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Motility > Block 11 > Flashcards

Block 11 Flashcards

1
Q

What is a strabismus

A

Person cannot not align both eyes simultaneously under normal conditions. It can move in, out, up, or down
Can be constant or intermittent

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2
Q

What are the causes of strabismus

A

Congenital
Accommodative ET
Abnormal visual development
Neurological

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3
Q

What are the types of strabismus

A

CN palsy
Neurological diseases
Post. Fossa tumor
Increased ICP

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4
Q

LR
Primary
Secondary
Tertiary action

A

1: abduct
2: none
3: none

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5
Q

MR
Primary
Secondary
Tertiary

A

1: adduct
2: none
3: none

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6
Q

SR
Primary:
Secondary:
Tertiary:

A

1: elevate
2: intort
3: adduct

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7
Q

IO
Primary
Secondary
Teritary

A

1: extort
2: elevate
3: abduct

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8
Q

IR
Primary:
Secondary:
Tertiary:

A

1: depress
2: extort
3: adduct

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9
Q

SO
Primary:
Secondary:
Tertiary:

A

1: intort
2: depress
3: abduct

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10
Q

What are the symptoms of cranial nerve paralysis

A 
Double vision
Blurry vision
Decreased peripheral vision
HA
Dizziness
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11
Q

CN 3 innervates what…

A 
SR
MR
IR
IO
Superior palpebral 
EW nucleus
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12
Q

How does a CN 3 palsy appear

A

Down and out
Ptosis
Dilated pupil, no accommodation

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13
Q

What are the common causes of CN3 palsy in children

A

Congenital
Vascular
Tumor

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14
Q

What are the common causes of CN 3 palsy in adults

A

Demyelination disease
Vascular
Tumor
Diabetes

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15
Q

What are the common causes of CN 3 palsy in elderly

A

Vascular

Tumor

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16
Q

What are some causes of CN3 palsy

A 
Ischemic/vascular
Intracranial aneurysm
Neoplasm
Trauma
Migraine
Inflammatory 
Infectious
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17
Q

What test would you do on CN 3 palsy

A 
CH
External exam
VA
CT (exo, hypo) 
EOMs
Pupils
NPC
Accommodation testing
Hess-lancaster
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18
Q

What palsy is most common in children

A

CN 4

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19
Q

What muscles are innervated by CN 4

A

SO

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20
Q

How does a CN 4 palsy appear

A

Eye is up and in

Compensatory head tilt to the opposite side of palsy

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21
Q

What nerve has the longest intracranial pathway

A

CN 4

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22
Q

Why can a CN 4 palsy cause ipsilateral Horner’s syndrome

A

Because it runs near the sympathetic fibers

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23
Q

What is the Horner’s syndrome triad

A

Miosis
Ptosis
Anhidrosis

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24
Q

What are common causes of CN 4 palsys in children

A

Abnormal development of CN4/peripheral nerves

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25
Q

What are the common causes of CN 4 palsy

A 
#1 idiopathic
#2 head trauma WITH loss of consciousness
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26
Q

What tests are performed for CN4 palsy

A 
CH
External exam 
CT 
EOMs
Pupils
Parks 3 step
NPC
Hess-Lancaster
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27
Q

What muscles are innervated by CN 6

A

LR

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28
Q

How does CN 6 palsy appear

A

Esotropia

Compensatory head turn towards the affected eye

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29
Q

What nerve has the longest external course through the cranium

A

CN 6

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30
Q

What injury is CN 6 susceptible to

A 
Injury
Increase ICP
Mastoid infection
Skull fracture 
Tumors
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31
Q

What is the presentation of CN 6 palsy

A

Ipsilateral paresis of LR
Convergent strabismus in temporal gaze
Lateral diplopia
Ipsilateral paresis of facial muscles

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32
Q

What palsy is most common in adults

A

CN 6

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33
Q

T/F the LR has 1 anterior ciliary muscle that innervates it

A

True

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34
Q

Why is the LR affected so much by ischemia

A

It has only one anterior ciliary muscle

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35
Q

What are some causes of CN 6 palsy

A 
Trauma
Aneurysm
Ischemia 
Idiopathic
Demyelination diseases
Neoplasms
Inflammation 
Meningitis
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36
Q

What tests are done in CN 6 palsy

A 
CH
External exam
VA
CT
EOMs
Hess-Lancaster
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37
Q

