The patient with diplopia

2.  Diplopia is the most common symptom for which the
patient needs urgent ophthalmic care
 The two most common mechanisms for diplopia are
ocular misalignment and ophthalmic aberrations

3. What does the faculty of BSV require?
 Perfect ( or near perfect ) alignment of the visual axes
simultaneously on the object of regard
 Perfect ( or near perfect ) retinal correspondence
 Perfect central ( or paracentral ) fusional capability.
 Perfect ( or near perfect ) alignment of the retinal
receptors
 Perfect ( or near perfect ) optics to allow only one
image to be formed on the retina and the same single
image to be formed on the other

4. What is Diplopia ?
 It is when more than one image ( two ) of the object of
regard are seen simultaneously
 Physiological
 Pathological

5. Monocular vs Binocular Diplopia
Key question
Is the double vision present even on monocular eye
closure?

6. Monocular diplopia
 More than one image of the object of regard is
formed in the retinae of one or both eyes…..
 Irregular astigmatism ( corneal scars, haze, corneal
distortion)
 Subluxated clear lenses
 Poorly fitting contact lenses
 Early cataract
 Macular disorders – edema, CNVM etc

7. Binocular Diplopia
The eyes lose their simultaneous alignment with the object of regard
in one or more directions of gaze
Key clues
 Anomalous Head Position
 Vision Blurry in one gaze position, better in another
 Obviously misaligned eyes,
 proptosis
 Presence of partial ptosis
 Nystagmus

8. History:
A detailed history will be required to enquire about the
patient current status:
 i.e. Either the diplopia eliminates after closing one eye
(binocular diplopia)
 The diplopia remains after closing one eye (monocular
diplopia)
 Monocular diplopia must not be confused with
metamorphopsia secondary to maculopathy

9. Questions about the nature of the
particular condition:
Key questions
Is the diplopia more for distance or near?
Is the diplopia predominantly horizontal or vertical?
In which direction of gaze are the images maximally
separated?
To which eye does the “outer” image belong?
Is there a predominant tilt?
In which position of gaze does the tilt increase
maximally?

10. Physical examination:
 Movement of both eyes
 External examination for proptosis /ptosis, redness
 Ductions
 Versions
 Assessment of eye movements in all position of gazes
 Comparison between near and far fixation

11. Identifying muscle/s involved
 AHP
 Predominant face turn – horizontal recti
 Predominant chin elev/dep – vertical recti, pattern
strabismus
 Predominant tilt – Obliques

12. Purpose:
 Wether the misalignment is comitant or Incomitant
 Comitant strabismus are congenital in nature while
Incomitant gives a picture of acquired abnormality /
disorder

13. Initial Assessment:
Gross examination
 Alternating cover test in all 9 position of gazes
 Maddox rod test
 Double Maddox rod test (torsional misalignment)
 Red/Green goggles
 Prism cover test

14. Differentiating Paretic From
Restrictive Etiologies of Diplopia

15. Restrictive causes:
 Proptosis
 Enophthalmos
 Orbital trauma
 Thyroid ophthalmopathy
 Post surgery

16. Differential diagnosis:
Restrictive disorder Paretic disorder
Saccadic movements are normal Saccadic movements are slower
Mechanical restriction on FDT FDT is normal
Increase IOP at eccentric fixation No change in IOP at any gaze
Duction =Version Duction more than version

17. Causes of Diplopia:
 Supranuclear
 Nuclear
 Internuclear
 Infranuclear
 Myopathic
 Restrictive
 Orbital

18. Supranuclear causes:
 It includes any afferent input to the ocular motor
nerves
 It controls vestibular input to adjust the relative
position of the eyes within the head
 It allow accurate calculation of saccadic velocity and
direction
 Most supranuclear disorders affect both eyes equally
and do not cause diplopia

19. Continue:
It involves:
1. Skew Deviation
2. Thalamic esodeviation
3. Vergence Dysfunction

20. Skew Deviation
 Skew deviation is an acquired vertical misalignment of
the eyes resulting from asymmetric disruption of
supranuclear input from the otolithic organs (the
utricle and saccule of the inner ear, both of which
contain otoliths, which are tiny calcium carbonate
crystals).
 These organs sense linear motion and static head tilt
via gravity and transmit information to the vertically
acting ocular motoneurons, as well as to the interstitial
nucleus of Cajal (INC), all of which are in the
midbrain.

