Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

My Own Deck > Neuro Ophthalmology > Flashcards

Neuro Ophthalmology Flashcards

1
Q

What are the 2 different visual pathways controlling pupil reactions?

A

Sympathetic- Dilator

Parasympathetic- sphincter

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

When is the pupil at its max dilation and minimum constriction?

A

Dilation- apprehensive in the dark

Constriction- bored while sunbathing

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What is the primary driver of pupil light responses?

A

Parasympathetic pathway

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What is the process from afferent to efferent response?

A

The afferent section allows RGCs light signals to reach midbrain (Edingerwest phal nucleus). This is responsible for generating afferent to efferent constriction signal.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What does the sympathetic pathway contributes to?

A

Light response via activation of dilatory muscle

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Where does the sympathetic pathways passes over in the body?

A

Sites that exposes nerve fibre to local and systemic diseases i.e. lung tumours and internal carotid artery

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What conditions do not give rise to an RAPD?

A
  1. Cataracts
  2. Amblyopia
  3. Visual pathway lesions post to Chiasm
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

When is it an exception for a post to the chiam lesionto cause an RAPD?

A

If more in 1 eye than the other, INCONGROUS homo hemiamopia or quadrantanopia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

When is an RAPD caused?

A

If there is an imbalance in strengths of right and left afferent signals

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What conditions that are associated with RAPD?

A
  1. Anterior Ischaemic Optic Neuropathies (Arteritic or non Arteritic?
  2. Optic Neurits
  3. Advanced glaucoma
  4. Unil ON tumour
  5. Tumours compressing ON
  6. Unil ON Trauma
  7. Orbital disease
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What are key signs for an RAPD to be present?

A

Unilateral and Aysmmetric VF defects

Also depends on degree and depth/extent

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Which area is effected to cause AION or NA AION?

A

Short posterior ciliary arteries

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What tumours may cause an RAPD?

A

Meninginoma, pituitary lesion, ON glioma

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What are the conditions that show a normal reacting pupil?

A
  1. Physiological anisocoria

2. Horners syndrome

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What are the conditions that show an abnormal reacting anisocoia?

A
  1. Adies tonic pupil

2. 3rd nerve palsy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What are the signs of a physiological anisocoria and how common is it?

A

15-20% of the population Asymptomatic
Normal vision
No GH association
No ptosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Which pathway is effected in horners syndrome?

A

Sympathetic pathway

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

What are the causes of horners syndrome?

A
  1. Brainstem damage
  2. Carotid or Aorotic artery dissection
  3. ‘Pancoast tumour’ (Apical lung tumour)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Where are the potential pathologys located to cause horners syndrome?

A
  1. Sup cervical symp ganglion
  2. Internal carotid artery
  3. Long ciliary nerve
  4. Ciliary ganglion
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

What symptoms are likely to be seen in an carotid artery dissection?

A 
HAs 
Numbness/weakness
Neck and shoulder pain 
(If ophthalmic artery effected- Amarausis fugax)
Painful acute horners syndrome
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

What is a carotid artery dissection?

A

A tear in the internal artery wall

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

What are the ocular signs of horners syndrome?

A
  1. Miosis
  2. Ptosis
  3. Anhidrosis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Which muscle has reduced innervation in ptosis?

A

Superior or inferior tarsal muscles

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

If both upper and lower tarsal muscles were seen to have reduced innervation, what may this be misdiagnosed as?

A

Endophthalmos

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

What symptoms are there in horners?

A

No ocular/visual symptoms

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

What us Annhydrosis?

A

Drying of the skin on the same side as the sympathetic nerve fibres
…also runs along carotid artery and arise parasympathetic nerve fibres damaged

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

Management on horners syndrome…

A

… sudden onset horners= urgent!

Pharmacological pupil testing and imaging

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

If a involvement of the pupil is absent in a 3rd nerve palsy, what features are expected?

A

Other features of 3NP but light reflexes remain intact

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

What is the meaning of partial total and absent mean in 3NP?

A

Partial- dilated with sluggish direct
Total- fixed dilated (no direct response
Absent- normal light reflexes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

What are the 2 oculomotor signs when checking for 3NP?

A

Cover test and ocular motility

Ptosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

What position is the eye in, in 3NP and what muscles would be effected?

A

Down and out = u/a medial rectus
Depressed= SR, IR and IO u/a

Ptosis= u/a levator muscle

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

What are the ocular symptoms presented in 3NP?

A
  1. Hz, vz, oblique binocular sudden dip
  2. Intermittent dip- subtle fusion reserves still present
  3. Constant dip- significant lack of EOM innervation
  4. No dip sxs- ptosis complete
  5. Significant pupil involvement(glare/photophobia)
  6. Possible Non ocular sxs depending on pathology.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

What are the non ocular symptoms in 3NP?

