patient's eye?
Did you measure an elevation of 5 mmHg of greater?
As we briefly mentioned before,
suggests that there is a restriction in the movement of an extraocular muscle. These can be distinguished by careful observation of the patient's eye motility, as well as other symptoms in addition to double vision, and by ordering various laboratory testing.
Graves ophthalmopathy (Thyroid orbitopathy)
- Idiopathic inflammation of extraocular muscles would produce pain and ophthalmoplegia, leading to restriction
- Congenital restriction due to shorter tendon of superior oblique muscle
a careful ocular examination may reveal a complicated underlying disorder that could be potentially life-threatening
Monocular vs. binocular diplopia
- horizontal vs. vertical vs. oblique
- worse at near vs. far
- tropia vs. phoria
- esodeviation vs. exodeviation
- hyper vs hypo-deviations
Have your patient
one eye at a time.
Is the diplopia resolved when covering one eye?
Lets figure out first if the problem is in
one eye (monocular)
or if it involves
both eyes (binocular)
- Most common cause of restrictive strabismus
- Thyroid function testing results may be normal
- Other signs of hyperthyrodism:
- Any rectus muscle can be involved, but most commonly affected are the inferior and medial
- Diplopia will be worsen at specific directions of gaze:
if inferior m. involved - note vertical diplopia with increased deviation at upward gaze
if medial m. involved - note horizontal diplopia increasing with lateral gaze
if bilateral eye involvement would lead to V-shaped pattern of eye movement, with
right-hyperdeviation with left gaze and vice verse.
- Mostly due to a blowout fracture of the orbit and entrapment of extraocular muscle (usually the inferior rectus, but medial rectus possibly as well)
- May involve direct damage to involved muscle, associated with edema and
hemorrhage, which could further lead to compartment syndrome, and later to fibrosis and scarring
- Involvement of the intramuscular septa can lead to restriction in eye motility as well without necessarily a direct involvement of a muscle in the
- Restriction in extraocular movement can result due to a neoplastic process extending from near by sinuses
- Metastases rarely involve the eye muscles directly
- Other possible symptoms are proptosis, chemosis, and conjunctival hyperemia
- Radiography may show enlargement of extraocular muscles and associated tendons
- may be secondary to systemic illness. Consider testing
for SLE, Sarcoidosis, Granulomatosis with polyangiitis
and other appropriate disorders.
- Eye will deviate outward in up gaze. Note hypodeviation increases on contralateral upgaze. Patient will compensate by tilting his head backwards.
- Can be acquired due to inflammation of the superior oblique tendon sheath (in Rheumatoid arthritis, "Click syndrome"), sinusitis, surgery,
and rarely trauma.
. Have your patient move his/hers eyes in the 9 cardinal positions of gaze relative to primary position, which is looking straight ahead.
up & left
up & right
down & right
down & left
This exam result tells us that your patient monocular diplopia is not due to an optical aberration. Here are other possible causes you should consider at this point.
Note any impairment in motility:
Even if you did not notice any, move on to the next exam to help you localize the problem
with abduction (eye can't move laterally) or adduction (eye can't move medially)
with elevation or depression
with divergence, diplopia worsened with object at distance
with convergence , diplopia worsened at near, for example, when patient is attempting to read.
Let's do the
. Ask the patient to look at an object with both eyes open. Cover one of the patient's eyes and observe any corrective movement in the other (unoccluded) eye needed to fixate. Repeat test for the opposite eye. If you notice any movement in the unoccluded eye, a
if the patient was unable to maintain fixation or if you were not able to perform this test, try to do the next exam using a penlight.
Even if you did not notice any deviation, move on to the next exam to help you localize the problem.
corneal light reflection test (Hirschberg test)
is an objective test that can be performed instead of the cover-uncover test. Ask the patient to stare ahead (eyes at primary gaze). While standing in front of the patient, shine a light at the patient's eyes and observe where it is reflected on each cornea.
If eyes are normally aligned, the light will be reflected slightly nasally from the center of each cornea, and if comparing both eyes, the reflection will be symmetric (meaning, with same relative position).
if there is misalignment, reflection would be asymmetric; light shined at the center of one pupil will be reflected on the cornea in the other eye in a direction opposite to the deviation of the eye.
if the eye is deviated upwards (hypertropic), reflection will appear below the pupil.