21. Skew Deviation
 An alternating skew deviation on lateral gaze usually
manifests as hypertropia of the abducting eye (ie, right
hypertropia on right gaze) that switches when gaze is
directed to the opposite side (ie, becoming left
hypertropia on left gaze).
 Responsible lesions are located in the cerebellum,
cervicomedullary junction, or dorsal midbrain.
 This disorder must be distinguished from bilateral
fourth nerve palsies,

22. Thalamic Esodeviation
 Thalamic esodeviation is an acquired horizontal
strabismus that may be observed in patients with
lesions near the junction of the diencephalon and
midbrain, most often thalamic hemorrhage.
 The esodeviation may develop insidiously or acutely
and, in the case of expanding tumors, may be
progressive.
 It is especially important to consider the possibility of
a central nervous system lesion in children being
evaluated for strabismus surgery.

23. Vergence Disorders
 Although vergence disorders are common, their
diagnosis can be challenging because convergence
depends heavily on patient effort.
 These disorders most commonly are classified as
convergence insufficiency, convergence spasm, or
divergence insufficiency.
 Unlike other supranuclear disorders, vergence
disorders usually result in diplopic symptoms.

24. Convergence paralysis
 Convergence paralysis may be secondary to various
organic processes such as encephalitis, diphtheria,
multiple sclerosis and occlusive vascular disease
involving the rostral midbrain
 Patients usually present with exotropia and diplopia
for near fixation.
 They will have normal adduction of either eye
 The deviation can be said to be concomitant across the
field of gaze.

25. Common supra nuclear
disorders

26. INO
 INO is a lesion of the Medial longitudinal fascicules (MLF)
resulting in a palsy of the MR muscle and a dissociated
gaze evoked nystagmus in the abducting eye .

27. INO
 INO may be unilateral or bilateral.
 Aetiology:
 Multiple Sclerosis in younger patients.
 Brainstem tumor
 Trauma etc.

28. INO
 For right lateral gaze:
 The PPRF signals the right CN VI (Abducens) nucleus
to turn the right eye outwards
 It also signals the left CN III (Occulomotor) nucleus,
via the left MLF to simultaneously turn the left eye
inwards
 Thus, a lesion of the left MLF, prevents the impulse
from reaching the left medial rectus
 The right eye abducts, left eye does not adduct
 And nystagmus is seen in the right eye

29. “LOOK TO THE RIGHT!!!”
III III
VI VI
PPRF PPRF
RIGHT LEFT
INTERNUCLEAR OPHTHALMOPLEGIA

30. Left internuclear ophthalmoplegia

31. INO
Symptoms and Signs:
 Painless onset of visual disturbance
 Diplopia
 usually not in the primary position
 horizontal diplopia in the lateral gaze
 Convergence usually normal

32. INO Clinical and diagnostic features:
 The principle feature is abducting nystamus.
 Limitation of the MR of the affected eye in
adduction during conjugate movement.
 There is usually an exophoria or exotropia in the
primary position.
 Which increases in the direction of affected MR in
horizontal gaze movement.