A
  1. HAs/orbital facial pains
  2. GCS sxs
  3. CVA sxs
  4. Demylinating disease sxs
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

What are the potential causes to 3NP?

A
  1. Compressive lesions (tumour)
  2. Ischaemic (interruption to 3NP blood supply)
  3. Inflammatory (Multiple sclerosis)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

Which is the most common cause of 3NP?

A

Ischaemia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

What is the pathway the 3rd nerve goes to get to the eye?

A

The 3rd nerve start MIDBRAIN, passes through the CAVERNOUS SINUS sinus which is close to INTRACRANIAL STURCTURES I.e. circle of Willis, pituitary gland.
Once entering the orbit, 3rd nerve splits into 2 branches: superior and inferior branch

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

What muscles are supplied by the 3rd nerve in the superior and inferior branch?

A

Superior- SR and levator

Inferior- MR, IR and IO

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

What structures do the 3rd nerve follow to reach the iris sphincter and ciliary muscle?

A

INFERIOR OBLIQUE… then the fibres enter the CILIARY GANGLION where the SHORT CILIARY NERVES supply these structures

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

Where would a lesion responsible for 3NP more commonly found?

A

Posterior to the orbit

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

How is a 3NP managed?

A

Acute= emergency referral (same day phone call)

… include CT/MR fo risk of intracranial pathology

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

Which muscles is the 4th nerve supply?

A

Superior oblique

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

What are the risk factors of ischaemia?

A

DM
HT
GCA

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

What are the signs of 4NP?

A
  1. Incomitant ipsilateral hypertropia (elevation)
  2. Deviation greater in adduction
  3. Compensating head tilt (away)
  4. Torsional deviation
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

What are the sxs of 4NP?

A

Acute- sudden vz, torsional, oblique diplopia
Head tilt minimises effect
Poss longstanding

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

What can cause 4NP?

A

Commonly CONGENITAL and UNILATERAL
Acquired (compressive/ ischaemic/inflamm path)
Trauma- head injury

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

How is 4NP managed?

A

Acute- emergency referral

Congenital- non urgent (if no previous investigation)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
47
Q

Which muscle is effected in 6NP?

A

Lateral rectus muscle

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
48
Q

What are the signs of 6NP?

A 
Sudde onset SOT
Head turn (towards effected side)
Poss VF defect
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
49
Q

What are the ocular sxs of 6NP?

A

Sudden Hz dip (max when effected eye adducts, dip greater at Dist)
Asthenopia
Reduced corneal sensitivity (if trigeminal nerve involved)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
50
Q

What are the possible non ocular sxs of 6NP?

A

HAs/ pain around eye/ nausea
Facial numbness/pain
Masticulation disorder
Hearing loss

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
51
Q

What are the possible causes of 6NP?

A

Any/all vasc/comp/inflamm

More susceptible to COMPRESSIVE damage due to ICP

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
52
Q

Why makes 4NP more vulnerable to damage?

A

Its a thin and long pathway (midbrain to SO)

Located/passes over petrous temporal bone

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
53
Q

Which other cranial nerves could be effected by he 6NP?

A

5th (Trigeminal nerve)- reduced facial sensation

8th (auditory nerve)- acoustic neuromas

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
54
Q

What is the management for 6NP?

A

Acute= emergency referral

CT/MR scans needed

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
55
Q

If a bitemporal NP is present, what would the lesion be effecting?

A

Pan cranial (whole head) i.e. ICP, Meningitis, demylinating disease

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
56
Q

Which structure would be effected to damage multiple cranial nerves?

A

Cavernous sinus

57
Q

What can midbrain or pons lesions give rise to?

A
  1. Intranuclear ophthalmopegia
  2. Supranuclear ophthalmopegia
  3. Acquires Nystagmus
  4. Myasthenia Gravis
58
Q

What is INO responsible for where is it located?

A

Gaze control centre and is found in the 6th nerve nucleus

59
Q

What sxs are associated with INO and when are these sxs worse?

A

Diplopia
Oscillopsia (unstable visual world, no balance)
Worse when looking in side gaze

60
Q

What is the most common cause for INO and SNO?

A

Midbrain pathology

61
Q

What is the key feature of SNO?

A

Difficulty with eye movements

Can’t look UP and RIGHT

62
Q

What is the management for SNO and INO?

A

Emergency referral

63
Q

How are majority of nystagmus formed?

A

Congenital

Maybe caused by mid brain lesion

64
Q

What is myasthenia gravis?

A

Autoimmume disease which muscular functions are reduced via neuromuscular junctions.

65
Q

What other condition can this may appear as?

A

A nerve palsy, hard to differentiate but end result is the same

66
Q

What are the signs of myasthenia gravis?

