Week 3 - Neuro 2.2 Flashcards

1
Q

What is Nystagmus and what may cause it?

A

Abnormal eye movements may occur because:
• Inability to maintain fixation
• Loss of normal inhibitory influences on eye movement control system
• Loss of normally symmetrical input from one of the vestibular pathways to the ocular motor nuclei

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2
Q

Why do Albino’s have Albinism?

A

• Inability to maintain fixation, with OCT of a patient with albinism:
Absence of a normal foveal contour, therefore no central point of fixation

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3
Q

What are the different phases of Nystagmus, and what does amplitude and frequency relate to nystagmus?

A

• Slow phase and rapid recovery phase
• slow phase - abnormal movement, drifting away from object of interest
• Rapid phase - recovery saccadic motion

• Amplitude (how far eyes move): coarse or fine
• Frequency (how fast eyes move): low, moderate, high

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4
Q

What are the 3 types of eye movements with nystagmus?

A

• Jerk: Slow drift, fast saccadic correction
• Pendular: Non-saccadic in both directions, slow
• Mixed: Pendular in primary position
Jerk on lateral gaze

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5
Q

What are the 8 types of acquired nystagmus?

A

• See-Saw
• Downbeat
• Upbeat
• Abducting nystagmus of INO
• Periodic alternating
• Pendular nystagmus
• Spasmus Nutans
• Gaze evoked

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6
Q

What causes See-Saw and downbeat nystagmus?

A

• See-Saw
- Midbrain lesions
- Pituitary tumours
- Severe visual loss
• Downbeat
- Cerebellum lesions
- Medulla lesions
- Idiopathic

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7
Q

What causes Upbeat and Abducting nystagmus of INO?

A

• Upbeat
- Medullary lesions
- Cerebellum lesions
- Benign positional paroxysmal vertigo
• Abducting nystagmus of INO
- Demyelination
- Brainstem stroke

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8
Q

What causes Periodic alternating and Pendular nystagmus?

A

• Periodic Alternating
- Arnold-Chiari
- Demyelination
- Trauma
- Encephalitis
- Syphilis
- Posterior fossa tumours
- Visual deprivation
• Pendular nystagmus
- Demyelination
- INO
- Brain stem dysfunction

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9
Q

What causes spasmus Nutans and Gaze-evoked nystagmus?

A

• Spasmus Nutans
- Idiopathic in children
- Glioma
• Gaze-evoked
- Drugs
- Alcohol

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10
Q

What needs to be asked during history of nystagmus?

A

• Onset
- Age, constant or intermittent, aggravating or alleviating factors (head position)
• Associated symptoms
- Symptoms of demyelinating disease
- Vertigo or oscillopsia; vestibular system abnormality
- Deafness/tinnitus in vestibular lesions
- Blurred vision
- Double vision in particular positions of gaze

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11
Q

How must motility be assessed with nystagmus?

A

First assess ocular stability in primary position.

Then examine in 9 cardinal positions to:
• Monocular or binocular
• Conjugation - do eyes behave similarly?
• Abnormal movements are horizontal, vertical, torsional or mixed
• Abnormal movements are continuous or are induced by particular eye positions
• Only, slow, fast, both phases are seen
•There is a null point

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12
Q

How is Nystagmus managed?

A

• Acquired - investigate for cause
• Advice
• Refractive management; spectacle choices
• Low vision aids

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13
Q

What is a Migraine?

A

• Periodic headaches with complete resolution between attacks
• 80% have 1st attack before 30yrs
• Prevalence increases until 40yrs then decreases
• 6-8% of men, 15-25% of women
• 15% of females only have attacks around menstruation

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14
Q

What are migraines caused by and what are the stages?

A

Can be associated with:
• certain foods (cheese, chocolate, coffee, red wine, shell fish)
• nausea or vomiting
• photophobia

Typical stages of an attack:
• Prodrome (warning symptoms of attack)
• Aura (visual disturbance, motor or sensory disturbance)
• Headache
• Resolution
Many types, variations of the above

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15
Q

What is a common migraine and its symptoms?

A

• Migraine without aura
• Headache and autonomic nervous system dysfunction (pallor, nausea)

• Prodrome: changes in mood, yawning, poor concentration
• Headache: pounding/throbbing, can start anywhere and spreads to half or whole head, photophobic and sensitive to sound
• Lasts from hours to a day

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16
Q

What is a classical migraine?

A

• Visual aura ; 20mins
• Paracentral scotoma: bright, positive
• Fortification spectrum enlarges after a few mins, lined on inner edge with negative scotoma
• Scotoma expands and moves towards temporal periphery before breaking up
• Full visual recovery within 30min
• Headache follows, usually opposite the hemianopia, associated with nausea and photophobia, can vary in severity - absent, trivial, severe

17
Q

What is a cluster headaches?

A

• Typically affects men in 30s and 40s
• Almost every day for a period of weeks, can go years between clusters
• Headache severe, starts suddenly, lasts 10min-2hrs
• Associated ocular features;(lacrimation, conjunctival injection and rhinorroea)

18
Q

What is a focal migraine, migraine sine migraine and a retinal migraine?

A

• Focal migraine
Symptoms of migraine as well as transient dysphasia, hemisensory symptoms, focal weakness
• Migraine sine migraine
Episodic visual disturbances without headache, typically elderly with history of classical migraine
• Retinal migraine
Unilateral visual loss, differential diagnosis retinal embolism.

19
Q

What is an Ophthalmoplegic migraine and familial hemiplegic migraine?

