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Duke Elder: SB Deck > Neuro-Ophth 2, pupils, gaze and conditions > Flashcards

Neuro-Ophth 2, pupils, gaze and conditions Flashcards

1
Q

What is Anisocoria?

A

the presence of asymmeterical pupillary size between the two eyes

physiological or pathological

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2
Q

What is the normal pupil size in light and dark?

A

2-4mm and 4-8mm

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3
Q

In what % of the population is physiological aniscoria present?

A

20% of the population

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4
Q

What is unique about physiological aniscoria?

A

unchanged in light and dark environments

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5
Q

What is horner syndrome caused by?

A

lesion in the sympathetic pathway

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6
Q

What is horner syndrome characterised by?

A

Ptosis: mild eyelid droop due to Muller muscle dysfunction

Miosis: dysfunction of dilator pupillae

Ipsilateral facial anhydrosis: not present in third order neurons

Affected iris is lighter in colour

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7
Q

What are some causes of Horner’s syndrome?

A

first order: lateral medullary syndrome and syrinomyelia

second order: pancoast tumour and neck trauma

third orders: internal carotid dissection (painful), cluster headache and cavernous sinus lesions

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8
Q

What 4 investigations are used in Horner’s syndrome?

A

Topical apraclonidine

topical cocaine

topical hydroxyamphetamine

CT or MRI

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9
Q

How is topical apraclonidine used in Horner’s syndrome?

A

used to confirm horner’r pupil

it is an alpha-1 and alpha-2 adrenergic agonist

causes dilation in horner’s pupil due to denervation hypersensitivity

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10
Q

How is topical cocaine used in horner’s syndrome?

A

used to confirms horner’s pupil

cocaine blocks re-uptake of noradrenaline

causes dilation of normal pupil > than horner’s pupil

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11
Q

How is topical hydroxyamphetamine used in horner’s syndrome?

A

used to differentiate between preganglionic and post ganglionic horner’s pupils

hydroxyamphetamine releases norepinephrine from normal post ganglionic adrenergic nerve endings, causing pupil dilation

failure of dilation - third order (post ganglionic), dilation - first or second order

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12
Q

How are CT / MRI used in horner’s syndrome?

A

if tumours / carotid arteries suspected

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13
Q

What is Adie’s pupil?

A

Unilateral condition characterised by loss of postganglionic parasympathetic innervation to the iris sphincter and ciliary muscle

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14
Q

What are the features of Adie’s pupil?

A

large pupil

poor response to light

intense pupillary response to near stimuli (miosis)

slow re-dilation

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15
Q

What is light-near dissociation?

A

pupillary reaction to near stimulus is greater than reaction to light

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16
Q

What is holmes-adie syndrome?

A

Adies pupil + diminished deep tendon reflex of lower limbs

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17
Q

What investigations are used in Adie’s pupil?

A

Slit lamp: vermiform movements of pupillary borders

pharmacological: 0.1% (low dose) of topical pilocarpine into both eyes causes constriction of affected pupil due to denervation hypersensitivity

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18
Q

What is an Argyll robinson pupil?

A

bilateral, irregular small pupils

both pupils do not react to light

constrict normally on accommodation (light-near dissocaition)

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19
Q

What is the most common cause of argyll pupil?

A

diabetes, previous neuro symphillis

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20
Q

What does homonymous hemianopia with macular sparing looking like?

A

‘half a donut’ of the visual field is blacked out

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21
Q

What type of visual loss do large pituitary tumours lead to?

A

chiasmatic

bitemporal superior quadrantanopia –> bitemporal hemianopia

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22
Q

What type of visual loss do craniopharyngiomas lead to?

A

chiasmatic

bitemporal INFERIOR quadrantopia –> bitemporal hemianopia

also casues growth failure, delayed puberty, headaches, diabetes inspidus, obesity and hypothyroidism in kids

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23
Q

What type of visual field loss doe tuberculum sellae meningiomas lead to?

A

chiasmatic (affects anterior angle of chiasm)

junctional scotoma

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24
Q

What type of visual field loss do aneurysms cause?

A

a large ANTERIOR COMMUNICATING ARTERY ANEURYSM –> bitemporal hemianopia

bilateral internal carotid aneurysms –> biNASAL hemianopia as they affect temporal lobes of the chiasm

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25
Q

What can lesions to the optic tract cause?

A

contralateral incongruous (asymmeterical) homonymous hemianopia

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26
Q

What do lesions of the temporal radiations cause?

A

contralateral, incongruous superior homonymous quadrantopia ‘pie in the sky’

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27
Q

What do lesions of the parietal radiations cause?

A

Contralateral incongrous inferior homonymous hemianopia ‘pie on the floor’

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28
Q

What do lesions of the main optic radiations cause?

A

contralateral incongruous homonymous hemianopia

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29
Q

What do lesions in the occipital cortex cause?