If you were not able to detect any abnormality, it might be because your patient has either full ocular motility, or it may be unnoticeable because the ocular deviation is very small or when it is congenital and is being suppressed.
When the misalignment is not noticeable, try to elicit it by interrupting the synchronization
between the eyes, as described in the next examination step.
*Use the same terminology we used when we were describing tropias (for example, eso
if eye is deviated medially)
To confirm our suspicion, let's do the
cross-cover test (aka alternate cover test)
. In an alternating fashion, cover one of the patient's eyes and then the other, to "break fusion". If the unoccluded eye moves to fixate, a
Great! now we can move on to the next step!
We are left to figure out whether the amount of the patient's ocular deviation varies with gaze.
If you observed that the deviation was the same regardless of direction of
gaze, the patient's tropia/phoria is
If it varied (increased/decreased) with changes in the direction of gaze, the
patient's tropia/phoria is
note that generally, the size of deviation tends to increase (=diplopia is worsened) in the direction of action of the affected extraocualr muscle
- Incomitant misalignment are frequently acquired (=not congenital) and cause diplopia when deviation is large enough (if deviation is small enough, fusional amplitudes may prevent from noticing double vision).
Created by: Orly Moshe-Lilie, OHSU SOM
Preceptor: William L. Hills, MD
- noninflammatory corneal disease that decrease visual acuity and can cause blurriness
Astigmatism (corneal defect)
- Most Common cause of monocular diplopa
- The eyes may produce less tears
- gradually with age, noticeable in patients around mid-40s, the eyes lose their ability to actively focus on objects at near
- Due to an imperfection in corneal curvature or distorted lens, leading to distorted or blurred images.
- Gradually with age, most notably and patients older than 65, the lens become less transparent (cloudy).
- Smoking, diabetes, steroids use, radiation treatment and/or trauma to the eye can increase the risk for cataract.
- Cataracts causes light to be scattered or can either partially or completely block it from reaching the retina.
Band keratopathy: calcification of the cornea due to hypercalcemia and appears as gray bands
Bollous keratopathy: permanent swelling of the cornea due to endothelial pathology
- it tends to worsen as we age until ~65 years of age.
- vision becomes blurred so that reading a book can become an annoying and difficult task to do.
- Tears may evaporate more extensively as patients may sleep with their eyes open, or when their oil ducts become clogged enough so that the tear film (usually consists of watery tears and a lipid layer) can no longer retard evaporation
- This may lead to blurred vision, and in cases of severe dry eyes, ghost images may appear as well (monocular polyopia),
especially at night
- epiretinal membrane
- choroidal folds
Drusen (leading to macular edema)
See bilateral monocular diplopia later in this guide
Does the patient experience monocular diplopia in both eyes?
This could be a
- Rarely, in cases of binocular monocular diplopia, the etiology may be neurologic; post-chiasmal, cerebral cortical disease. Look for signs of diplopia, polyopia, or palinopsia and order further testing to support your diagnosis
binocular monocular diplopia
Comitant misalignment is most common with congenital strabismus. Be aware that your patient may not complain of diplopia because of
, a cortical mechanism to eliminate diplopia by suppressing images in one eye, usually the non-dominant eye.
Patients can experience diplopia with comitant misalignment due to breakdown of pre-existing eso- or exophoria.
- A lack of coordination between the extraocular muscles leads to misalignment of the eye .
- Since the eyes bring the gaze of each eye to the same point in space, binocular vision and depth perception are hampered.
- Esodeviation is greater at distance (rather than at near) since eyes are not able to diverge sufficiently
- Consider bilateral sixth nerve palsies (eyes will cross due to lack of lateral rectus muscle function), myasthenia gravis, and congenital (decompensated) esophoria.
- A result of asymmetrical involvement of internuclear connections within the brainstem, leading to problems with vertical eye movements.