33. Defective left adduction Normal left gaze
Intact convergence
INO involving left MLF

34. INO
 Deferential diagnosing
 Myasthenia gravis
 Medial wall blow out fracture
 Duane's retraction syndrome
 MR palsy

35. Bilateral INO
 Lesions that affect the interneurones running in the MLF
from both sixth nerve nuclei result in bilateral INO
 With loss of adduction of each eye on attempted
contralateral version
 Abducting nystagmus is present in each eye on lateral
gaze
 Provided the lesion is limited to the interneurones,
convergence is retained.
 Bilateral INO is often asymmetric

36. INO
 Management
 Neurological investigation.
 Identify and treat the underlying cause.
 Monitor the condition.

37. One and a half eye syndrome

38.  Description:
 One-and-a-half syndrome consists of a unilateral
internuclear ophthalmoplegia and a contralateral
horizontal gaze palsy.
 Causes include demyelination, vascular, tumour and
inflammation

39. One and a half eye syndrome
 lesion involving MLF and ipsilateral 6-nerve
nucleus and PPRF
 Ipsilateral gaze palsy
 Defective ipsilateral adduction
 Normal contralateral abduction with ataxic
nystagmus

40. Features
 The only remaining horizontal movement is abduction by
the unaffected lateral rectus, which is associated with the
typical abducting nystagmus
 When the patient attempts to fixate with this eye in the
primary position, the nystagmus will reduce or cease.
 There is therefore a palsy of conjugate gaze on one side
and an INO on looking to the other side

41. Defective left gaze
Defective left side adduction with
normal right side abduction
Left side 1 ½ Syndrome

42. Nuclear palsies

44. Nuclear Portion
 Anatomy
 Nucleus lies at the level of superior
colliculus in the periaqueductal gray
mater of midbrain.
 It is a complex of subnuclei
 Levator muscles show projection form
single midline subnucleus
 Superior rectus subnucleus has a
crossed projection

 Edinger-westphal nucleus gives
parasymathetic input to ipsilateral
pupil

45. Nuclear Portion
 Causes
 Infraction
 Hemorrhage
 Neoplasia
 Abcess

46. NUCLEAR PORTION
 Clinical features
 Symptoms of iii cn dysfunction
 Diplopia mixed horizontal and vertical,
binocular)
 Ptosis of varying degrees)
 Glare due to pupil dilatation
 In nuclear lesions
 Ptosis should be bilateral or absent
 Sr muscle may be
 Involved contralaterally and spared ipsilaterally
 But commonly affected bilaterally

47. FASCICULUS
 Anatomy
 Passes through the red nucleus, and exits the brain stem
through the medical portion of each cerebral peduncle
 Causes
 Infraction
 Hemorrhage
 Neoplasia

48. FASCICULUS:
 CLINICAL FEATURE
III CN palsy may be associated with
 Cerebellar ataxia (Nothnagel
syndrome)
 Ipsilateral flapping hand tremor (rubral tremor)
and contralateral sensory loss (Benedikt syndrome)
 Contralateral hemiplegia or hemiparesis (Weber syndrome)

49. SUBARACNOID PORTION:
 ANATOMY
 Passes between posterior cerebral and superior cerebellar
arteries
 Parallels the tentorial edge and the posterior communicating
artery
 Pupillomotor fibers are located superficially and derive their
blood supply from pial blood vessels while the main trunk is
supplied by vasanervosum

50. SUBARACNOID PORTION:
 CAUSES
 Aneurysm
(of post communicating artery) (most common cause)
 Infectious meningitis
Bacterial, fungal/parasitic, viral
 Granulomatous inflammation
(sarcoidosis, lymphomatoid granulomatosis, Wegener
 Meningeal infiltration
(carcinomatous, lymphomatous or leukemic)
 Head trauma
resulting in temporal lobe herniation.

51. SUBARACNOID PORTION:
 CLINICAL FEATURE
 III CN palsy may be associated with
 Signs and symptoms of subaracnoid hemorrhage
 like severe headache, stiff neck and loss of consciousness.
(bleeding from berry aneurysm)
 Sign and symptoms of meningitis
 (basal meningeal infection)
 Progressive involvement of other cranial nerves
 (inflammatory and neoplastic infiltration)
 Early pupil involvement in cases of compressive lesions and
relative sparing in cases of microangiopathies.

