History and examinations

1. Evaluation Of A Patient With
Diplopia
Priyanka Bharti
01-09-2014

2. Introduction
 Diplopia is the subjective complaint of seeing 2 images instead of one and is
often referred to as double-vision in lay parlance
 The term diplopia is derived from 2 Greek words: diplous, meaning double, and
ops, meaning eye
 One of the common presenting symptom to ophthalmologists
 Breakdown in the fusional capacity of the binocular system

3. Normal binocular single vision (BSV)
Involves simultaneous use of both eyes with bifoveal fixation, so that each eye
contributes to a common single perception of the object of regard
 Conditions necessary for normal BSV

4. Confusion

5. Pathological diplopia

6. Suppression
 Involves active inhibition by the visual cortex of the image from one eye when both
eyes are open
 Stimuli include diplopia, confusion and a blurred image from one eye resulting
from astigmatism/anisometropia

7. EVALUATION

8. History
 single most useful evaluation in treating patients with diplopia
 Patient typically presents with a history of double vision, where single objects
appear as double
 Specific inquiry should be made
 Progression
 Variability with head posture or gaze direction
 Previous similar episodes
 Spontaneous resolution

9. History
 Three important symptoms should be elicited:
 Does covering either eye make the diplopia disappear?
Monocular vs Binocular diplopia
 Is the double vision the same in all directions of gaze or does it vary with
gaze directions?
Comitant vs Incomitant diplopia
 Is the double vision horizontal, vertical, or oblique?

10.  History of
 Diabetes
 Vascular disease
 Hypertension
 Headache
 Muscle fatigue or weakness
 Medications and drugs being used
 Past medical and surgical history
 History of trauma

11. Physical Examination
 2 specific aspects
 Physiological
Sensory function
Motor function
 Anatomical

12. Sensory Component
 Monocular or Binocular
 Does covering each eye in turn alleviate the problem, or does the diplopia
persist despite covering the "good" opposite eye?

13. Monocular Diplopia
 Results from abnormalities of refractive media
 Typically improves with a pinhole
 No need for neurological work-up
 Causes:
 Refractive error
 Corneal irregularities
 Keratoconus
 Iris injury/ defects
 Multiple pupils

14.  Cataract
 Retinal pathology (less common)
 Maculopathy with retinal distortion by fluid, haemorrhage, or fibrosis
 Epiretinal membrane, choroidal folds

15. Binocular Diplopia
 Results from misalignment of visual axis
 Relieves by closing either eye

16. Causes:

17.  Evaluate magnitude of difference in spectacle correction required for each eye
 Marked differences between the eyes (anisometropia) will frequently produce disabling
diplopia, especially in extremes of gaze
 Determine the visual acuity in each eye separately, with and without spectacle
correction and with a pinhole
 Does a pinhole improve the visual acuity, or does it improve monocular diplopia?
 Major improvement in visual acuity with a pinhole suggests intraocular or refractive
problems

18.  Is the diplopia the same in the 9 cardinal directions of gaze?
 Tests weaknesses of individual muscles
 Evaluate how tilting the head to the left or to the right alters the diplopia
 increase when the head is tilted to same side, if vertical diplopia is
present due to weakness of the superior oblique muscle (innervated by
the fourth cranial nerve)
 Evaluate the integrity of the other cranial nerves (eg, facial sensation, facial
muscle movements)

19. Motor component
 Movement of the eyes should be assessed individually
(ductions), together (versions) and in all positions of gaze
 Determine if diplopia worsens when the muscles are fatigued
(eg, after strenuous use, at the end of the day)
 Myasthenia gravis
 Determine that other ocular motor functions are normal
 Is the lid in a normal position?
 Is the pupil response normal and symmetric with the other
pupil?

