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2nd year > Eye movements in health and disease > Flashcards

Eye movements in health and disease Flashcards

1
Q

what are the extraocular muscles of the eye?

A 
superior rectus
inferior rectus
medial rectus
lateral rectus
superior oblique
inferior oblique
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2
Q

what are the extraocular muscles of the eye?

A 
superior rectus
inferior rectus
medial rectus
lateral rectus
superior oblique
inferior oblique
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3
Q

Rectus muscles

A

originate from common tendinous ring and attach to anterior sclera

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4
Q

superior rectus

A

elevates eye
adduction
medial rotation
innervated by oculomotor nerve

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5
Q

inferior rectus

A

depresses eye
adduction
lateral rotation
innervated by oculomotor nerve

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6
Q

medial rectus

A

adduction

innervated by oculomotor nerve

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7
Q

lateral rectus

A

abduction

innervated by abducens nerve

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8
Q

oblique muscles

A

attach to posterior sclera

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9
Q

superior oblique

A

depresses eye in adduction
medial rotation/ intorsion
innervated by trochlear nerve

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10
Q

inferior oblique

A

elevates eye when in adduction
lateral rotation/ extorsion
innervated by oculomotor nerve

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11
Q

what happens when the superior tract is damaged?

A

inferior vision affected

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12
Q

what happens when the inferior tract is damaged?

A

superior vision affected

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13
Q

lesion at optic chiasm

A

tunnel vision

non-homonymous bitemporal hemianopia

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14
Q

what happens when there is a lesion in the primary visual cortex?

A

macular sparing

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15
Q

efferent visual pathway

A

upper motor neurone from fronto-parietal cortex to brainstem then lower motor neurone - cranial nerve to muscles of the eye
travel through cavernous sinus to orbit

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16
Q

motor pathway to eye

A

conjugated eye movement requires modification to the basic primary motor pathways to achieve convergence and conjugation

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17
Q

what is convergence?

A

alignment as objects become closer together

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18
Q

what is conjugation?

A

simultaneous tracking of objects

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19
Q

how to test superior rectus?

A

look laterally and upwards

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20
Q

how to test inferior rectus?

A

look laterally and downwards

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21
Q

how to test medial rectus?

A

look medially

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22
Q

how to test lateral rectus?

A

look laterally

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23
Q

how to test inferior oblique?

A

look medially and upwards

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24
Q

how to test superior oblique?

A

look medially and downwards

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25
Q

what are the components of MS?

A

inflammation - autoimmune mediation
demyelination
axonal loss

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26
Q

efferent opthalmic manifestations of MS

A 
extraocular muscle palsy
internuclear opthalmoplegia
nystagmus
saccadic abnormalities
uveitis
oscillopsia
diplopia
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27
Q

afferent opthalmic manifestations of MS

A

demyelinating optic neuritis

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28
Q

visual field defects

A

prechiasmal
chiasmal
post-chiasmal

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29
Q

pre-chiasmal defects

A

optic neuritis

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30
Q

chiasmal defects

A

junctional scotoma

bitemporal hemianopia defect - rare

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31
Q

post-chiasmal defects

A

optic tract

geniculocalcarine pathway

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32
Q

what is optic neuritis?

A

common early presentation of MS - 20%

acute demyelination of optic nerve

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33
Q

clinical features of optic neuritis

A 
more commonly unilateral than bilateral
pain on eye movement
loss of vision
blurred vision
partial/ complete
typically central
reduced visual acuity
central scotoma
loss of colour vision
pale disc
relative afferent pupil defect 
no fundoscopy findings
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34
Q

potential fundoscopy findings

A

can develop papillitis - blurred margins caused by swollen disc on fundoscopy

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35
Q

what is central scotoma?

A

blurred spot in centre of vision

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36
Q

what is a relative afferent pupillary defect?

A

pupils don’t send impulse back to brain to cause dilation or constriction of pupil

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37
Q

clinical features of a relative afferent pupillary defect

A

affected eye will dilate when light shone in swinging torch test
because of the consensual reflex from when light shone in unaffected eye is removed and there is dilation but the light is not detected by the affected eye so no constriction can occur

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38
Q

prognosis for optic neuritis

A

often self-resolves in 2-3 weeks
5-10% will not recover fully
can get recurrent attacks

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39
Q

treatment for optic neuritis

A

oral steroids have no long-term improvement but can speed recovery
IV steroids - methyprednisolone has been shown to reduce progression of MS