52. INTRACAVEROUS PORTION:
 ANATOMY
 Runs dorsal to IV CN in the lateral wall of cavernous sinus
 Causes
 Tumor
 pituitary adenoma, meningioma, craniopharyngiona, metastatic carcinoma
 Gaint intracavernous aneurysm
 Carotid artery-cavernous sinus fistula
 Cavernous sinus thrombosis
 Ischemia
 from microvascular disease in vasa nervosa
 Inflammatory
 Tolosa-Hunt syndrome (Idiopathic or granulomatous inflammation)

53. INTRACAVEROUS PORTION:
 CLINICAL FEATURES
 III CN palsy is often accompanied by other cranial nerve
palsies in the vicinity like IV, VI & V cranial nerve.
 An important exception is nerve infraction associated with
microvascular disease.
 Significant pupillary involvement may occur in 10% of cases.

54. ORBITAL PORTION:
 ANATOMY
 Enters the orbit through superior orbital fissure and
divides into :
 Superior branch
 SR & L.P. Superiors muscles
 Inferior branch
 IR, MR, IO muscles
 Parasympathetic fibers to the ciliary ganglion

55. ORBITAL PORTION
 CAUSES
 Trauma
 Inflammatory
 orbital inflammatory pseudotumor
 Orbital myositis
 Endocrine
 thyroid orbitopathy
 Tumors
 hemangioma, lymphangioma, meningioma
 CLINICAL FEATURES
 III CN palsy may be associated with inflammatory signs e.g. lid
swelling, conjunctival injection and chemosis
 IV & VI CN may be involved.

56.  posterior communicating artery
aneurysm
 and third cranial nerve palsy

57.  . Complete right third-nerve palsy
resulting in hypotropia,
exotropia, and pupillary
mydriasis. The ptotic eyelid is
manually elevated.

58.  Right third nerve palsy
 showing limitation of elevation
 Same patient as in Figure 2
showing
 limitation of adduction
 Same patient showing limitation
of depression

59. Table 1. Acquired lesions of the oculomot or nerve
Anatomic Localization Cause Associated Symptoms Diagnostic Evaluation Therapy
Nuclear Infarction, mass, infection,
inflammation,
compression
Bilateral ptosis and paresis
of the contralateral
superior rectus; lid
function may be spared
MR imaging Stroke resuscitation,
antiplatelet therapy,
coumadin
Wernicke-Korsakoff
syndrome
Ataxia, abducens palsy,
nystagmus, altered
mentation
Stroke workup* Thiamine
Fascicular Infarction, mass, infection,
inflammation,
compression
Contralateral hemiparesis
or tremor; pupil may be
spared
MR imaging Stroke resuscitation,
antiplatelet therapy,
coumadin
Demyelination Stroke workup* Interferon-β1, Copaxone
Subarachnoid space Aneurysm Headache, stiff neck,
pupil-involved, aberrant
regeneration
MR imaging, MR
angiography, angiogram
Interventional radiology,
surgical clipping
Vasculopathic Pupil generally spared, no
aberrant regeneration
Check BP, serum glucose,
ESR, RPR, cholesterol
Spontaneous recovery
Meningitis Headache, cranial nerve
involvement,
meningismus, fever
LP, MR imaging Antibiotics, steroids,
supportive care
Miller-Fisher syndrome Areflexia, ataxia, previous
viral illness
NCS/EMG, LP Plasmapheresis, IVIG
Migraine Headache, positive family
history, pediatric age
group
MR imaging on initial
event
Rocovery generally good
Uncal herniation Early pupil involvement,
altered mentation,
ipsilateral hemiparesis
Emergent CT scan Emergent
hyperventilation, osmolar
therapy