20.  Anatomical evaluation
 Inspection
Head position
Eyes
Eyelids
Orbits
Facial asymmetry or displacement
Inflammation or vascular congestion
 Palpation
Orbital rim
Soft tissues

21.  Percussion
orbital rim to disclose focal tenderness from sinus inflammation
 Auscultation
Bruit in carotid cavernous fistula

22. Comitant and incomitant deviations
 Comitant misalignment, characteristically seen in patients with
congenital or early-onset strabismus
 Do not report diplopia because of suppression
 Incomitant deviation is most frequently acquired
 Patients report diplopia

23. Localization of lesion

24. Supranuclear causes of diplopia
 Includes any afferent input to the ocular motor nerves (CNs Ill, IV, VI)
 Most important supranudear pathways are the Corticobulbar pathways
 Typically, disruption of supranuclear pathways symmetrically limits the movements
of both eyes- No diplopia
 Supranuclear ocular motor lesions that produce Strabismus and Diplopia
 Alternating skew deviation
 Convergence insufficiency or spasm
 Divergence insufficiency
 Ocular tilt reaction
 Skew deviation
 Thalamic esodeviation

25.  Skew deviation
 Is an acquired vertical misalignment of the eyes resulting from asymmetric disruption of
supranuclear input from the otolithic organs
 Sense linear motion and static tilt of the head via gravity and transmit information to the
vertically acting ocular motoneurons
 Central causes of skew deviation are more common and can occur anywhere within the
posterior fossa (brainstem and cerebellum)
 Alternating skew deviation on lateral gaze usually manifests as hypertropia of the
abducting eye
 right hypertropia on right gaze that switches when gaze is directed to the opposite side,
becomes left hypertropia on left gaze

26.  Ocular tilt reaction
 Is a combination of a head tilt, skew deviation, and cyclotorsional abnormalities of both
 Develops because of loss of otolithic input to the interstitial nucleus of Cajal (INC) from a
central lesion
 Can alter the sense of true vertical, drives head and rotates the eyes toward the same side
 Should be differentiated from normal response of head tilt as well as from fourth nerve

27.  Thalamic esodeviation
 Acquired horizontal strabismus
 Seen in patients with lesions near the junction of diencephalon and midbrain
Thalamic haemorrhage is most common
 Esodeviation may develop insidiously or acutely
 Expanding tumors presents with progressive esodeviation

28. Nuclear causes of diplopia
 Third nerve nucleus- nuclear complex
 Contains:
 Subnuclei for superior, inferior, medial recti and inferior oblique muscles
 Single subnucleus- central caudal for Levator muscle
 Paired subnuclei- Edinger Westphall nuclei for pupillary constrictor muscles
 Lesions uncommon
 Can affect or spare both upper eyelids and may bilaterally affect superior rectus muscle

29.  Fourth nerve nucleus
 Lesions are rare
 Sixth nerve nucleus
 Causes horizontal gaze palsy
 Isolated abduction paresis in one eye- not seen
 Patient may not experience diplopia

30. Internuclear causes of diplopia
 Includes one that disrupts medial longitudinal fasciculus (MLF)
 Produces Internuclear Ophthalmoplegia (INO)
 Unilateral INO
 Slowed adducting saccadic velocity in one eye
 Adducting nystagmus of fellow eye
 Convergence may be spared or disrupted
 Named for the side of limited adduction

31.  Bilateral INO
 Bilateral adduction lag
 Bilateral abducting nystagmus
 large-angle exodeviation may occur- "wall-eyed" bilateral lNO, or WEBlNO, syndrome
 Caused by a midbrain lesion near the third nerve nuclei
 Causes of INO
 Demyelination
 Stroke

32. Infranuclear causes of diplopia
 Involves lesions of the nerve distal to its nucleus but within the brainstem
 Can damage either third, fourth nerve or sixth nerve
 Third nerve involvement
 Benedikt syndrome
 Weber syndrome
 Nothnagel syndrome
 Claude syndrome
 Fourth nerve involvement- uncommon

33.  Sixth cranial nerve involvement
 Foville syndrome
 Millard-Gubler syndrome
 May also injure seventh cranial nerve

34.  Ischemic cranial nerve palsies
 Involves Sub-arachnoid segment of ocular motor nerves
Extends from brainstem to cavernous sinus
 Typically occur in isolation
 Pain may or may not be present
 Almost always improves and diplopia usually resolves within 3 months
 Risk factors
Diabetes mellitus
Hypertension
Elevated serum lipid levels