A

• Ophthalmoplegic migraine
- Rare
- Usually starts before age 10
- Recurrent 3rd nerve palsy after headache
• Familial hemiplegic migraine
- Neurological features continue after migraine attack subsides

20
Q

What is a Basilar migraine?

A

• Basilar migraine
- Affects children
- Bilateral numbness/tingling of extremeties and lips
- Ataxia of gait and speech can occur
- Sometimes loss of consciousness

21
Q

What are the differential diagnosis of migraine and other visual phenomena?

A

• Acute posterior vitreous detachment (flashes)
• Retinal detachment
• Transient ischaemic attack
• Transient visual obsurcations
• Occipital epilepsy (coloured circles during epileptic attack)

22
Q

what are the 3 types of facial spasm?

A

• Essential blepharospasm
• Facial hemispasm
• Bell’s Palsy

23
Q

What is an essential Blepharospasm?

A

• Uncommon but distressing Presents in 50s, F:M 3:1
• Progressive bilateral involuntary spasm of orbicularis oculi and upper facial muscles
• Cause unknown, likely to be mixture of genetic and environment
• Predisposing factors: reading, driving, stress, bright light
• Alleviated by: talking, walking, relaxing

24
Q

What is facial Hemispasm?

A

• Unilateral
• Age: 40s to 50s
• Brief spasm of orbicularis oculi spreading along facial nerve
• Idiopathic most commonly (aberrant blood vessels compressing on facial nerve) or due to irritation to nucleus of nerve (e.g. tumour, stroke, multiple sclerosis
• May occur several months/years after Bell’s palsy

25
What is Bell’s Palsy and it’s risk factors?
• Paralysis of facial nerve (VII cranial nerve) • Bell's Palsy constitutes 72% of all facial palsy: - Annual incidence 20 per 100,000 - Especially between 15 & 45 yrs - M = F (except in pregnancy) Bell's Palsy is more common in: • pregnancy • diabetes • HIV
26
What is the cause if Bells Palsy?
Unknown! Sometimes associated with: • latent virus infection (HSV type 1, HZ) • influenza • respiratory tract infections • depleted immune system • stress
27
What are Bell’s Palsy systemic symptoms?
• Sharp pain in the inner ear during the onset of paralysis • Impaired or altered sense of taste • Sensitivity to loud noises • Difficulty eating and speaking • Distressing cosmetic change due to loss of muscle tone on one side of face
28
What does the ocular exposure from bells palsy cause?
• redness • discomfort • pain • photophobia • watering of eye (epiphora)
29
What are some Bells Palsy facial signs?
• Brow droop • Upper lid retraction • Intercanthal line • Lower limbal line • Ptotic palpebral malar sulcus and nasojugal sulcus • Loss of nasolabial fold • Drooping corner of mouth
30
What are the ocular Bells Palsy signs?
• Unilateral orbicularis oculi weakness • Incomplete blink resulting in corneal drying, affects nighttime (Lagophthalmos), causing corneal exposure • Loss of lacrimal pump mechanism, pooling and epiphora caused • Conjunctival hyperaemia/oedema/staining
31
What happens if the corneal erosions:punctuate etc in Bells palsy is left to develop?
• Corneal desiccation ranges from mild superficial punctate erosions to frank ulceration (usually inferior)
32
What are Bell’s Palsy differential diagnosis?
• part of a stroke (cerebro-vascular accident with hemiplegia) • infection (e.g. otitis media, Lyme disease) • trauma (e.g. cranial fracture, facial laceration) • tumour (e.g. acoustic neuroma: damage to nerve by tumour or secondary to surgical trauma)
33
What are ocular differential diagnosis of bells palsy and Lagopthalmos?
• Entropion/ectropion Other causes of lagophthalmos: • orbital (thyroid eye disease) • mechanical (cicatricial - look for lid scarring) • physiological (patient's partner to check for full lid closure at night)
34
What is the prognosis for Bell’s Palsy?
• Fair prognosis without treatment • 82% recover normal function within 9 months • Most improvement occurs within 3 weeks
35
What is the prognosis for Bell’s Palsy? (Which don’t recover) and the risks associated with non recovery?
• In the remaining 20-30%, px is left with a degree of permanent facial paralysis Severe nerve damage is more likely to occur if the px: • Is over 60; • Had severe pain at onset; • Had complete rather than partial paralysis at onset; • Has diabetes or high blood pressure; • Was pregnant at the time of onset; • If recovery had not begun after six weeks.
36
What are the Complications of Bell’s Palsy?
Contracture of muscles • shortening of facial muscles over time : side of face appear to be slightly 'lifted’ • affected eye may appear smaller than the unaffected eye. • the fold between the outer edge of the nostril and the corner of the mouth may seem deeper due to the increased contraction of cheek muscles on that side.
37
What are the Complications of Bell’s Palsy?
• Crocodile tears The affected eye waters involuntarily, particularly whilst eating due to faulty 're-wiring' of the nerves during recovery phase • Synkinesis When intentionally trying to move one part of the face, another part automatically moves, e.g. on smiling, the eye on the affected side automatically closes.
38
How can Bells Palsy be managed by an optometrist?
• First aid measures and emergency referral in new cases - Improved prognosis with systemic corticosteroids 72hrs of onset • Recovering/established cases: no referral • Advice: Tape lids at night, sunglasses for photophobia, artificial tears during day, ointment at night, therapeutic lenses
39
How can Bells Palsy be managed by an Opthalmologist?
• Urgent medical treatment for new cases with systemic steroid • Surgery for permanently unrecovered cases