2. Types of heterotropias
1. Concomitant
2. Non-concomitant (deviation differ by 10 Pd)
Is a type of Heterotropia In which the amount of deviation
varies in different directions of gaze. Further, amount of
deviation may also vary depending on which eye is fixing.
3. Types of Incomitant deviations
1. Non-paralytic (Special types of Strabismus)
i. vertically incomitant horizontal heterotropias e.g.:
A-, V-, X-, Y- and λ- pattern heterotropias
ii. Special restrictive ocular motility defects: e.g.:
Duane’s Retraction syndrome, Brown’s syndrome,
Grave’s ophthalmopathy, etc.
2. Paralytic (Paralysis of Cranial Nerve/s)
4. Vertically incomitant horizontal
heterotropias
Refers to those horizontal deviations that change in
magnitude with upgaze and downgaze
A pattern Horizontal heterotropia:
Increasing convergence (decreasing divergence) in
upgaze and increasing divergence in downgaze.
Considered significant if deviation differ by 10 Pd
A esotropia- esotropia will increase in upgaze and decrease
in downgaze
A exotropia: exotropia will decrease in upgaze and increase
in downgaze
6. Vertically incomitant horizontal
heterotropias
V pattern Horizontal heterotropia:
Increasing convergence (decreasing divergence) in
downgaze and increasing divergence in upgaze.
Considered significant if deviation differ by 15 Pd
V esotropia- esotropia will increase in downgaze and
decrease in upgaze
V exotropia: exotropia will increase in upgaze and decrease
in downgaze
8. Vertically incomitant horizontal
heterotropias
Y pattern Horizontal heterotropia:
Have exotropia only in upgaze
λ- pattern Horizontal heterotropia:
Exotropia in down gaze only
X- pattern Horizontal heterotropia:
No deviation or a small one in primary position, but a
significant exotropia in upgaze as well as in downgaze
9. Ex: Non-Paralytic
Special Types of Strabismus
Duane Syndrome
(face turn to left)
Brown’s Syndrome LE
(head tilt towards affected side)
10. Muscle Innervation
Each EOM is innervated by a specific cranial nerve
1. medial rectus (MR)—cranial nerve III (Inferior branch)
2. superior rectus (SR)—cranial nerve III (Superior
Branch)
3. inferior rectus (IR)—cranial nerve III (Inferior Branch)
4. inferior oblique (IO)—cranial nerve III (Inferior Brach)
5. lateral rectus (LR)—cranial nerve VI
6. superior oblique (SO)—cranial nerve IV
7. Levator Palpebral Superiosis (LPS) - cranial nerve III
(Superior
Branch)
LR6(SO4)3.
11. Paralytic Deviation
Ocular deviation resulting from complete or
incomplete paralysis of one or more
extraocular muscles.
Complete called as palsy
Incomplete called as paresis
19. General features:
Diplopia
Confusion
Ocular deviation : i . primary
ii . Secondary
Ocular movements
Past pointing
Nausea, vertigo & dizziness
Muscle sequelae :
20. Muscle sequelae :
Changes that take place in EO muscle after
sometime of paralysis or paresis of one or
more EO muscle.
i . Overaction of contralateral synergistic
muscle.
ii . Contracture of direct antagonist
iii . Secondary inhibitional palsy of the
contralateral antagonist muscle.
21. Muscle sequelae following
paresis of EO
Paretic muscle Overaction of
contra. Synergist
Contracture of
direct agonist
Sec.inhibitional
palsyofcontra.
Antagonist
RLR LMR RMR LLR
RMR LLR RLR LMR
RSO LIR RIO LSR
RIO LSR RSO LIR
RSR LIO RIR LSO
RIR LSO RSR LIO
30. Cover test:
Both for distance & near , with & without
abnormal head posture
Presence of any manifest or latent deviation
Type of deviation
Primary versus secondary deviation
Normally fixing eye : for the dominant eye.
35. Different types of test :
Diplopia test
Bielschowsky three step test
Haploscopic test
Field of binocular fixation
Other test : FDT , EMG , EOG , Orbital USG ,
Computerised tomographic scanning.
38. Differential diagnosis in
paralytic squint :
Comitant versus incomitant squint
Congenital versus acquired palsies
Paralytic versus restrictive palsies.
39. Clinical varieties of ocular
palsies :
Isolated ocular muscle paralysis : SO (4TH
nerve palsy) and LR (6TH
nerve palsy).
