Neuro-Ophth 2, pupils, gaze and conditions Flashcards

(79 cards)

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
What can lesions to the optic tract cause?
contralateral incongruous (asymmeterical) homonymous hemianopia
26
What do lesions of the temporal radiations cause?
contralateral, incongruous superior homonymous quadrantopia 'pie in the sky'
27
What do lesions of the parietal radiations cause?
Contralateral incongrous inferior homonymous hemianopia 'pie on the floor'
28
What do lesions of the main optic radiations cause?
contralateral incongruous homonymous hemianopia
29
What do lesions in the occipital cortex cause?
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
30
What medical problems cause CNIII lesions?
diabetes, HTN - affect blood supply to nerve usually pupil sparing
31
Why are medical problems leading to CNIII damage pupil sparing?
pupillomotor fibres are located superficially, supplied by pial blood vessels
32
What surgical problems can lead to CNIII lesions?
posterior communicating artery aneurysm, uncal herniation and trauma NOT PUPIL SPARING
33
What are the features of CNIII lesions?
ptosis abduction and dpression of eye in primary position ophthalmoplegia (only abduction of eye is normal) dilated pupil and accommodation abnormalties
34
What are some vascular syndromes of CNIII palsies?
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
What are some causes of CNIV lesions?
congenital CNIV palsy, closed head trauma and microvascular ischaemia
36
What are the features of CNIV lesions?
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
What are the 3 steps of the Park-Bielschowsky test for CNIV lesions?
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
What are some causes of CNVI lesions?
microvascular ischaemia (most common) other causes: trauma, idiopathic and ICP
39
What are some features of CNVI lesions?
HORIZONTAL double vision, worsened on looking at distant targets esotropia in primary position limited abduction
40
What are some syndromes that cause sixth nerve palsies?
Foville syndrome Millard Gaublar syndrome Gardenigo syndrome
41
What is fovile syndrome?
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
What is millard-Gublar syndrome?
Lesions to VENTRAL pons CNVI palsy Contralateral hemiplegia due to damage to corticospinal tract ipsilateral CNVII palsy
43
What is gardenigo syndrome?
Causes: otitis media, mastoiditis or petrositis unilateral periorbital pain diplopia otorrhoea
44
What is internuclear ophthalmoplegia?
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
What is one and half syndrome?
lesion to the PPRF and MLF on the same side, usually due to stroke ONLY abduction of the contralateral eye can still occur
46
What is parinaud syndrome?
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
What is progressive supranuclear palsy?
neurodegenerative disorder characterised by vertical gaze palsy, slowing of vertical saccades postural instability parkinsonism
48
What is nystagmus?
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
What is end point nystagmus?
nystagmus at extreme gaze
50
Waht is optokinetic nystagmus?
nystagmus due to fast moving objects
51
Describe congenital nystagmus
horizontal, pendular / jerky DISAPPEARS DURING SLEEP
52
What are some causes of congenital nystagmus?
sensory deprivation (bilateral cataracts) optic nerve hypoplasia foveal hypoplasia
53
Describe latent nystagmus
horizontal and jerky only present on monocular occlusion (direction is away from the covered eye) most commonly associated with infantile esotropia
54
What is convergence-retraction nystagmus?
co-contraction of horizontal muscles on attempted upgaze causing the globe to retract caused by dorsal midbrain lesions e..g parinaud syndrome
55
Which EOM is the most powerful?
Medial Rectus
56
What is upbeat nystagmus?
downward drifting of the eye followed by a fast upward corrective saccade or beat mainly due to medulla lesions
57
What is downbeat nystagmus?
upward drifting of eye followed by fast downward corrective saccade mainly due to lesions at the craniocervical junction such as Arnold-Chiari malformation
58
What is peripheral vestibular nystagmus?
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
What is myasthenia gravis?
AI condition affecting post synaptic, nicotinic acetylcholine receptors leads to muscle fatiguability
60
When does myasthenia gravis present?
3rd decade of life female predominance
61
Which muscles are affected in myasthenia gravis?
voluntary muscles smaller ones first
62
What are the features of myasthenia gravis?
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
What investigations are used for myasthenia gravis?
Ice test antibodies: anti-AChR antibodiy and anti MUSK repetitive nerve stimulation (decrement of muscle action potential amplitude) CT thorax: may reveal thymoma
64
How is myasthenia gravis managed?
acetylcholinesterase inhibitors e.g. pyridostigmine steroids immunomodulators thymectomy if thymoma
65
What is myotonic dystrophy?
abnormal muscular relaxation and muscle wasting AD condition, due to tri-nucleotide repeats on chromosome 19
66
what are the features of myotonic dystrophy?
inability of muscle relaxation early-onset cataracts: polychrmatic opacities, Christmas tree cataracts Ptosis Ophthalmoplegia
67
What is Kearns-Sayre syndrome?
mitochondrial inherited myopathy due to deletion of mitochondrial DNA
68
What does histopathology of kearns-sayre syndrome show
ragged red fibres (increased intramuscular accummulation of mitochondria)
69
how does kearns-sayre present?
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
What is miller fisher syndrome?
variant of Gullain Barre Anti-GQ1b may be present
71
Describe the features of miller fisher
tetrad ataxia areflexia ophthalmoplegia facial diplegia
72
What is NF1?
AD multisystem disorder due to mutation in the neurofibromin 1 gene on Chr 17
73
What are the features of NF1?
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
What is NF2?
less common than NF1 mutation on neurofibromatin 2 gene on chr 22
75
What are the features of NF2?
posterior SUBSCAPULAR cataracts bilateral / unilateral acoustic neuromas causing decreased sensorineural hearing loss, tinnitus and loss of corneal reflex Meningiomas
76
What is tuberous sclerosis?
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
What is benign essential blepharospasm?
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
What is meige syndrome?
blepharospasm and oromandibular dystonia
79
How is benign essential blepharospasm managed?
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