35. Third nerve palsy
 Results in dysfunction of the superior, inferior, and medial recti; inferior oblique; and
levator palpebrae superioris muscle
 And pupillary sphincter and ciliary muscles
 Complete third nerve palsy
 Complete ptosis, with eye positioned downward and outward and unable to
adduct, infraduct, or supraduct, and a dilated pupil that responds poorly to light
 Partial third nerve palsy
 Are more common and present with variable limitation of upward, downward, or
adducting movements; ptosis; or pupillary dysfunction

36.  Pupil- involving third nerve palsy
 'Surgical’ lesions such as aneurysms, trauma
 Pupil- sparing third nerve palsy
 ‘Medical' lesions such as hypertension and diabetes

37. Fourth nerve palsy
 Typically causes diplopia that worsens in downgaze
 Cover-uncover or Maddox rod test- to demonstrate hypertropia that
 Worsens on contralateral downgaze
 Ipsilateral head tilting usually increases the vertical strabismus
 Patients typically tilt their head to the opposite side to avoid diplopia
 long-standing nature of the head tilt can often be confirmed by reviewing old
photographs

38.  Patients older than 50 years-
 Isolated fourth nerve palsy is typically caused by microvascular ischemic
disease, typically resolves within 3 months
 Full medical evaluation
 Lack of recovery after 3 months- neuroimaging needed

39. Sixth nerve palsy
 Most common cause of an isolated ocular motor palsy
 Typically presents as horizontal diplopia that worsens on ipsilateral gaze
 Abduction deficit, typically associated with an esodeviation that increases with gaze
to the affected side
 Isolated sixth nerve palsies in adults over the age of 50 are usually ischemic
 Ocular motility in these cases always improves and typically resolves within 3
months

40.  Cranial MRI is mandatory if obvious improvement has not occurred after 3 months
 Younger individuals- appropriate neuroimaging
 If negative
 Neuromuscular junction disease
 Thyroid eye disease with medial rectus involvement

41. Carotid cavernous sinus fistula
 Abnormal connections between the carotid artery and the cavernous sinus
 High arterial pressure into the normally low-pressure venous contents of the cavernous
sinus
 Reverse blood flow within the superior ophthalmic vein and produce venous congestion
within the orbit
 Trauma is responsible for 75% of cases

42.  Clinically
 Elevated intraocular pressure
 Proptosis (pulsatile)
 Conjunctival chemosis
 Severe epibulbar injection
 Ptosis (3rd nerve involvement)
 Anterior segment ischemia- corneal edema, aqueous cells and flare
 Ophthalmoplegia – 6th nerve frequently affected
 Angiography- determine the location and configuration of fistula

43. Neuromuscular Junction Causes of Diplopia
 Myasthenia gravis - produces variable diplopia and ptosis with any pattern of
pupil-sparing, painless ocular misalignment

44. Myopathic, Restrictive, and Orbital Causes
of Diplopia
 Thyroid Eye Disease
 Most common cause of restrictive strabismus in adults
 Any of the extraocular muscles may be involved
 Inferior and medial recti are most commonly affected

45.  Post-traumatic restriction
 Blowout fractures of the orbit often develop diplopia
 Most commonly involves fracture of the inferior orbital floor with entrapment of
the inferior rectus muscle
 Orbital myositis
 Idiopathic inflammation of one or more extraocular muscles typically produces
ophthalmoplegia and pain
 Conjunctival hyperemia, chemosis, and sometimes proptosis
 CT / MRI- enlargement of one or more of the extraocular muscles, with
involvement of tendon

46. Tests for diplopia

47. Differentiating Paretic From Restrictive Etiologies
Forced duction test

48.  Positive result:
 Difficulty or inability to move the globe indicates a restrictive problem such as
thyroid myopathy or muscle entrapment in an orbital floor fracture
 Negative result:
 No resistance will be encountered in either eye if the muscle is paretic as a
result of a neurological lesion