A

Ptosis (bilateral and assymetrical)
Motility defects
Diplopia (unless ptosis complete)

67
Q

As MG is a systemic condition what sxs could be present?

A 
Change in facial expression
Difficulty swallowing 
Shortness of breath
Impaired speech
Limb weakness
68
Q

How is MG managed?

A

Pharmacological treatment?

Referred- non urgently via GP

69
Q

What tests are carried out to help dx and compare optic neuropathies?

A 
VF
VA
Colour vision
Pupil reaction 
Sxs
ONH Assessment
70
Q

What are the 2 main signs/sxs of the presence of opic neuropathy?

A
  1. Acquired colour vision defect

2. Disc swelling/ pseudo swelling

71
Q

What colour vision test would detect a red/green deficiency and a tritan defect?

A

Ishihara colour vision test- red/green deficiency

City test- tritan defect

72
Q

What is the key point in acquired color vision defects?

A

That there are likely going to be sxs

73
Q

What is a key feature of congenital color vision defect?

A

Its bilateral

74
Q

What does the nature of the defect depend on?

A

Cone type effected by the RNFL

ONH pathology

75
Q

Which benign conditions mimic disc swelling?

A

Optic disc drusen
Crowded optic disc
Tilted disc
Disc pseudo swelling

76
Q

What are the signs and onset of disc drusen?

A 
Congenital- visible in teen yrs
Bilateral and Assymetrical 75%
Asymptomatic 
Normal VA
VF- irregular pattern possible
77
Q

What is the referral criteria for optic disc drusen?

A

Irregular VF pattern present or unsure= non urgent referral to rule out papilloedema

78
Q

What is another name for crowded optic disc?

A

Congenital optic disc hypoplasia

79
Q

What is “bunching up” referring to?

A

RNF passing through small apertures in small diameter discs

80
Q

What is associated with tilted discs?

A

Myopia
Astimatism
VF loss

81
Q

What type VF loss is present in a tilted disc?

A

Commonly bitemporal and superior and does no respect vz midline (mimics a chiasmal lesion)

82
Q

What are the signs of disc pseudo swelling?

A
  1. No blurring of RNFL
  2. No obstruction of opic disc blood vessels
  3. Cup intact
  4. No dilation of disc arteries/veins
  5. No flame haemm at disc margins
  6. No syst/ocular sxs related to GCA, ICP, Demylinating disease
83
Q

What leads to acute ischaemia of the ONH?

A

Sudden reduction in blood flow in the posterior ciliary artery

84
Q

How does acute ischaemia effect the RNFL?

A

Causes infarction

85
Q

What other pathology is acute ischaemia similar to?

A

Retinal artery occlusion

86
Q

Why is acute ischaemia different to chronic ischaemia?

A

This is a slow starvation I.e. conditions like DM retinopathy

87
Q

Where is the ischaemia located?

A

Posterior to the lamina cribrosa

88
Q

What happens to retinal nerves during ischaemia?

A

Sudden painless loss of function. Also referred as stroke of optic nerve

89
Q

Whatis the single biggest risk factor for AION?

A

Age

90
Q

What are the sxs of AION?

A 
Unilateral, sudden painless loss of vision 
Amarausis fugax (intermittent transient vasc occl)
91
Q

What are the signs of AION?

A
  1. Decreased colour vision
  2. Marked RAPD
  3. VF Altitudinal and unil loss (inferior attitudinal common)
  4. Disc appearance- pale disc, oedema and hypereamia from swelling, splinter haemm
92
Q

How long does the oedema and hyepreamia resolve?

A

6/52

93
Q

What do AAION and NA AAION both have in common?

A
  1. Acute and chronic disc appearance
  2. VA loss
  3. RAPD
  4. VF defects
94
Q

What is the key difference between AAION and NA AION?

A

Sxs assco c GCA

95
Q

How is AAION caused?

A

Inflamm leading to vasc occl of the post ciliary artery

96
Q

What are the potential risk factors for NA AAION?

A 
Systemic vasc factors
Arteriosclerosis 
High BP
High cholesterol level 
DM
SMOKERS!
97
Q

What makes PION different to AION?

A

PION arteries effected are found far posterior b/w ON and chiasm- disc appears normal but will show other signs of AION.

98
Q

How are ION managed?

A

Acute= emergency
Recent hx of Amarausis fugax= same day phone call
GCA sxs but no other sxs= Emergency

99
Q

What is optic neuritis?

A

Inflammation of the RNF (not the blood vessels!!!!)

100
Q

What is the cause of optic neuritis?

A

Demyelinating disease

101
Q

What is demylinating disease?

A

Autoimmune disorder where nerves looses the myelin sheath and disrupt neural transmit

102
Q

What is the age group that are at risk of ON?