- This syndrome most commonly reveals incomitant misalignments
- Most often, incomitant deviations may be caused by
one of the extraocular muscles to relax results in resistance of the eye to movment in certain directions.
nerve paresis leading to underaction of one or more extraocular muscles).
another possible etiology (less common than the two above) is primary muscle overaction. Syndromes to consider:
Superior oblique myokymia
- look for vertical diplopia and vertical / torsional oscillopsia
- look for tonic deviation of the eye laterally due to spont. activity of CN VI
- note increased convergence tone leading to "pseudo CN VI palsy"
key clue to look for is miosis of the eye when patient is attempting
to abduct the eye
This is where things can get even trickier, but don't give up just yet, we will get through this! We've briefly covered nerve paresis, but we have not yet discussed the (many) syndromes that may arise from it.
To differentiate among the various syndrome, the most sensible thing to do next is to localize the pathological involvement. We will divide there syndromes by the anatomical localization of the paresis.
Ocular motor nerves
A significant extraocular muscle weakness can cause diplopia. Do you suspect a myopathy?
To confirm your suspicion of myopathy, you should
Look for signs of weakness in other cranial or skeletal muscles
Ask patient if he/she has been experiencing muscle weakness since early childhood
Ask patient if he/she knows of disorders causing muscle fatigue in his/hers family history
Depending on your finding, click on one of the following three options:
Note that myopathies caused by inflammatory etiology (some researches would argue) do not involve extraocular muscle weakness. In these cases, you should order other tests to figure out the cause for your patient diplopia.
muscle weakness evident in second
decade of life
drooping eye lids
limited eye motility
exercise intolerance / patient fatigues easily
abnormal heart rhythm
other signs: deafness, blindness, nausea, headaches
problems with breathing
problems with swallowing (Dysphagia) and eating
a group of neuromuscular diseases caused by damage to the mitochondria. prognosis ranges in severity from progressive weakness to death. on DDx: chronic progressive external ophthamoplegia (CPEO), Kearns-Sayre syndrome (CPEO plus pigmentary retinopathy noted), mitochondrial encephalopathy (MELAS, dementia noted), and myoclonus epilepsy.
a group of muscle diseases present at birth due to genetic defects in muscle development, non-progressive. Conduct appropriate testing to figure out which of the 4 major groups (based on genetic and morphological features) your patient's disorder is part of; myopathies with protein accumulation, with cores, with central nuclei, or with fiber size variation
progressive muscle weakness
frequent falls, waddling gait
difficulty getting up from seated/laying position
enlarged calf muscles
a group of genetic diseases involving unusual susceptibility of muscle fibers to damage. Onset of most syndromes is at young age, and primarily boys are affected. on DDx: Duchenne muscular dystrophy, Becker muscular dystrophy (progresses more slowly and milder than Duchenne), and more.
Does the patient's diplopia
vary throughout the day?
Is the patient's muscle weakness intermittent/irregular?
Neuromuscular junction dysfunction (in pre- or post-synaptic portions of the synapse) prevents the neurotransmitter acetylcholine from reaching and/or binding to its receptor, leading to an abnormal transmission of information. Look for:
fluctuation in muscle weakness
ptosis in more than 50% of patients
diurnal variation in diplopia
- don't confuse this with 3rd nerve palsy; MG typically spares the pupils and does NOT cause pain.
There are many neuromuscular junction disorders (such as Lambert-Eaton, Isaac's syndrome (aka NMT), Kennedy's disease and more). We will focus on (MG) since it is the most common.
an autoimmune disorder. The body (in ~80% cases) makes antibodies against the acetylcholine receptor leading to intermittent muscle weakness. Only 1/2 of the patients with MG will experience ocular symptoms. MG may affect and one eye muscle initially and therefore can resemble any of the eye movement problems previously discussed. Fatigability is key here - symptoms tend to worsen in the evening and with muscle usage, and will improve with rest. Other important signs are dysphagia, hoarseness, and dyspnea.
Lesion to one or more of the cranial nerves that innervate the extraocular muscles may lead to diplopia. Injury to a CN can occur at any of the following sites along its pathway:
superior orbital fissure
Cranial nerves palsies
It's time to go back and review your ocular exam notes. Based on your patient's ocular movements, do you suspect your patient's diplopia is due to an isolated cranial nerve palsy (use the image above to figure this out), or do you believe multiple cranial nerves are involved (in this case, patient's eye movements don't follow a simple pattern)?