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40
Q

Rectus muscles

A

originate from common tendinous ring and attach to anterior sclera

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41
Q

superior rectus

A

elevates eye
adduction
medial rotation
innervated by oculomotor nerve

How well did you know this?
1
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2
3
4
5
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42
Q

inferior rectus

A

depresses eye
adduction
lateral rotation
innervated by oculomotor nerve

How well did you know this?
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2
3
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5
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43
Q

medial rectus

A

adduction

innervated by oculomotor nerve

44
Q

lateral rectus

A

abduction

innervated by abducens nerve

45
Q

oblique muscles

A

attach to posterior sclera

46
Q

superior oblique

A

depresses eye in adduction
medial rotation/ intorsion
innervated by trochlear nerve

47
Q

inferior oblique

A

elevates eye when in adduction
lateral rotation/ extorsion
innervated by oculomotor nerve

48
Q

what happens when the superior tract is damaged?

A

inferior vision affected

49
Q

what happens when the inferior tract is damaged?

A

superior vision affected

50
Q

lesion at optic chiasm

A

tunnel vision

non-homonymous bitemporal hemianopia

51
Q

what happens when there is a lesion in the primary visual cortex?

A

macular sparing

52
Q

efferent visual pathway

A

upper motor neurone from fronto-parietal cortex to brainstem then lower motor neurone - cranial nerve to muscles of the eye
travel through cavernous sinus to orbit

53
Q

motor pathway to eye

A

conjugated eye movement requires modification to the basic primary motor pathways to achieve convergence and conjugation

54
Q

what is convergence?

A

alignment as objects become closer together

55
Q

what is conjugation?

A

simultaneous tracking of objects

56
Q

how to test superior rectus?

A

look laterally and upwards

57
Q

how to test inferior rectus?

A

look laterally and downwards

58
Q

how to test medial rectus?

A

look medially

59
Q

how to test lateral rectus?

A

look laterally

60
Q

how to test inferior oblique?

A

look medially and upwards

61
Q

how to test superior oblique?

A

look medially and downwards

62
Q

what are the components of MS?

A

inflammation - autoimmune mediation
demyelination
axonal loss

63
Q

efferent opthalmic manifestations of MS

A 
extraocular muscle palsy
internuclear opthalmoplegia
nystagmus
saccadic abnormalities
uveitis
oscillopsia
diplopia
64
Q

afferent opthalmic manifestations of MS

A

demyelinating optic neuritis

65
Q

visual field defects

A

prechiasmal
chiasmal
post-chiasmal

66
Q

pre-chiasmal defects

A

optic neuritis

67
Q

chiasmal defects

A

junctional scotoma

bitemporal hemianopia defect - rare

68
Q

post-chiasmal defects

A

optic tract

geniculocalcarine pathway

69
Q

what is optic neuritis?

A

common early presentation of MS - 20%

acute demyelination of optic nerve

70
Q

clinical features of optic neuritis

A 
more commonly unilateral than bilateral
pain on eye movement
loss of vision
blurred vision
partial/ complete
typically central
reduced visual acuity
central scotoma
loss of colour vision
pale disc
relative afferent pupil defect 
no fundoscopy findings
71
Q

potential fundoscopy findings

A

can develop papillitis - blurred margins caused by swollen disc on fundoscopy

72
Q

what is central scotoma?

A

blurred spot in centre of vision

73
Q

what is a relative afferent pupillary defect?

A

pupils don’t send impulse back to brain to cause dilation or constriction of pupil

74
Q

clinical features of a relative afferent pupillary defect

A

affected eye will dilate when light shone in swinging torch test
because of the consensual reflex from when light shone in unaffected eye is removed and there is dilation but the light is not detected by the affected eye so no constriction can occur

75
Q

prognosis for optic neuritis

A

often self-resolves in 2-3 weeks
5-10% will not recover fully
can get recurrent attacks

76
Q

treatment for optic neuritis

A

oral steroids have no long-term improvement but can speed recovery
IV steroids - methyprednisolone has been shown to reduce progression of MS

77
Q

what are the types of nystagmus?

A 
unilateral
bilateral 
purely downward
purely torsional 
pendular is most common
78
Q

oculomotor nerve palsy

A

eye moves down and out
ptosis
pupil involvement
diplopia

79
Q

why does an oculomotor palsy cause diplopia?

A

no conjugation of eyes

80
Q

why does an oculomotor palsy cause pupil involvement?

A

carries parasympathetic fibres to sphincter and ciliary muscles

81
Q

causes of oculomotor nerve palsies

A 
posterior circulation aneurysm
brainstem lesions
microvascular ischaemia
cavernous sinus disease 
strokes
82
Q

abducens nerve palsy

A

limited abduction
most common nerve palsy of eye
esotropia
head turn for compensation

83
Q

what is esotropia?