60. Uncal herniation Early pupil involvement,
altered mentation,
ipsilateral hemiparesis
Emergent CT scan Emergent
hyperventilation, osmolar
therapy
Cavernous sinus Neoplasm CSS, pain, sensory
changes, potential
sympathetic involvement
MR imaging Surgery, radiation therapy,
possible hormonal
modulation
Fistula Exophthalmos, bruit,
chemosis
MR imaging, angiography Surgical ligation
interventional radiology
Thrombosis Previous infection/trauma,
pain, exophthalmos,
chemosis
MR imaging, angiography Antibiotics, thrombolysis
Tolosa-Hunt syndrome Pain, pupil may be spared MR imaging, evaluate for
collagen-vascular disease
Steroids
Apoplexy Headache, bilateral
ophthalmoplegia, altered
mentation, vision loss
MR imaging, electrolyte
and hormonal workup
Surgical decompression,
electrolyte maintenance
Superior orbital fissure Neoplasm Superior division
involvement (ptosis and
superior rectus paresis)
MR imaging Surgery, radiation therapy,
possible hormonal
modulation
Neuromuscular junction Myasthenia gravis No pupil involvement,
frequent fluctuation,
ptosis, ophthalmoparesis,
orbicularis oculi
weakness, dysarthria
Tensilon test,
electrodiagnostics,
antiacetylcholine receptor
antibody titer
Immunosuppression,
mestinon
* B

61. TROCHLEAR NERVE: (IV CN)
 Underlying etiology of the congenital IV CN palsy remains
obscure
 Acquired IV CN palsy may be
 Idiopathic
 Traumatic
 Microvasculopathy secondary to diabetes, atherosclerosis or
hypertension
 Thyroid ophthalmopathy
 Myasthenia gravis
 Iatrogenic injury
 Tumors (pinealoma, teratoma)
 Aneurysms

62. IV CN PALSY:
 CLINICAL FEATURE
 Patient reports vertical, torsional or oblique diplopia. It is
worse on downgaze & gaze away from the side of affected
muscle
 Pt. often adopts characteristic head tilt away from affected
side
 Bielschowsky head tilt test is extremely useful
 Double maddox rod test can be used to measure
excyclotorsion
 3o – 10o excyclotorsion
 unilateral IV CN palsy
 > 100 excyclotorsion
 Bilateral IV CN palsy

63.  A 2-year-old girl with
compensatory left head tilt due to
congenital right superior oblique
palsy.
 Patient with traumatic bilateral
superior oblique palsy; note right
hypertropia on right head tilt and
left hypertropia on left head tilt.

64. IV CN NUCLEUS
 Lies in periaqueductal gray mater
in the midbrain
 Nuclear lesions may involve the
descending sympathetic fibers
leading to contralateral IV CN
palsy with ipsilateral Horner
syndrome
 SUBARACHNOID COURSE
 From the dorsal brainstem it runs
just below the tentorial edge and
may be damaged by
neurosurgical procedure and
head trauma.

65. Table 2. Acquired lesions of the trochlear nerve
Anatomic Localization Cause Associated Symptoms Diagnostic Evaluation Therapy
Nuclear Infarction Internuclear
ophthalmoplegia, Horner's
syndrome, afferent
pupillary defect
MR imaging, stroke
workup*
Stroke resuscitation,
antiplatelet therapy,
coumadin
Truma, tumor, infection,
inflammation
As above MR imaging, LP Depends on cause
Fascicular Infarction Internuclear
ophthalmoplegia, Horner's
syndrome, afferent
pupillary defect
MR imaging, stroke
workup*
Stroke resuscitation,
antiplatelet therapy,
coumadin
Trauma, trmor, infection,
inflammation
As above MR imaging, LP Depends on cause
Demyelination Isolated or with midbrain
signs above
MR imaging Interferor-β1, Copaxone
Subarachnoid space Trauma, hydrocephalus May be bilateral Neuroimaging Neurosurgical consult
Vasculopathic Usually isolated Check BP, serum glucose,
ESR, RPR, cholesterol
Spontaneous recovery
Mass lesion Contralateral hemiparesis
or ipsilateral ataxia
MR imaging Neurosurgical consult
Cavernous sinus As in third nerve palsy Cavernous sinus syndrome
Herpes zoster
ophthalmicus
Rash, trigeminal sensory
loss in the V1 or V2
distribution
Antiviral medications
Orbit Inflammation, trauma,
tumor
Oculomotor, abducens,
optic nerve dysfunction,
proptosis
MR imaging of the orbit
or orbital ultrasound