49. The differential intraocular pressure test
 Positive result:
An increase of 6 mmHg or more denotes resistance transmitted to the
globe by muscle restriction- Braley sign
 Negative result:
 an increase of <6 mmHg suggests a neurological lesion
Saccadic eye movements
 Reduced in velocity- neurological lesions
 Normal saccadic velocity- restrictive defects

50. Measurement of deviation
 Hirschberg test

51.  Krimsky and prism reflection tests

52.  Cover- uncover test
Two parts:
Cover test

53.  Uncover test

54.  Alternate cover test
 Prism cover test

55. Maddox rod test

56. Double Maddox rod test

58. Maddox wing test

59. Motility tests
 Ocular movements
Versions
Ductions
 Near point of convergence
Normal NPC- nearer than 10 cm
 Near point of accommodation
At 20 years- 8 cm
By 50years- 46 cm

60. Diplopia Chart

61. Electronic Hess test

64. Worth four dot test

65. Bagolini striated glasses

66. Park three-step test
First step
Find the side of hypertropia in primary position

67.  Second step
Determine if the hypertropia is greater on left or right gaze
In 4th nerve palsy the deviation is Worse On Opposite Gaze – WOOG

68.  Third step (Beilschowsky test)
Determine if the hypertropia is greater in right or left head
tilt
In 4th nerve palsy the deviation is Better On Opposite Tilt – BOOT

69.  Tensilon test
 Neostigmine test
 Amsler grid test

70. Imaging studies
 CT scan or MRI of the skull and orbits to rule out intracranial masses or other
pathologic processes, such as:
 A blow-out fracture requires imaging of the orbital floor
 Enlarged muscles from thyroid ophthalmopathy help explain a vertical diplopia
 Tumor of orbit
 Tumor along cranial nerve pathway

71.  Carotid cavernous fistula: Angiography may be required
 Aneurysm of intracranial carotid artery or posterior communicating artery:
Cerebral angiogram
 Disease of sinuses (eg, infection, tumor) or bony disorders can account for
displacement of the eye

72.  Traditional guidelines for imaging patients with new-onset diplopia
 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

73. Medical care
 Patching one eye
 Stick-on occlusive lenses can be applied to glasses
 Fresnel prisms:
 can be stuck to glasses
 severely blur the image from one eye and function like occlusive lens
 Myasthenia gravis: Anticholinergic agents
 Monocular diplopia or polyplopia associated with corneal astigmatism
 rigid gas-permeable lenses may be beneficial

74. Surgical care
 Strabismus surgery is occasionally necessary
 Recession/ Resection procedure
 Transposition surgery (Hummelsheim surgery):
 With permanent paralysis of the lateral rectus muscle, overcoming the unopposed tone of
the medial rectus muscle is possible by splitting the superior and inferior recti muscles and
by reinserting the lateral half of each muscle at the lateral rectus insertion
 Superior oblique muscle paralysis:
 Weakening the yoke muscle of the opposite eye (superior rectus muscle) as well as the
direct antagonist (inferior oblique muscle) in the same eye, together with a shortening of the
affected muscle, to minimize the deviation

75.  Chemodenervation:
 helps prevent the contracture in eyes with extraocular muscle paresis
 Multiple injections over several months of botulinum toxin into the medial rectus muscle
reduce contracture due to a weak lateral rectus from a sixth nerve paralysis
 Opposing un-injected muscle may develop a degree of permanent shortening and
contracture

76. Summary

78. Bibliography
 Theory & Management Of Strabismus, Von Noorden & Emilio
Campos, 6th edition
 Myron Yanoff & Jay Duker. Ophthalmology,3rd edition, 2008
 American Academy of Ophthalmology. Neuro-ophthalmology,
2013-14.
 Jack J Kanski.Clinical Ophthalmology,7th edition, 2012
 Alison Finlay, The differential diagnosis of diplopia, October 6, 2000
 Victoria S. Pelak, Evaluation of diplopia: An anatomic and systemic
approach, March 2004
 Jitander Dudee, Diplopia, emedicine.Medscape. com, September
2013

79. THANK YOU