A

eye turned inwards

84
Q

causes of abducens nerve palsy

A 
trauma
space occupying lesion
raised ICp 
ischaemia
inflammation
cavernous sinus disease
85
Q

why is abducens nerve palsy the most common?

A

most superficial/ on the outside

86
Q

trochlear nerve palsy

A

head tilt to compensate
torsional diplopia
worse on downward gaze
cannot look down

87
Q

causes of trochlear nerve palsy

A

trauma
aneurysm
cavernous sinus disease
space occupying lesion

88
Q

internuclear opthalmoplegia

A

most common abnormality in MS

often bilateral

89
Q

causes of internuclear opthalmoplegia

A

cerebrovascular disease

lesion in medial longitudinal fasciculus

90
Q

clinical features of internuclear opthalmoplegia

A

disorder of conjugate lateral gaze
adduction deficit in ipsilateral affected eye
pendular nystagmus in abducting contralateral eye
patients present with horizontal nystagmus

91
Q

what is cavernous sinus thrombosis?

A

blood clot in cavernous sinus

can be life-threatening

92
Q

causes of cavernous sinus thrombosis

A
  • oral contraceptives
  • pregnancy
  • blood clotting disorders
  • haematological diseases
  • malignancies
  • head trauma
  • neurosurgical procedures
  • IBS
  • collagen vascular diseases
  • blood vessel disorders
  • hyperhomocysteineamia
  • haematological conditions
  • nephrotic syndrome
  • dehydration
  • infections
93
Q

what infections can cause cavernous sinus thrombosis?

A

In paranasal region

  • rhinogenic infections
  • mid-facial infections
  • dental infections
  • otogenic infections
  • meningitis
  • pharyngitis
  • tonsillitis
  • orbital and periorbital cellulitis
94
Q

what is the pathophysiology of cavernous sinus thrombosis?

A

thrombogenesis occurs in vertebral venous system
decreases cerebral drainage, increasing ICP
oxygenated blood in brain decreases
causes cerebral oedema and infarcts/ strokes

95
Q

clinical features of cavernous sinus thrombosis

A
  • symptoms depend on the size and location of thrombosis
  • non-specific symptoms
  • raised ICP
  • cerebral ischaemia
  • headache – acute, subacute or chronic and may progress in severity over days/ weeks
  • bilateral papilloedema
  • vision impairment – diplopia/ vision loss
  • nausea and vomiting
  • impaired consciousness
  • seizures – focal or generalised
  • cranial nerve dysfunction – diplopia, tinnitus, unilateral deafness, facial palsy
  • paralysis
  • aphasia
  • behavioural changes
  • delirium
  • amnesia
  • progressive and slow development of symptoms
96
Q

diagnosis of cavernous sinus thrombosis

A

neuroimaging

lab tests

97
Q

neuroimaging for cavernous sinus thrombosis

A

MRI with venography, if not CT with venography

98
Q

neuroimaging findings in cavernous sinus thrombosis

A 
absence of flow
intraluminal venous thrombus 
focal oedema secondary to ischaemia
intraparenchymal haemorrhage 
empty delta sign
99
Q

lab tests for cavernous sinus thrombosis

A 
D-dimer - elevated in acute disease
FBC
coagulation studies
baseline renal function tests prior to starting treatment
CRP
blood cultures
lumbar puncture
ESR
antibody studies 
LFTs
thrombophilia screening 
EEG
100
Q

treatment for cavernous sinus thrombosis

A

general stabilisation
treat raised ICP
treat underlying cause
anticoagulation
antimicrobial therapy if infection present
surgical intervention if no improvement with medical therapy or if anticoagulation is contraindicated

101
Q

medical management of cavernous sinus thrombosis - anticoagulation

A

1st line = LMW heparin
2nd line = unfractionated heparin
long-term = vitamin K antagonists (warfarin) for 3-12 months

102
Q

antimicrobial therapy for cavernous sinus thrombosis

A

vancomycin
3rd/4th generation cephalosporin
metronidazole for 3-4 weeks
rarely caused by fungal infection but if the case = immunosuppression, amphotericin B

103
Q

other medical managements of cavernous sinus thrombosis

A 
fluids
neuroprotective measures
ICP management 
anticonvulsants if seizures present
corticosteroids in certain conditions
104
Q

invasive procedures for cavernous sinus thrombosis

A

endovascular thrombolysis

catheter thrombectomy

105
Q

surgery for cavernous sinus thrombosis

A

decompressive hemicraniectomy
haematoma evacuation
shunt placement
abscess drainage

2nd year (48 decks)

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