What is affected in Cavernous sinus palsy

A

CN 3, 4, V1, V2, 6, Horner’s

NOT the optic nerve

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38
Q

What is the number one cause of cavernous sinus palsy

A

Neoplasms

Carotid cavernous fistula, aneurysm, fungal infxn, inflammation

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39
Q

What is affected in orbital apex syndrome

A

CN 3, 4, v1, 6, Horner’s, Optic Nerve

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40
Q

What are the common causes of orbital apex syndrome

A

1 neoplasms

Fungal, inflammation

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41
Q

MR palsy causes

A

Exo

N>D

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42
Q

IR palsy

A

Hyper/exo

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43
Q

SR palsy

A

Bilateral

V exo pattern

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44
Q

IO palsy

A

Eso

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45
Q

What is affected in double elevator palsy

A

SR and IO of the SAME eye

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46
Q

How does double elevator palsy present

A

No elevation in abduction or adduction

Bells pheromones IS present

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47
Q

What is double depressor palsy (monocular depression deficiency)

A

IR and SO in the age eye are affected

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48
Q

How does double depressor syndrome appear

A

No depression in ab/adduction

Head is tilted down

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49
Q

What are causes of neurogenic palsys

A 
Congenital 
Traumatic
Inflammation
Neoplastic
Ischemic
Toxic
Demyelination diseases
Idiopathic
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50
Q

Supranuclear palsy

A

Lesions above the oculomotor nerve nuclei

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51
Q

How does a supranuclear palsy appear

A 
Gaze palsy
Tonic gaze deviation
Vergence anormality
Saccadic/smooth pursuit disorders
Nystagmus
Ocular oscillations
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52
Q

What is internuclear palsy

A

Lesion of the medial longitudinal fasciculus

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53
Q

What are causes of internuclear palsy

A

MS in younger patients

Vascular in elderly

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54
Q

What is nuclear palsy

A

Unilateral CN3 with bilateral ptosis or SR underaction
Palsy of IR, IO, or MR
Browns syndrome
Bilateral CN 3- sparred levator function

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55
Q

What is infranuclear palsy

A

CN 3, 4, 6

56
Q

If CN 3 is affected in infranuclear palsy how does it appear

A

Central pupil sparing

Peripheral with pupil

57
Q

In infranuclear if the pupil is spared what caused it?

A

Vascular

58
Q

In infranuclear if the pupil is NOT spared what casued it?

A

Aneurysm

59
Q

What are some management tests done for strabismus

A

CH
CT, Hess-Lancaster, EOMs
Differential diagnosis
Additional tests (MRI, blood work)

60
Q

What are the causes of strabismus

A

Aneurysm
Neoplasms
Ischemic

61
Q

In ischemic causes how do they happen?

A

> 40 yoa
Sudden onset
Resolves in 3 months
Treat systemic factors

62
Q

What is the first step in strabismus treatment

A

Glasses

Fresnel prism

63
Q

What are som either treatements for strabismus besides glasses

A

Occlusion
Botox
Surgery

64
Q

When is Botox commonly used

A

In CN 6 palsy

65
Q

What are the side effects of Botox

A 
Soreness at injection site
Weakness in injected muscle
Muscle soreness in whole body
Difficulty swallowing
Red rash
66
Q

What is a mechanical restriction

A

EOM is tethered or a systemic disease reduces the elasticity of one or more muscles

Incomitant nonparetic deviations

67
Q

What are some common characteristics of mechanical restrictions

A

Gross limitation of ocular movement in one or more gazes

Small deviation of ortho in primary
Normal binoularity vision aided by compensatory head movement
Positive forced duction testing

68
Q

What tests are done for mechanical restrictions

A 
Alternate CT
Maddox rod (prism over affected eye)

Both eyes: Hirschberg/Krimsky

69
Q

What is Duanes syndrome characterized by

A

Limitations in ABDuction, ADDuction, or both

70
Q

Type 1 Duanes

A

Limited ABDuction

71
Q

Type 2 duanes

A

Limited ADDuction

72
Q

Type 3 duanes

A

Limited ABDuction and ADDuction

73
Q

T/F a patient with limited abduction in the absence of a significant strabismus in primary position should be considered Duane’s syndrome until otherwise proven

A

True

74
Q

What are some characteristics of Duanes

A 
Congenital 
Unilateral
No strab in primary 
Enopthalmos in primary
A/V pattern
75
Q

What is the most common onset of Duanes

A

Sporadic during infancy

76
Q

What causes Duanes syndrome

A

Fibrotic LR
MR that is inserted too far posteriorly
Anomalous innervation

77
Q

How is binocularity in Duanes Syndrome patients

A

High level
Compensatory head posture toward affected eye
Amblyopia and diplopia are rare