66. Anatomic Localization Cause Associated Symptoms Diagnostic Evaluation Therapy
Nuclear Infarction Internuclear
ophthalmoplegia, Horner's
syndrome, afferent
pupillary defect
MR imaging, stroke
workup*
Stroke resuscitation,
antiplatelet therapy,
coumadin
Truma, tumor, infection,
inflammation
As above MR imaging, LP Depends on cause
Fascicular Infarction Internuclear
ophthalmoplegia, Horner's
syndrome, afferent
pupillary defect
MR imaging, stroke
workup*
Stroke resuscitation,
antiplatelet therapy,
coumadin
Trauma, trmor, infection,
inflammation
As above MR imaging, LP Depends on cause
Demyelination Isolated or with midbrain
signs above
MR imaging Interferor-β1, Copaxone
Subarachnoid space Trauma, hydrocephalus May be bilateral Neuroimaging Neurosurgical consult
Vasculopathic Usually isolated Check BP, serum glucose,
ESR, RPR, cholesterol
Spontaneous recovery
Mass lesion Contralateral hemiparesis
or ipsilateral ataxia
MR imaging Neurosurgical consult
Cavernous sinus As in third nerve palsy Cavernous sinus syndrome
Herpes zoster
ophthalmicus
Rash, trigeminal sensory
loss in the V1 or V2
distribution
Antiviral medications
Orbit Inflammation, trauma,
tumor
Oculomotor, abducens,
optic nerve dysfunction,
proptosis
MR imaging of the orbit
or orbital ultrasound
* V

67. ABDUCENS NERVE PALSY:

68. VI CN PALSY:
 CAUSES
 Idiopathic
 Trauma
 Ischemic
 Aneurysm
 inflammatory gaint cell arteritis
 Neoplastic demyelinating disorders
 intracranial pressure

69. VI CN PALSY:
 CLINICAL FEATURES
 Esotropia
 Face turn
 Diplopia
 Vision loss
 Pain
 Hearing loss

70.  abducens palsy caused by
vasculopathic injury. There is a
large angle esotropia in left lateral
gaze.

71. VI CN PALSY: NUCLEUS
 It contains both motor neurons
and interneurons that project
along the contralateral MLF to
the contralateral MR subnucleus,
so lesions result in gaze palsy.

72. VI CN PALSY: FASCICULES
 If the damage to the fasciculus occurs in the ventral
pons the pyramidal tract is involved causing
contralateral hemiplegia (Millard-Gubler syndrome)
 In subarachnoid space
 Trauma may affect as it ascends the clivus or as it crosses
the petrous pyramid e.g. Basilar skull fracture
 Raised intracranial presure can cause streching of VI CN
 Lesions arising in the cerebellopontine angle may
involve e.g. Acoustic neurinomas and meningioms

73. VI CN PALSY:
 PETROUS PYRAMID
 Can be compressed by dilated inf. Petrosal sinus in Dorellos
canal e.g. CC Fistula
 Petrositis secondary to otitis media or mastoiditis (Gradenigo
syndrome)
 INTRA CAVERNOUS
 May be associated with postganglionic Horner syndrome

74. Table 3. Acquired lesions of the abducens nerve
Anatomic Localization Cause Associated Symptoms Diagnostic Evaluation Therapy
Nuclear Infarction Ipsilateral facial
paralysis, INO
MR imaging, stroke
workup*
Stroke resuscitation,
antiplatelet therapy,
coumadin
Infiltration, trauma,
inflammation
MR imaging Varies with cause
Wernicke-Korsakoff
syndrome
Ataxia, nystagmus,
altered mentation
Thiamine
Fascicular Infarction, tumor,
inflammation, MS
Ipsilateral facial nerve
paralysis and
contralateral hemiplegia
(Miller-Gubler
syndrome)
MR imaging, stroke
workup*
Stroke resuscitation,
antiplatelet therapy,
coumadin, surgical
treatment, interferon-β1
or Copaxone
Anterior inferior
cerebellar artery
infarction
Ipsilateral facial
paralysis, loss of taste,
ipsilateral Horner's
syndrome, ipsilateral
trigeminal dysfunction,
and ipsilateral deafness
(Foville's syndrome)