A

occlusion of calcrine artery of posterior cerebral artery: contralateral, CONGRUOUS, homonymous hemianopia with macular sparing

damage to tip of occipital cortex due to systemic hypoperfusion or following an injury to the back of the head: CONGRUOUS homonymous hemianopic central scotoma

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30
Q

What medical problems cause CNIII lesions?

A

diabetes, HTN - affect blood supply to nerve

usually pupil sparing

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31
Q

Why are medical problems leading to CNIII damage pupil sparing?

A

pupillomotor fibres are located superficially, supplied by pial blood vessels

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32
Q

What surgical problems can lead to CNIII lesions?

A

posterior communicating artery aneurysm, uncal herniation and trauma

NOT PUPIL SPARING

33
Q

What are the features of CNIII lesions?

A

ptosis

abduction and dpression of eye in primary position

ophthalmoplegia (only abduction of eye is normal)

dilated pupil and accommodation abnormalties

34
Q

What are some vascular syndromes of CNIII palsies?

A

weber syndrome - CNIII palsy, contralateral hemiparesis

benedikt syndrome - CNIII palsy, contralateral hemiataxia and hemitremor (damage to the red nucleus)

nothangel syndrome - CNIII palsy (ipsilateral cerebellar ataxia) (damage to superior cerebellar peduncle)

claude syndrome - benedikt + nothangel

35
Q

What are some causes of CNIV lesions?

A

congenital CNIV palsy, closed head trauma and microvascular ischaemia

36
Q

What are the features of CNIV lesions?

A

vertical diplopia: worse on walking / looking down

hypertropia: affected eye is higher than the other, worsened on tilting head to ipsilateral shoulder

eye depression is limited, noted on eye adduction

compensatory head posutre to avoid diplopia - contralateral head tilt and face turn

bilateral CNIV palsies may present with depressed chin and posture and crossed hypertropia

37
Q

What are the 3 steps of the Park-Bielschowsky test for CNIV lesions?

A
  1. identify hypermetropic eye in primary position
  2. eyes are examined in left and right gazes, hypertropia increases on opposite gaze in CNIV palsy (worse on opposite gaze, WOOG)
  3. Ask patient to fix at a target ahead, assess hypertropia on right and left head tilts, hypertropia improves on contralateral head tilt in CNIV (better on opposite tilt, BOOT)
38
Q

What are some causes of CNVI lesions?

A

microvascular ischaemia (most common)

other causes: trauma, idiopathic and ICP

39
Q

What are some features of CNVI lesions?

A

HORIZONTAL double vision, worsened on looking at distant targets

esotropia in primary position

limited abduction

40
Q

What are some syndromes that cause sixth nerve palsies?

A

Foville syndrome

Millard Gaublar syndrome

Gardenigo syndrome

41
Q

What is fovile syndrome?

A

lesion to the inferior medial pons

CNVI palsy

ipsilateral facial numbness

ipsilateral facial paralysis

loss of taste sensation to the anterior two third of tongue

horner syndrome

42
Q

What is millard-Gublar syndrome?

A

Lesions to VENTRAL pons

CNVI palsy

Contralateral hemiplegia due to damage to corticospinal tract

ipsilateral CNVII palsy

43
Q

What is gardenigo syndrome?

A

Causes: otitis media, mastoiditis or petrositis

unilateral periorbital pain

diplopia

otorrhoea

44
Q

What is internuclear ophthalmoplegia?

A

lesion to the medial longitudinal fasciculus due to demyelination or stroke

defective adduction of the eye ipsilateral to the lesions and abducting nystagmus of the contralateral eye

may have horizontal diplopia

45
Q

What is one and half syndrome?

A

lesion to the PPRF and MLF on the same side, usually due to stroke

ONLY abduction of the contralateral eye can still occur

46
Q

What is parinaud syndrome?

A

lesion to the dorsal midbrain

causes: pinealoma or aqueductal stenosis in children and vascular problems in adults

supranuclear upgaze palsy

lid retraction (collier sign)

convergence-retraction nystagmus

large pupil with light-near dissociation

47
Q

What is progressive supranuclear palsy?

A

neurodegenerative disorder

characterised by vertical gaze palsy,

slowing of vertical saccades

postural instability

parkinsonism

48
Q

What is nystagmus?

A

involuntary rapid and repetitive oscillation of the eye which can be physiological or pathological

risk of amblyopia in young patients tf. important to correct

49
Q

What is end point nystagmus?

A

nystagmus at extreme gaze

50
Q

Waht is optokinetic nystagmus?

A

nystagmus due to fast moving objects

51
Q

Describe congenital nystagmus

A

horizontal,

pendular / jerky

DISAPPEARS DURING SLEEP

52
Q

What are some causes of congenital nystagmus?

A

sensory deprivation (bilateral cataracts)

optic nerve hypoplasia

foveal hypoplasia

53
Q

Describe latent nystagmus

A

horizontal and jerky

only present on monocular occlusion (direction is away from the covered eye)

most commonly associated with infantile esotropia

54
Q

What is convergence-retraction nystagmus?

A

co-contraction of horizontal muscles on attempted upgaze causing the globe to retract

caused by dorsal midbrain lesions e..g parinaud syndrome

55
Q

Which EOM is the most powerful?

A

Medial Rectus

56
Q

What is upbeat nystagmus?

A

downward drifting of the eye followed by a fast upward corrective saccade or beat

mainly due to medulla lesions

57
Q

What is downbeat nystagmus?

A

upward drifting of eye followed by fast downward corrective saccade

mainly due to lesions at the craniocervical junction such as Arnold-Chiari malformation

58
Q

What is peripheral vestibular nystagmus?

A

conjugate, horizontal and jerky nystagmus that occurs due to a vestibular lesion (e.g. labyrinthitis)

slow drifting of the eyes towards the side of the lesions followed by a fast corrective saccade in the other direction

59
Q

What is myasthenia gravis?

A

AI condition

affecting post synaptic, nicotinic acetylcholine receptors

leads to muscle fatiguability

60
Q

When does myasthenia gravis present?

A

3rd decade of life

female predominance

61
Q

Which muscles are affected in myasthenia gravis?

A

voluntary muscles

smaller ones first

62
Q

What are the features of myasthenia gravis?

A

ptosis: bilateral, worse at end of day or prolonged upgaze

cogan lid twitch: brief upshoot of the lid elicited by making patient look down then up

diplopia

ophthalmoplegia

fatiguability ad weakness of muscles of facial expression and proximal limb muscles

respiratory depression

63
Q

What investigations are used for myasthenia gravis?

A

Ice test

antibodies: anti-AChR antibodiy and anti MUSK

repetitive nerve stimulation (decrement of muscle action potential amplitude)

CT thorax: may reveal thymoma

64
Q

How is myasthenia gravis managed?

A

acetylcholinesterase inhibitors e.g. pyridostigmine

steroids

immunomodulators

thymectomy if thymoma

65
Q

What is myotonic dystrophy?

A

abnormal muscular relaxation and muscle wasting

AD condition, due to tri-nucleotide repeats on chromosome 19

66
Q

what are the features of myotonic dystrophy?

A

inability of muscle relaxation

early-onset cataracts: polychrmatic opacities, Christmas tree cataracts

Ptosis

Ophthalmoplegia

67
Q

What is Kearns-Sayre syndrome?

A

mitochondrial inherited myopathy due to deletion of mitochondrial DNA

68
Q

What does histopathology of kearns-sayre syndrome show

A

ragged red fibres (increased intramuscular accummulation of mitochondria)

69
Q

how does kearns-sayre present?

A

within the first two decades of life

triad:

bilateral, symmeterical ptosis and ophthalmoplegia

pigmentary retionopathy with sale and pepper appearance involving macula

cardiac conduction defects

70
Q

What is miller fisher syndrome?

A

variant of Gullain Barre

Anti-GQ1b may be present

71
Q

Describe the features of miller fisher

A

tetrad

ataxia

areflexia

ophthalmoplegia

facial diplegia

72
Q

What is NF1?

A

AD multisystem disorder

due to mutation in the neurofibromin 1 gene on Chr 17

73
Q

What are the features of NF1?

A

cafe-au-lait on trunk commonly

axillary freckling

opthalmic:

  • optic nerve glioma
  • bilateral lisch nodules (Irish hamartomas)
  • plexiform neurofibromas (bag of worms) feeling on the lid
  • choroidal naevi: patients with this have a higher risk of choroidal malanoma
74
Q

What is NF2?

A

less common than NF1

mutation on neurofibromatin 2 gene on chr 22

75
Q

What are the features of NF2?

A

posterior SUBSCAPULAR cataracts

bilateral / unilateral acoustic neuromas causing decreased sensorineural hearing loss, tinnitus and loss of corneal reflex

Meningiomas

76
Q

What is tuberous sclerosis?

A

AD multisystem disorder characterised by:

  • facial angiofibromas
  • ash-leaf spots
  • seizures

cognitive impairment

multiple intracranial / retinal astrocytic hamartomas

  • glial tumours of retinal fibre layers from astrocytes
  • referred to as mulberry lesions due to their multinodular appearance
  • -on fundoscopy appear as well-dined elevated creamy white lesions

associations: tuberous sclerosis, neurofibromatosis and retinitis pigmentosa

77
Q

What is benign essential blepharospasm?

A

bilateral idiopathic condition characterised by involuntary contraction of the orbicularis oculimuscle due to basal ganglia dysfunction

present in sixth decade of life with female predominance

78
Q

What is meige syndrome?

A

blepharospasm and oromandibular dystonia

79
Q

How is benign essential blepharospasm managed?

A

artifical tears for dry eyes

botulinum toxin injection to orbicularis oculi

-side effects: ptosis, dry eye, diplopia, lagophthalmos and corneal exposure

surgical myomectomy if these don’t work

Duke Elder: SB Deck (9 decks)

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