Neuro Ophthalmology 1 Flashcards

1
Q

Where is early papillaedema first apparent?

A

Inferior and superior fields

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2
Q

What percentage of the general population exhibit spontaneous venous pulsations?

A

80%

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3
Q

What neurological findings can be found in idiopathic intracranial hypertension?

A

CN VI, other neurological deficits are not found except in juvenile IIH

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4
Q

What is the etiology of naion?

A

Presumably compromised micro circulation in discs at risk

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5
Q

What is the 5 year risk of contalateral involvement in naion?

A

15%

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6
Q

What is pseudo-foster Kennedy syndrome?

A

Contralateral involvement of naion which shows disc edema while the initial naion eye shows atrophy/palor

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7
Q

What layers of the lgb receive uncrossed fibers?

A

2, 3, 5

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8
Q

“Pie in the sky” VF defect is caused by injury to what fibers?

A

Meyers loop (temporal fibers)

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9
Q

Object agnosia

A

Inability to recognize objects. Localizes to bilateral occipitotemporal (ventral pathway) dysfunction.

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10
Q

Prosopagnosia

A

Inability to recognize faces. Localizes to bilateral occipital lobe. Seen in patients with Alzheimer’s.

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11
Q

Akinetopsia

A

Loss of perception of motion

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12
Q

Alexia without agraphia

A

Can’t read but can write, disruption between occipital lobe and the dominant angular gyrus

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13
Q

Simultanagnosia

A

Inability to see several events in a scene and integrate a total picture/scene

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14
Q

Balint syndrome

A

Injury to bilateral occipitoparietal lobes resulting in triad of simutanagnosia, optic ataxia, oculomotor apraxia

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15
Q

Anton syndrome

A

Denying visual deficits when in fact cortical blindness is reality.

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16
Q

Riddoch phenomenon

A

Preservation of the perception kinetic but not static vision. Portends a better outcome. Also termed staticokinetic dissociation.

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17
Q

When evaluating anisicoria, what other parts of the ocular exam should you pay close attention to?

A

Eom and lid position (for cn 3 involvement)

18
Q

Tadpole pupil

A

Focal spasm of iris dilator muscle causing a peaking of the pupil lasting minutes occurring numerous times intermittently. May harbor

19
Q

Midbrain corectopia

A

Eccentric or oval pupils from rostral midbrain disease.

20
Q

What is the gtt sequence used in testing for a horners pupil?

A
  1. Apply 10% cocaine and anisicoria will increase (miotic horners pupil does not dilate well)OrApply 1 or 5% apraclonidine and see reversal of miotic versus dilated pupil2. >24 hours later apply paredrine (hydroxyamphetamine) to decipher which order neuron
21
Q

What is the differential for anisicoria greater in dark? (Abnormally small pupil)

A

Pharmocoligic, inflammatory (synechia binds down), horners, chronic adies, argyll Robertson (although always bilateral)

22
Q

What is the differential for anisicoria greater in the light (abnormal pupil is large)?

A

Iris sphincter tear, physiologic, 3rd nerve palsy, adies, pharmocologic,

23
Q

What are other ophthalmic signs of horners syndrome besides the classic triad?

A
  1. Lower iop on affected side2. Conjunctival hyperemia (decreased sympathetic vascular tone)3. Iris heterochromia (congenital horners)4. Transient increase in accommodation (older patients hold the near card closer on the affected eye.
24
Q

Are argyll Robertson pupils always bilateral?

A

Yes, although may be asymmetric

25
Q

What is a basic differential for light-near dissociation?

A

Bilateral optic neuropathy or severe retinopathyArgyl Robertson pupilsAdies tonic pupilsDorsal midbrain (paranauds) syndromeDiabetes, alcoholismAberrant 3rd nerve regeneration

26
Q

The saccadic system generates eye movements how fast? Smooth pursuit system?

A

400-500 degrees/sec; 30-60 degrees/sec

27
Q

What is the active forced generation test?

A

Patient is asked to look in a directin against force of an instrument grasping,

28
Q

Congenital ocular motor apraxia is characterized by….

A

Absence or defect in controlled, purposeful, and voluntary eye movementpatients must turn their heads to seeno nystagmus induced on okn drum testing horizontally

29
Q

At what point should a patient with optic neuritis start to demonstrate vision improvement?

A

1 month. If no improvement or worsening nmo should be considered

30
Q

What is the diagnostic criteria for NMO?

A

-Optic neuritis-Myelitis-2 of the following1. Spinal cord lesion spanning >3 vertebral segments2. MRI brain non-diagnostic for ms3. Nmo IgG positive

31
Q

What is a good way to differentiate skew vs superior oblique palsies that have similar appearing deviation patterns?

A

There is in torsion in skew deviation vs ex torsion in superior oblique palsy

32
Q

Excyclotorsion of how much suggests bilateral superior oblique palsy?

A

More than 10 PD

33
Q

What AHP (abnormal head position) would someone with bl so palsy show?

A

Chin down (doesn’t make sense to me bc there is a V pattern deviation)

34
Q

What percentage of the visual cortex is devoted to macular fibers?

A

80%

35
Q

The occipitotemporal pathway is also called the “what” or “where” pathway? Is it ventral or dorsal? How about the occipitoparietal pathway?

A

“what” pathway which is ventral; “where” pathway which is dorsal

36
Q

Ocilopsia would localize to failure of which of the 6 eye movement pathways?

A

Vestibular

37
Q

What is the purpose of the optokinetic pathway?

A

To track full field visual motion

38
Q

There are two main categories of brainstem saccade generators, the horizontal saccades and the vertical saccades. Where do the exitatory neurons originate for the horzontal and vertical saccades respectively?

A

Horizontal: PPRF (paramedian pontine reticular formation)Veritcal: riMLF (rostral interstitial nucleus of the medial longitudinal fasiculus)

39
Q

Does upward saccadic exitatory stimulation project bilateral or ipsilateral from the riMLF? Downward?

A

bilateral; ipsilateral

40
Q

Which center coordinates vergence movements?

A

MRF (midbrain reticular formation) premotor neurons project to CN nuclear complex to stimulate the near triad