75. Subarachnoid space Mass Contralateral
hemiparesis
MR imaging
Ischemia Usually isolated MR imaging if no
recovery after 3 months
Trauma Papilledema, headache Diamox,
ventriculoperitoneal
shunt
Intracranial
hypertension
Headache CSF study† Blood patch
Intracranial
hypotension
Petrous apex Mastoiditis, skull
fracture, lateral sinus
thrombosis, neoplasms,
tumor
Ipsilateral facial
paralysis, severe facial
pain
CT or MR imaging Antibiotics,
neurosurgical
intervention,
anticoagulation
Cavernous sinus As with third nerve
palsy
Cavernous sinus
syndrome
* † I

76. Neuromyotonia
 Neuromyotonia, a rare but important cause of episodic
diplopia, is thought to be neurogenic in origin.
 Prior skull-base radiation therapy, typically for
neoplasm (eg, meningioma), is the most common
historical feature.
 Months to years post radiation, patients experience
episodic diplopia lasting typically 30-60 seconds.
 Neuromyotonia may affect any of the ocular motor
nerves or their divisions.

77. Neuromyotonia
 Diplopia is often triggered by activation of the affected
nerve, during which overaction of the nerve produces
ocular misalignment
 ( eg, abducens nerve neuromyotonia episodes produce
abduction of the involved eye and attendant
exotropia).
 The disorder generally responds quite well to medical
therapy; carbamazepine and its derivatives are the
first-line treatment

78. Myopathic, Restrictive, and
Orbital Causes of Diplopia
 Thyroid Eye Disease
 The most common cause of restrictive strabismus in
adults is thyroid eye disease (TED).
 Any of the extraocular muscles may be involved, but
the inferior and medial recti are most commonly
affected.

79. Posttraumatic Restriction
 Blowout fractures of the orbit often cause diplopia.
 The most typical presentation involves fracture of the
orbital floor with entrapment of the inferior rectus
muscle or its fascial attachments to the orbital tissues.

80. Post- Cataract Extraction
Restriction
 Binocular diplopia can result from injury to or
inflammation within the inferior rectus or
 other muscles after retrobulbar injection for cataract
or other ocular surgery.
 The onset of vertical diplopia just after surgery initially
suggests nerve damage or myotoxicity from the local
anesthetic.

81. Orbital Myositis
 Idiopathic inflammation of one or more extraocular
muscles typically produces ophthalmoplegia and pain,
often with conjunctival hyperemia, chemosis, and
sometimes proptosis.
 The pain may be quite intense and is accentuated by
eye movements
 Orbital myositis related pain usually responds within
24 hours to systemic corticosteroid therapy, whereas
diplopia may take longer to resolve.

82. Neoplastic Involvement
 Infiltration of the orbit by cancer, especially from the
surrounding paranasal sinuses, can impair eye
movements because of either extraocular muscle
infiltration or involvement of the ocular motor cranial
nerves.
 Relative enophthalmos or associated eyelid "hang-up"
on downgaze may accompany the diplopia.
 Occasionally, extraocular muscles may be the site
of a metastatic tumor.

83. Brown Syndrome
 Brown syndrome is a restrictive ocular motor disorder that
produces limited up gaze when the affected eye is in the
adducted position (Fig 8-14).
 This pattern of motility is usually congenital but can be
acquired.
 which produces an ipsilateral hypodeviation that increases
on upgaze to the opposite side
 Acquired cases result from damage or injury to the
trochlea, which may cause a "click" that the patient can
feel.
 Caused by Inflammatory disease, or trauma, but it may,
rarely, be a manifestation of a focal metastasis of a
neoplasm to the superior oblique muscle.

84. THANK YOU