Paralysis of 3rd
cranial nerve
External ophthalmoplegia
Total opthalmoplegia
Internuclear ophthalmoplegia
41. Differences
Paralytic Strabismus Non-Paralytic Strabismus
Types of Onset Usually sudden, rarely may be
slow or since birth
Usually gradual
Age of Onset Any age During Childhood
H/O Head Trauma Common Uncommon
Hering’s Law Follows (20
> 10
Deviation) May not follow
ARC/ Amblyopia Uncommon Possible / Common
Comitancy In Late Stage Common
Head Posture Abnormal Commonly Normal
Past Pointing Present (Recent onset) Rare
Diplopia Usually present Usually absent
Ocular movements Limited in direction of paralyzed
muscle
Usually full
42. Congenital/ Old Paralysis Recent Onset
(Acquired)
Abnormal Head Posture May persist on covering paretic eye Disappears on covering
paretic eye
Diplopia (??) Rare Always Present
Amblyopia May be present Absent
Facial Asymmetry Common with long standing torticollis Absent
Comitancy Spread of Comitancy Incomitant
Past Pointing Absent Present
Abnormal head posture May persist on covering paretic eye
bcoz of scoliosis and contracture of
neck muscle
Disappear in covering
paretic eye
Force duction test May be positive negative
Abnormal head posture
In old photographs
May be present absent
Onset of symptoms Usually indefinite and intermittent Usually definite and sudden
44. Prevalence Of Nerve Paralysis
Nerve Prevalence
(Variable)
III 11%
IV 30% <
VI 45%
Multiple 14%
Holmes n et al
45. Stages of EOM Paralysis
First Stage
After Onset : Weakness of the paralyzed muscle
Maximum Deviation is in the field of action of Paralyzed
Muscle
Second Stage
Direct Overaction (Contracture) Ipsilateral Antagonist
With time: Overshadow the defective action of affected Muscle
Third Stage
Recovery
Deviation will spread to all fields of gazes – Increase in
Comitancy : Spread of Comitancy
46. Consequences of a EOM Paralysis
1. Contracture of Ipsilateral Antagonist
2. Overaction of Contraleral Synergist (yolk muscle)
3. Inhibition Palsy of Contralateral Antagonist
Ex: LLR Palsy
1. LMR Contracture
2. RMR Overaction
3. RLR Under action
47. Consequences of EOM Paralysis
Ex: LLR Palsy
1. LMR Contract
2. RMR Overaction
3. RLR Under action
49. Oculomotor Nerve Paralysis
(III Cranial Nerve)
III Nerve – Superior Branch – LPS/ SR
- Inferior Brach – MR/IO/ IR
- Intrinsic Muscles (Iris/ Ciliary Body)
Rarely Isolated Muscle Paralysis
50. IIIrd
Cranial Nerve Paralysis
PATHOPHYSIOLOGY
Results from damage to the oculomotor nerve anywhere in its
the nucleus in the dorsal mesencephalon
fascicles in the brainstem parenchyma,
the nerve root in subarachnoid space, or
in the cavernous sinus or
posterior orbit.
Interesting Facts (Involvement of IIIrd Nerve Nucleus)
Damage to the third nerve nucleus results in
an ipsilateral third nerve palsy with contralateral superior rectus under action
and bilateral ptosis.
Damage to the third nerve fascicles results in an ipsilateral third nerve
palsy with contralateral hemiparesis (Weber's syndrome),
51. IIIrd
Cranial Nerve Paralysis
Damage to Course of IIIrd Nerve
Damage at the level subarachnoid space produces
an isolated third nerve palsy.
causes
Cavernous sinus involvement
Rarely isolated IIIrd
Nerve palsy
May include pareses of cranial nerves IV, VI and V-1, and an
ipsilateral Horner's syndrome.
Common Causes
metastatic disease, inflammation, herpes zoster, carotid artery
aneurysm, pituitary adenoma and apoplexy, and sphenoid wing
meningioma.
52. IIIrd
Cranial Nerve Paralysis
Isolated Muscle Involvement :
Rare and often congenital
1. Superior Rectus (SR) : Congenital / Secondary to Trauma
2. Medial Rectus (MR) : Very Rare / Congenital
Synergistic Divergence Phenomenon
Simultaneous abduction of both eyes on attempted gaze in
the field of action of paralyzed MR.