A

15-45 years

103
Q

What is the key difference between AION and ON?

A

Age!
Early age onset- ON
Later stage onset- AION

104
Q

What are the sxs of ON?

A
  1. Episodic
  2. Sudden blurred vision
  3. Pain on eye movements
105
Q

As the ON condition is episodic what is the time scale for the blurred vision to dissipitate?

A

Increases over 2/52 and slowly improves over 4/52

106
Q

What 2 conditions can cause ON?

A

Multiple sclerosis

Epstein bar virus

107
Q

Between makes and females c ON, what is the likely chance of developing MS?

A

66% females

33% men

108
Q

ON is the 1st sign of what?

A

Multiple sclerosis

109
Q

What are the sxs of MS?

A 
All episodic:
Numbness
Pins and needles 
Muscle spasm
Limb pain
110
Q

What are the signs of MS?

A

Reduced VA
Reduced colour vision
VF defect
RAPD

111
Q

What is the disc appearance of ON?

A

Normal in 66% during and after episodes
Of inflammation retro bulbar- signs are subtle

33% show mild-mid unil disc OEDEMA and HYPEREAMIA

112
Q

How is optic neuritis managed?

A

Same day phone call

HES will assess approx 1/52

113
Q

Why are the RGCs unmylinated?

A

Minimise shadow effects induced on underlying retinal layers

114
Q

What can a myelin sheath look like?

A

Cotton wool spots

115
Q

Where do myelin sheaths start and end ?

A

At the midbrain- LGN and end at the lamina cribrosa

116
Q

How is a myelin sheath managed?

A

No referall necessary
Inform and reassure px
Document size and position

117
Q

What is papilloedema?

A

Disc swelling in presence of ICP

118
Q

How can papilloedma be confirmed?

A

Neuroimaging and lumbar puncture

119
Q

What causes ICP?

A
  1. Idiopathic IC Hypertension
  2. Intracranial space occupying lesion
  3. Decreased CSF drainage
120
Q

Name some conditions that would cause decreased CSF drainage?

A

Meningitis
Hydrocephalus
Subarachnoid papilloedema

121
Q

What is IIH strongly associated with?

A

Obesity (90%)

122
Q

What are the sxs of ICP?

A

HAs
Postural element
Other neurological sxs

123
Q

What are the ocular signs of papilloedema?

A

Disc swelling (from axoplasmic build up)
Dilated and haemm disc vessels (ischaemia)
VF Defects (presence depends on severity)
VA and colour vision reduced (recovery possible)

124
Q

How is papilloedema managed?

A

Suspected?= potential emergency
Any signs and sxs c no disc swelling= Emergency
Persistent HAs and other neurogical sxs= Advise to see GP if all else normal

125
Q

What are the sxs of amarausis fugax?

A 
Monocular vision loss 
Painless
Whole VF effected
Last several minutes= <1hr-<10mins
Described- 'dim, black, spreading in one direction
126
Q

What is the common cause of amarausis fugax?

A

Transient acute retinal ischaemia induced by carotid disease

127
Q

What are the other causes for amarausis fugax?

A

Papilloedema and migraines

128
Q

In what form is permanent vision loss precuror to?

A

CRAO, BRAO and AAION

129
Q

If signs are not present in Amarausis fugax, what action is taken?

A

Seek medical advise and ask px about strokes sxs

130
Q

What is the most common type of visual defect when thinking about strokes?

A

Homonymous hemianopia

131
Q

What is the 1st and 2nd most common lesion locations to cause VF defect?

A

1st- occipital lobe

2nd- Parietal lobe

132
Q

What are the actions take for potential stroke VF defects?

A
  1. New hemianopia c other strokes sxs (<1/52)— Emergency via A+E
  2. Symptomatic hemianopia c no other steoke sxs (>1/52)— urgent outpx and seen <1/52- 10 days
  3. Asymptomatic hemianopia and VF defect incidental finding—- GP appointment (traige c stroke team)
133
Q

What is visospatial neglect and how is it managed?

A

One side of the vision is ignored (usually opposite side of the brain injury)— ROUTINE REFRRAL

134
Q

What is a thyroid eye disease?

A

Autimmune disorder causing inflammation of orbital fat tissue and EOM

135
Q

Who are at risk of thyroid eye disease?

A

Age 40-50 yrs

F>m

136
Q

What does thyroid eye disease lead to?

A

Proptosis- a retraction of the upperlid

137
Q

What are the sxs of proptosis?

A

Constant intermm diplopia

Dry eye

138
Q

What are the signs of proptosis?

A

VF defect

Bilateral or unilateral

139
Q

How is proptosis managed?

A

Non urgent referral via GP

My Own Deck (18 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions