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neuro-optham 2 Flashcards

1
Q

causes of chiasmatic lesions and their visual defect

A

large pituitary adenoma
- Bitemporal superior quadrantanopia which progress to bitemporal
hemianopia.

craniopharyngioma
- Bitemporal inferior quadrantanopia which can progress to bitemporal hemianopia.

tuberculum sellae meningioma
- Can affect the anterior angle of chiasm causing a junctional scotoma.

aneurysms

  • A large anterior communicating artery aneurysm may cause bitemporal hemianopia.
  • Bilateral internal carotid aneurysms may cause binasal hemianopia as they affect the temporal portions of the chiasm.
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2
Q

causes of cranipharyngioma

A

growth failure

delayed puberty

headaches

diabetes insipidus

obesity

hypothyroidism in children

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3
Q

visual defect of optic tract

A

● Contralateral incongruous (asymmetrical) homonymous hemianopia.

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4
Q

visual defect if temporal radiations, parietal radiations, main radiations

A

● Temporal radiations: Contralateral incongruous superior homonymous quadrantanopia ‘pie in sky’.

● Parietal radiations: Contralateral incongruous inferior homonymous quadrantanopia ‘pie in floor’.

● Main radiations: Contralateral incongruous homonymous hemianopia.

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5
Q

visual defect it occipital cortex

A

● Occlusion of the calcarine artery of the posterior cerebral artery: Contralateral congruous homonymous hemianopia with macular sparing.

● Damage to the tip of the 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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6
Q

causes of CNIII lesions

medical
surgical

A

Medical problems
- diabetes
- hypertension
—- they affect the blood supply to the nerve. However, they are usually pupil- sparing, as pupillomotor fibres are located superficially within the nerve and are
supplied by pial blood vessels (which are not affected in these conditions).

Surgical problems, however, are pupil involved, as the pupillomotor fibres are damaged or compressed. Surgical causes include posterior communicating artery
aneurysm, trauma and uncal herniation.

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7
Q

features of CNIII lesions

A

● Ptosis.
● Abduction and depression of the eye in primary position (‘down and out’)
with ophthalmoplegia (only abduction of the eye is fully normal).
● Dilated pupil and accommodation abnormalities.

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8
Q

vascular syndromes of CNIII palsies and their effect

A

Weber syndrome
● CNIII palsy
● Contralateral hemiparesis (damage to the cerebral peduncle)

Benedikt syndrome
● CNIII palsy
● Contralateral hemiataxia and hemitremor (damage to the red nucleus)

Nothangel syndrome
● CNIII palsy
● Ipsilateral cerebellar ataxia (damage to the superior cerebellar peduncle)

Claude syndrome
● Benedikt + Nothangel

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9
Q

CNIV lesions aetiology

A

congenital CNIV palsy

closed head trauma

microvascular ischaemia.

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10
Q

features of CNIV lesions

A

● Vertical diplopia: Worse on walking downstairs or looking down.
● Hypertropia: The affected eye is higher than the contralateral eye. It is made
worse on tilting the head to the ipsilateral shoulder.
● Depression of the eye is limited: Most noted on adduction.
● Compensatory head posture to avoid diplopia: Patients tend to develop a
contralateral head tilt and face turn.
● Bilateral CNIV palsies can present with compensatory depressed chin
posture and crossed hypertropia.

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11
Q

Examination of CNIV lesions and the name of the test

A

Park-Bielschowsky three-step test can be used to identify a superior oblique palsy.

  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. With the patient fixating at a target ahead, assess hypertropia on right and left head tilts. Hypertropia gets better on contralateral head tilt in CNIV palsy (better on opposite tilt [BOOT]).
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12
Q

aetiology of CNVI lesions

A

● Microvascular ischaemia (most common).

● Other causes: Trauma, idiopathic and ICP.

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13
Q

features of CNVI lesions

A

● Horizontal double vision: Worse on looking at distant targets.
● Esotropia in primary position.
● Abduction is limited.

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14
Q

what is foville syndrome

A 
● Lesion to the inferior medial pons
● CNVI palsy
● Ipsilateral facial numbness (CNV)
● Ipsilateral facial paralysis (CNVII)
● Loss of taste sensation to the anterior two-thirds of the tongue
● Horner syndrome
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15
Q

what is Millard-Gublar syndrome

A

● Lesion to the ventral pons
● CNVI palsy
● Contralateral hemiplegia due to damage to the corticospinal tract
● Ipsilateral CNVII palsy

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16
Q

what is gradenigo syndrome

A

● Causes: Otitis media, mastoiditis or petrositis
● Periorbital pain unilaterally (CNV)
● Diplopia (CNVI palsy)
● Otorrhoea

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17
Q

what is internuclear opthalmoplegia

A

● Lesion to the MLF, commonly caused by demyelination or stroke.
● Defective adduction of the eye ipsilateral to the lesion and abducting
nystagmus of the contralateral eye.
● Patients may complain of horizontal diplopia.

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18
Q

what is one and a half syndrome

A

● Lesion to the PPRF and MLF on the same side, commonly caused by a stroke.
● The only movement left is the abduction of the contralateral eye.

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19
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 (not reactive to light but constrict on
accommodation).
20
Q

what is progressive supranuclear palsy

A

A neurodegenerative progressive disorder characterized by vertical gaze palsy, slowing of vertical saccades, postural instability and parkinsonism.

21
Q

what is nystagmus

A

involuntary rapid and repetitive oscillation of the eye which can be physiological or pathological. There is a risk of amblyopia in young patients with nystagmus, so it is important to correct refractive error and treat the underlying cause.

22
Q

what is end-point nystagmus

A

nystagmus at extreme gaze

23
Q

what is optokinetic nystagmus

A

Nystagmus due to fast-moving repetitive objects.

24
Q

what is congenital nystagmus

A

● The nystagmus is horizontal, pendular or jerky and disappears during sleep. It often has a null point – a position of gaze where nystagmus is minimal.
● Common causes include sensory deprivation (e.g. bilateral cataracts), optic nerve hypoplasia or foveal hypoplasia (e.g. albinism).

25
Q

types of acquired nystagmus

A 
latent
convergence-retraction nystagmus
upbeat nystagmus
downbeat nystagmus 
peripheral vestibular nystagmus
26
Q

what is latent nystagmus

A

● Horizontal and jerky nystagmus, but only becomes present on monocular occlusion (direction is away from the covered eye).
● Most commonly associated with infantile esotropia.

27
Q

what is convergence-retraction nystagmus

A

● Co-contraction of horizontal muscles on attempted upgaze causing the globe to retract.
● The medial rectus is the most powerful EOM. This causes eye convergence.
● Caused by dorsal midbrain lesions (e.g. Parinaud syndrome).

28
Q

what is upbeat nystagmus

A

Downward drifting of the eye followed by a fast upward corrective saccade or beat. Caused mainly due to medulla lesions.

29
Q

what is downbeat nystagmus

A

Upward drifting of the eye followed by a fast downward corrective saccade or beat. Caused mainly due to lesions at the craniocervical junction such as Arnold-Chiari malformations.

30
Q

what is peripheral vestibular nystagmus

A

A conjugate horizontal and jerky nystagmus that occurs due to a vestibular lesion (e.g. labyrinthitis). There is a slow drifting of the eyes towards the side of the lesion followed by a fast corrective saccade in the other direction.

31
Q

what is myasthenia gravis and seen inwho mostly

A

Autoimmune disease affecting the post-synaptic nicotinic acetylcholine receptors (AChR) at neuromuscular junctions, leading to muscle fatigability.

It typically presents in the third decade of life and has a female predominance.
It affects voluntary muscles, and smaller muscles are affected first. Ocular involvement is commonly the presenting feature.

32
Q

features of myasthenia gravis

A

● Ptosis: Bilateral (can be unilateral initially), worse at end of the day or after prolonged upgaze.
● Cogan lid twitch: A brief upshoot of the lid elicited by making patient look downwards then upwards.
● Diplopia.
● Ophthalmoplegia.
● Fatigability and weakness of muscles of facial expression and proximal limb
muscles.
● Respiratory depression.

33
Q

Ix for myasthenia gravis adn what will u see in them

A

● Ice test: Ptosis improves after applying ice for 2 minutes.
● Antibodies: Anti-AChR antibody and anti-muscle-specific kinase (MUSK)
antibody.
● Repetitive nerve stimulation (decrement of muscle action potential amplitudes).
● CT thorax: Can reveal a thymoma.

34
Q

Mx for myasthenia gravis

A

● Acetylcholinesterase inhibitors (e.g. pyridostigmine), steroids and immunomodulators.
● Thymectomy if thymoma is present.

35
Q

what is myotonic dystrophy

A

abnormal muscular relaxation and muscle wasting. It is an AD condition due to tri-nucleotide repeats on chromosome 19.

36
Q

features of myotonic dystrophy

A 
● Inability of muscle relaxation.
● Early-onset cataract: Polychromatic opacities on the lens resembling a
‘Christmas tree’ cataract.
● Ptosis.
● Ophthalmoplegia.
37
Q

what is kearnS-SAYRE SYNDROME

A

Mitochondrial inherited myopathy due to deletion of mitochondrial DNA. Histopathology reveals ‘ragged red fibres’ due to increased intramuscular accumulation of mitochondria.

38
Q

triad of kearns-sayre syndrome

A

● Bilateral, symmetrical ptosis and ophthalmoplegia.
● Pigmentary retinopathy with ‘salt and pepper’ appearance involving the macula.
● Cardiac conduction defects.

39
Q

what is Miller FIsher syndrome and its features

A

A rare variant of Guillain-Barre syndrome. Anti-GQ1b antibodies may be present.

tetrad of ataxia, areflexia, ophthalmoplegia and facial diplegia.

40
Q

what is neurofibromatosis 1

A

Neurofibromatosis type 1 (NF1) is an AD multisystem genetic disorder due to a mutation in the Neurofibromin 1 gene on chromosome 17.

41
Q

features of neurofibroamtosis 1

A

● Café-au-lait spots: Brownish spots most commonly found on the trunk.
● Axillary freckling.
● Ophthalmic
Optic nerve glioma.
Bilateral Lisch nodules (iris hamartomas).

Plexiform neurofibromas: ‘Bag of worms’ sensation in the eyelids
- Choroidal naevi: Patients with this have a higher risk of choroidal melanoma

42
Q

what is neurofibromatosis type 2

A

Neurofibromatosis type 2 (NF2) is less common than NF1. It occurs as a result of a mutation to the Neurofibromin 2 gene on chromosome 22.

43
Q

features of neurofibromatosis type 2

A

● Posterior subcapsular cataracts.
● Bilateral/unilateral acoustic neuromas causing decreased sensorineural
hearing loss, tinnitus and loss of corneal reflex.
● Meningiomas.

44
Q

what is tuberous sclerosis and its characteristics

A

AD multisystem disorder characterized by the following.
● Facial angiofibroma.
● Ash-leaf spots: Hypopigmented macules on the skin.
● Seizures.
● Cognitive impairment.
● Multiple intracranial and/or retinal astrocytic hamartomas
Glial tumours of retinal fibre layer that arise from astrocytes.
They are commonly referred to as mulberry lesions due to their multinodular appearance. On fundoscopy they appear as well-defined elevated creamy white lesions.
Associations
– Tuberous sclerosis (most common association) – Neurofibromatosis
– Retinitis pigmentosa (less common; lesions are non-calcified)

45
Q

what is benign essential blepharospasm

A

A bilateral idiopathic condition characterized by involuntary contraction of the orbicularis oculi muscle due to basal ganglia dysfunction.

46
Q

presentation of benign essential blepharospasm

A

ixth decade of life, with a female predominance. Blepharospasm and oromandibular dystonia can occur together in Meige syndrome

47
Q

Mx of benign essential blepharospasm

A

● Artificial tears for dry eyes.
● Botulinum toxin injection to orbicularis oculi. Side effects: Ptosis, dry eye,
diplopia, lagophthalmos and corneal exposure.
● Surgical myectomy if the above does not work.

DEP (20 decks)

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