Looks like it's an isolated nerve palsy
It seems more complicated, probably
a multiple CN palsies
Third nerve palsy
- May involve the superior, inferior & medial recti, as well as inferior oblique muscle. CNIII also innervates levator palpebrae superioris, and the autonomic muscles (sphincter pupillae and cilliary body).
- Signs: ptosis, mydriasis (and pupil will respond poorly to light), eye is deviated "down and out" due to unopposed action of lateral rectus and superior oblique muscles.
- Palsy most commonly due to microvacular injury (diabetes, hypertension) or secondary to an aneurysm, but may be due to neoplasm, inflammation or other vasculopathic etiologies (lupus, granulomatosis with polyangitis)
- mostly, with involvement of cavernous sinus, ophthalmoplegia will demonstrate a combination of third, fourth and sixth cranial nerve dysfunction. Looks for signs of orbital venous congestion or increased intraocular and/or venous pressure. A key involvement in the case would be of CN V (trigeminal nerve), and the patient may experience facial pain and numbness.
- with involvement of the superior orbital fissure, dysfunction of the optic nerve may be detected. Signs may include decrease in vision, relative afferent pupillary defect, and noticeable change in the optic disc, such as edema or atrophy.
Divisional third nerve palsy
- CNIII divides into superior and inferior divisions within the anterior cavernous
sinus. Superior rectus dysfunction and ptosis suggest involvement of the superior division.
Intra-axial pathology in either midbrain or pons , as well as cerebellar involvement can result in diplopia and ocular misalignment. Brainstem injury to cranial nerve nuclei are likely to involve palsies in other cranial nerves, such as trigeminal (CN V) and facial (CN VII) nerves, and in addition may present signs of autonomic dysfunction.
May be due to a stroke, hemorrhage, a mass or a tumor, trauma, hydrocephalus and increased intracranial pressure, as well as multiple sclerosis (inflammatory) or other neurodegenerative disorders.
Since DDx list may be getting pretty long, at this point you probably should be ordering a CT scan or an MRI to help localize where the lesion might be.
Internuclear ophthalmoplegia (INO)
- comprised of one-and-a-half syndrome with ipsilateral facial palsy
- a large enough Pontine lesion that involves both MLF and the ipsilateral CNVI nucleus, leading to deficits in ipsi adduction and paresis of
conjugate gaze (ipsi as well). Most commonly due to a stroke. Pontine neoplasm can be considered as well.
- lesion to the medial longitudinal fasciculus (MLF) which connects CN III & CN VI nuclei to allow for coordinated conjugate
horizontal eye movements may lead to slow ipsi adduction, abducting nystagmus and perhaps skew deviation (if vertical fibers ascending from vestibular nuclei are involved).
- loss of lateral rectus muscle action leads to unopposed action of medial rectus and noted esotropia
- signs: horizontal diplopia worsens with lateral gaze and at distance
- Most likely etiology of an isolated CN VI palsy in adults is ischemic mononeuropathy due to diabetes, hypertension, or arteriosclerosis. Other etiologies to rule out are congenital, neoplastic, vasculopathic, traumatic and/or secondary to elevated intracranial pressure compressing the nerve as it passes through Dorello's canal.
Sixth nerve palsy
- This is the most vulnerable CN, longest and thinnest.
- Signs: head tilt contralateral to lesion (to minimize diplopia), vertical diplopia, worsens at near and with down gaze, cover-uncover test revels hypertropia (worsens with contralateral gaze)
- Palsy may be due to trauma, congenital, or vasculopathic (diabetes, hypertension)
Fourth nerve palsy
Well, some patients may experience diplopia without any pathological finding. Their diplopia is said to be
. These patients may experience other somatic or neurological symptoms as well.
Many thanks to Dr. Hills for an outstanding dedication to neuro-ophthalmology as well as medical education!
Thanks to all the helpful neurology and ophthalmology residents at the neuro-opthalmology clinic, located at OHSU's Center of Health & Healing!
Figure 1: eye exam (http://meded.ucsd.edu/clinicalmed/eyes.htm)
Figure 2: pinhole testing (http://meded.ucsd.edu/clinicalmed/eyes.htm)
Figure 3: ghost images (http://www.lasikdisaster.com/ghosting.htm)
Figure 4: cardinal positions of gaze (http://www.tedmontgomery.com/the_eye/eyesmove.html)
Figure 5: types of tropias (http://intranet.tdmu.edu.ua/data/kafedra/internal/lor/classes_stud/en/Ophtalmology/Medical/4%20course/1.%20anatomic%20and%20topographic%20peculiarities%20of%20the%20visual%20organ.htm)
For Example, in right
unoccluded right eye moves outward when left eye is covered, because it is deviated medially
Figure 6: cover-uncover test (http://intranet.tdmu.edu.ua/data/kafedra/internal/lor/classes_stud/en/Ophtalmology/Medical/4%20course/1.%20anatomic%20and%20topographic%20peculiarities%20of%20the%20visual%20organ.htm)
Types of tropia:
Figure 7: corneal light reflex test (Binocular Diplopia: A Practical Approach. Rucker, Janet; Tomsak, Robert; MD, PhD. Neurologist. 11(2):98-110, March 2005.)
Figure 8: https://www2.aofoundation.org/wps/portal/!ut/p/c1/04_SB8K8xLLM9MSSzPy8xBz9CP0os3hng7BARydDRwN39yBTAyMvLwOLUA93I4MQE6B8JJK8haGFgYFnqKezn7GTn4GBgQkB3X4e-bmp-gW5EeUAmUJP3w!!/dl2/d1/L2dJQSEvUUt3QS9ZQnB3LzZfQzBWUUFCMUEwR0dSNTAySkowOFVIRzIwVDQ!/?soloState=true&contentUrl=/srg/popup/additional_material/92/X70-examination.jsp
Figure 9: http://optical-casper-wyoming.com/vision/224/glaucoma-testing
Figure 10: actions of extraocular muscles and cranial nerves (http://www.turner-white.com/memberfile.php?PubCode=hp_mar04_diplopia.pdf)
Figure 12: forth nerve palsy (http://telemedicine.orbis.org/bins/content_page.asp?cid=1-2193-2360)
Figure 13: sixth nerve palsy (http://telemedicine.orbis.org/bins/content_page.asp?cid=1-2193-2360)
Figure 11: third nerve palsy (http://www.nanosweb.org/i4a/pages/index.cfm?pageID=3288 )
HOW TO USE THIS GUIDE:
press on the right arrow to move forward
when asked a question, use the mouse to press on a desired answer
when you get to a "diagnosis" screen, you are done! you can now press exit to leave the prezi.
Not it ah?
1. Binocular Diplopia: A Practical Approach. Rucker, Janet; Tomsak, Robert L. Neurologist. 11(2):98-110, March 2000.
2. Goldberg, Charlie, and Jan Thompson. A Practical Guide To Clinical Medicine. The Regents Of The University Of California, Sept. 2004.
3. Liesegang, Thomas J., Thomas A. Deutsch, and M G. Grand. 2015-16 Basic and Clinical Science Course: Section 6: Pediatric Ophthalmology and Strabismus. San Francisco, Calif: American Academy of Ophthalmology, 2015.
4. North K. What's new in congenital myopathies?. Neuromuscul Disord. Jun 2008;18(6):433-42
5. Pelak, Victoria S. "Evaluation of Diplopia: an Anatomic and Systematic Approach." Hospital Physician. Www.turner-white.com, Mar. 2004.
6. Spector RH. Diplopia. In: Walker HK, Hall WD, Hurst JW, editors. Clinical Methods: The History, Physical, and Laboratory Examinations. 3rd edition. Boston: Butterworths; 1990. Chapter 113.
7. UpToDate. Wolters Kluwer Health, n.d. Web. <http://www.uptodate.com/home>.
8. Von Noorden, Gunter K., and Emilio C. Campos. "Paralytic Strabismus." Binocular Vision and Ocular Motility:Theory and Managment of Strabismus. Mosby, 2001. 414+. Orbis Telemedicine.