78
Q

How is motility in Duanes syndrome

A

Up/downshoot of affected eye during adduction

Mimics overaction of IO and/or SO

Surgery will not help overshoot

79
Q

What is the differential diagnosis of Duanes

A

LR palsy

  • absence of retraction with adduction
  • esotropic angle larger in CN6P
  • rarely have vertical anomalous movements
80
Q

What are the treatments for Duanes

A

Surgery if significant strab in primary, help head posture, improve binocular field of vision

Prism to alleviate head posture

81
Q

What is Browns syndrome

A

Restricted elevation on adduction

82
Q

What are the characteristics of Browns

A

Unilateral
OD>OS
Females
Constant can be intermittent

83
Q

What is the cause of BRowns

A

Sue to thickening of the SO tendon

Cannot move through throchlea effectively
Congenital
Acquired (trauma)
May improve with time

84
Q

How is motility in Browns

A

Restricted elevation or absence of elevation in adduction

Positive forced duction
Minimal or no vertical deviation in primary

V pattern
Audible click

Head posture: chin elevated pointed towards posterior shoulder

Mild down shoot of affected eye
No overactin of ipsilateral SO
Widening of palpebral fissure in adduction

85
Q

How is binocularity in Browns

A

High level of bingo vision in primary

Ortho in primary
Rare amblyopia
Rare diplopia

86
Q

What is the differential for Browns

A

IO paresis

Hypotropia in primary
Head tilt to affected side/head Turn and elevation

A pattern
Can do parks 3 step

87
Q

How do you treat Browns

A

Most do not need treatment

Primary: surgery
Secondary: prism (BU or yoked)

vision therapy to improve elevation in adduction (no successful)

88
Q

What is MG

A

An autoimmune NM disorder of voluntary striated muscle

89
Q

Who is most often affected by MG

A 
Females
Females under 40
Men over 60
Neonatal or congenital 
Onset can follow stress
90
Q

What is the etiology do MG

A

Antibodies released and block and destroy ACh receptors
There are less receptors so less nerve signals so muscle weakness

Thymus gland could be involved (immune repsonse via T cells) larger thymus is MG patients

91
Q

What is the halllmark of MG

A

Muscle weakness that worsens after periods of activity and improves after periods of rest

92
Q

What are the 2 types of MG

A

Generalized (whole body)

Ocular (eyes)

93
Q

Generalized MG signs and symptoms

A

Weakness of arm and leg Muscles

Difficulty with speech, chewing, swallowing, and breathing

94
Q

What are the signs and symptoms of ocular MG

A

Ptosis (most common) (palsy of lev.,unilateral, progressive)

Diplopia

Nystagmus moments
Saccadic abnormalities

95
Q

MG causes issue with what muscles

A 
Skeletal muscle
Orbicularis oculi
Masseter (cant open jaw)
Sternocleidomastoid (head droop)
Tongue (poor gag repsonse)
Diaphragm (death)
96
Q

What is MG crisis

A

When muscels are too weak to control breathing

97
Q

What are teh most common associations of MG

A

Thymomas
Thymus hyperplasia
Thyroid disease
Autoimmune (rheumatoid factor)

98
Q

What do you use to diagnose ocular MG

A

Old photos
EOMs>fatigue

  • Ptosis with prolonged up gaze or rapid opening and closing of eye
  • Conan’s lid twitch (down gaze, the upper lid will twitch as patient looks up)

Ice test (2-5 minutes, ptosis will get improve) (cold makes the ACh breaks down much slower, there will be more ACH available)

99
Q

What is the clinical pearl of MG

A

Presence of an inconsistent deviation along with ptosis and restricted ocular motility

100
Q

What are some further tests that can be done in MG

A

Electromyography

Sleep test

Systemic antiAChase agents (tension and neostigmine test)

Pysical/Neuro exam

Blood test
MRI/CT scan
Pulmonary function

101
Q

How can you treat culver MG

A

Occlusion**
Prism (not successful)
Strabismus/ptosis surgery (not common)

Spontaneous remission occurs in 30% of cases

102
Q

What is teh systemic treatment for MG

A 
AntiAChase agents
Immunosuppressive drugs
Thymectomy
Plasmapheresis (severe)
IV immunoglobulin (severe)

