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
Q

What is Bell’s Palsy and it’s risk factors?

A

• 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
Q

What is the cause if Bells Palsy?

A

Unknown!
Sometimes associated with:
• latent virus infection (HSV type 1, HZ)
• influenza
• respiratory tract infections
• depleted immune system
• stress

27
Q

What are Bell’s Palsy systemic symptoms?

A

• 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
Q

What does the ocular exposure from bells palsy cause?

A

• redness
• discomfort
• pain
• photophobia
• watering of eye (epiphora)

29
Q

What are some Bells Palsy facial signs?

A

• 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
Q

What are the ocular Bells Palsy signs?

A

• 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
Q

What happens if the corneal erosions:punctuate etc in Bells palsy is left to develop?

A

• Corneal desiccation ranges from mild superficial punctate erosions to frank ulceration (usually inferior)

32
Q

What are Bell’s Palsy differential diagnosis?

A

• 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
Q

What are ocular differential diagnosis of bells palsy and Lagopthalmos?

A

• 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
Q

What is the prognosis for Bell’s Palsy?

A

• Fair prognosis without treatment
• 82% recover normal function within 9 months
• Most improvement occurs within 3 weeks

35
Q

What is the prognosis for Bell’s Palsy? (Which don’t recover) and the risks associated with non recovery?

A

• 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
Q

What are the Complications of Bell’s Palsy?

A

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
Q

What are the Complications of Bell’s Palsy?

A

• 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
Q

How can Bells Palsy be managed by an optometrist?

A

• 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
Q

How can Bells Palsy be managed by an Opthalmologist?

A

• Urgent medical treatment for new cases with systemic steroid
• Surgery for permanently unrecovered cases