?? Reason ? Overaction /Contracture of both LR
3. Inferior Rectus (IR) : Congenital / Rare
4. Inferior Oblique (IO) :
- Least likely to paralyzed
- Congenital / Blunt Trauma : Orbital floor fracture
53. IIIrd
Cranial Nerve Paralysis
Complete Paralysis : Acquired (total or partial)
Sign & Symptoms
Sudden onset with unilateral/ Bilateral Ptosis
Head Ache , Diplopia ??? (Partial Vs Complete)
The affected eye positions
Exotropic {non-comitant}, Hypotropic
position (down and out).
Limitation
Elevation, depression and adduction.
underaction of the superior, inferior, and medial recti
muscles and inferior oblique muscle
Pupillary involvement : dilated and minimally reactive to
light,
Pupillary sparing
54. Hess chart of right third nerve
palsy
Contraction of right chart and expansion of left
Right chart - underactions of all muscles except lateral rectus and superior oblique
Left chart - overactions of all muscles except medial rectus and inferior oblique
56. Trochlear Nerve (IV) Paralysis
SIGNS AND SYMPTOMS
Sudden onset
complaints of vertical diplopia,
which is especially manifest as the patient tries to
read.
Inability to look down and in.
Torticollis
Head tilt contralateral to the affected superior
oblique muscle.
Chin depressed There is frequently concurrent
hypertension and/or diabetes.
Amount of deviation
Hyper-deviation will increase in contralateral gaze,
reduce in ipsilateral gaze
Increase on ipsilateral head tilt, and decrease on
57. Trochlear Nerve (IV) Paralysis
PATHOPHYSIOLOGY
Damage to fourth cranial nerve nucleus (located in the
dorsal mesencephalon)
give a contralateral fourth nerve palsy
Causes
Trauma , hemorrhage, infarction, trauma, hydrocephalus and
demyelinization.
More likely, associated with palsy of cranial
nerves III (Cavernous sinus involvement)
??? Detection
Blunt Trauma to the head or orbit
can cause damage to the trochlea, resulting in superior
oblique muscle dysfunction.
58. Hess chart of right fourth nerve palsy
No significant difference in chart size
Right chart - underaction of superior oblique and overaction of inferior oblique
Left chart - overaction of inferior rectus and underaction of superior rectus
59. CRANIAL NERVE VI PALSY
(Abducen)
VI Supply – Lateral Rectus muscle
SIGNS AND SYMPTOMS
Sudden onset/ head pain
Present with horizontal uncrossed diplopia which
worsens at distance
An abduction deficit with either an esophoric or
esotropic position
Isolated palsy
Neither visual acuity nor visual field loss.
Normal fundus
Except in a bilateral cranial nerve VI palsy (Papilloedema)
60. CRANIAL NERVE VI PALSY
Abducen
PATHOPHYSIOLOGY
Originate from Pons
Close association with the facial nerve & PPRF
Damage to the sixth nerve at the brain stem
VII (facial) nerve palsy or an internuclear ophthalmoplegia.
Within the cavernous sinus
the sixth nerve is joined by
the oculosympathetic nerves and cranial nerves III, IV and V-1.
Damage
VI palsy and Horner's syndrome
Concurrent CN III and IV palsy.
Causes :
Aneurysm, meningioma, pituitary adenoma, inflammation, or fistula.
ischemic infarction
Diabetes and hypertension;
prime cause of isolated sixth nerve palsy.
61. Hess chart of Left CN VI palsy
Contraction of left chart and expansion of right
Left chart - marked underaction of lateral rectus and mild overaction of medial rectus
Right chart - marked overaction of medial rectus
62. Clinical Evaluation of Paralytic
Strabismus
1. Observation
2. EOM Evaluation
3. Cover Test
4. Measurement of deviation
5. Past Pointing
6. Head tilt Test
7. Diplopia/ Hess Charting
8. Force duction/ Force Generation test
9. Imaging Test (CT/ MRI)
68. Park’s Bielschwsky Head tilt Test
Park’s Procedure
Useful for only Isolated Nerve Palsy
Park’s Diagnostic Scheme
1. Which is the hyper eye in primary gaze?
RE/LE
2. Which horizontal field of gaze (right or left)
does the hyperdeviation increase?
3. Bielchowsky Head-Tilt Test: Toward which
shoulder does the hyperdeviation increase?
75. Hess Screen Chart
Additional infromation:
1. Contraction of ipsilateral antagonist
2. Overaction of contralateral synergist
3. Inhibtion palsy of contralateral antagonist.
Diagnosis
- Smallest field – Affected eye
- Field deviated maximum
towards the centre
- affected muscle