No cure, treat signs and symptoms

103
Q

What is Graves Disease

A

Autoimmune disorder that results from overproduction of thyroid hormone

Hyperthyroidism

104
Q

What are teh 2 types of Graves

A

Graves dermopathy

Graves Ophthalmopathy

105
Q

What are the signs and symptoms of Graves

A 
Enlargement of thyroid
Weight loss
He’s sensitivity
Change in menstruation
Fatigue
Thick red skin
Tachycardia
Budging eye **
ED
106
Q

What is Graves ophthalmopathy

A

Autoimmune inflammation of orbital tissue and muscles

Most common cause of spontaneous diplopia in middle aged people

107
Q

What is teh histology of Graves Ophthalmopathy

A

Enlargement of EOMs
Reduced elasticity and motility
Affected EOMs produces an incomitant deviation

108
Q

What are the characteristics of Graves Ophthalmopathy

A

Bilateral
Females
Younger than 40
Inherited

109
Q

What are the risk factors for Graves Ophthalmopathy

A

Stress
Pregnancy
Autoimmune
Smoking

110
Q

What are common signs of Graves Ophthalmopathy

A 
Periorbital congestion
Pro ptosis
Lid lag
Exophthalmos
Optic neuropathy
Impaired ocular motility

Dry gritty sensation, photophobia, tearing, double vision, pressure behind eyes, vison loss

111
Q

How is motility affected in Graves Ophthalmopathy

A 
Positive forced duction
IR most commonly affected
LR is least affected
(IR>MR>SR>LR)
In severe cases eye is tethered down
There will be a restriction in upgaze and hypotropia of affected eye
112
Q

What is Graves ophthalmopathy often mistaken for

A

SR paresis

113
Q

What is eye alignment in Graves

A

Diplopia worse in the morning

Restriction of elevation and abduction (hypotropia)

Could also have ET, XT, cyclotorsion)

114
Q

How do you diagnose Graves Ophthalmopathy

A

Tonometry (increased in up gaze)

Hertel exophthalmometer

Slit lamp (keratopathy)

Optic nerve eval (optic neuropathy)

CT of orbits, thyroid fxn tests (T3/T4/TSH)

115
Q

What is the prognosis for Graves Ophthalmopathy

A

Spontaneous improvement

Deviation may persist even with control

Improvement in motility can occur with decreased orbital edema

116
Q

What are the treatment options for Graves Ophthalmoscopy

A

Prism (Fresnel)

Surgery (in significant ocular deviations/restrictions)

Artificial tears
Cold compress for eyelid edema
Smoking cessation

117
Q

What is the systemic treatment for Graves ophthalmopathy

A

Radioactive iodine therapy
Corticosteroids
Anti-thyroid drugs
Thyroidectomy

These will not always improve ocular symptoms)
Ocular signs may worsen for 3-6 months)

118
Q

Versions

A

Conjugate movements of both eyes

119
Q

Ductions

A

One eye

120
Q

How do you record versions

A

SAFE

121
Q

How do you record ductions

A

Record as a percent of normal

122
Q

What is uncrossed diplopia

A

ESO

Light hits nasal retina

123
Q

What is uncrossed diplopia

A

EXO
Light hits temporal retina
Crosses the VA of the fixating eye

124
Q

Maddox Rod

Red Light through white dot

A

Ortho

125
Q

Maddox Rod

Red Line to the right

A

Eso

Uncrossed diplopia

126
Q

Maddox Rod

Red line to the left

A

Exo

Crossed diplopia

127
Q

Maddox Rod

Red line below

A

R hyper

128
Q

Maddox Rod

Red line above

A

L hyper

129
Q

What is fibrosis syndrome

A

Tissues of EOMs are abnormal

Replaced with fibrotic tissue

130
Q

What are some presentations of fibrosis syndrome

A

Severely restricted eye movements
Ptosis
Can elevation

131
Q

How many muscles are affected in fibrosis syndrome

A

All muscles or just 1

132
Q

What is the most common muscle affected by fibrosis syndrome?
How does it appear

A

IR

Hypodeviation 20-30 degrees below horizontal

133
Q

What is the onset of fibrosis syndrome

A

Congenital (Autosomal dominant)
Acquired (sporadic)
Stable, non-progressive

134
Q

How is bino in fibrosis syndrome

A

Poor

135
Q

What can occur in fibrosis syndrome

A 
Poor versions and ductions
Ptosis
Amblyopia
Assymmetrical
Cosmesis
Reduced stereopsis
136
Q

What are the treatments for fibrosis syndrome

A

Amblyopia therapy
Manage ptosis
Manage abnormal head movement
Difficult to treat with surgery

Motility (5 decks)

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