CM- Causes of Acute Vision Loss Flashcards Preview

Nervous System > CM- Causes of Acute Vision Loss > Flashcards

Flashcards in CM- Causes of Acute Vision Loss Deck (40)
Loading flashcards...
1
Q

Where is the likely lesion if a patient has unilateral vision loss?
Bilateral vision loss?

A
Unilateral = disease of the eye itself, or optic nerve 
Bilateral = lesion of the chiasm, or posterior to the chiasm [unless both optic nerves are blown]
2
Q

If vision loss is improved by viewing through a pinhole, what is the vision loss due to?

What if vision is NOT improved?

A
  1. uncorrected refractive error
  2. media disturbance- tear film abnormality, cataract, vitreous opacity]

If vision is not improved, the problem is structural or has some other physiologic etiology

3
Q

A patient experiences transient loss of vision and “sparkles” in both eyes lasting 15-20 minutes. What is this highly suggestive of?

A

Migraines [bilateral nature suggests occipital cortex involvement]

4
Q

What is transient painless monocular loss of vision due to?

A

emboli from the carotid arteries [Hollenhorst plaques] or from the heart

5
Q

What is the DDx for sudden unilateral visual loss?

A
  1. retinal vascular occlusion
  2. optic neuritis
  3. ischemic optic neuropathy
  4. embolic phenomenon
6
Q

What is the DDx for progressive visual loss with insidious onset?

A

compression of the optic pathway by:

  1. tumor
  2. aneurysm
7
Q

The visual phenomenon of _______ always recovers fully after 20 minutes. __________ is significantly resolved after 6-8 weeks. ____________ typically does not improve.

A

Migraines- recover in 20 min
Optic neuritis= 6 to 8 weeks
Ischemic optic neuropathy = no improvement

8
Q

What can color vision defects imply?

A
  1. optic nerve disease
  2. central macular disease
  3. congenital
9
Q

What 3 main things cause media opacity and acute vision loss?
How are they differentiated?

A

irregularity/opacity of the clear refractive media can cause blurred/decreased vision with NO pupillary changes

  1. acute-angle glaucoma causes corneal edema. it is a RAPID process with increased ICP
  2. cataracts opacify the lens. Usually it develops slowly& with age, but it cn arise quicker with trauma or inflammation. PUPIL WILL BE WHITE/CLOUDY, decreased red reflex
  3. vitreous hemorrhage- secondary to trauma or neovascularization [diabetes or retinal vein occlusion]
10
Q

A patient says that in his left eye he saw flashing lights and small black dots that drifted about. After that he experienced a shade of darkness over the vision in one eye that started peripherally and worked toward central vision. What is the most likely problem?
What will you notice when assessing his pupils?

A
Retinal detachment
He will have developed an afferent pupillary defect in the affected eye [left] 
So when you do the flashlight test:
1. light in right eye = both constrict
2. light in left eye = both dilate
11
Q

What is the pathological cause of retinal detachment?

How is it treated?

A

a hole in the retina allows fluid to flow under the sensory retina and detach it from the back of the eye.
It needs to be surgically treated prompty to close the hole and reattach the retina

12
Q

How do you differentiate retinal detachment from migraine in terms of presentation?

A

Migraine- bilateral “sparkles’ and vision loss that lasts 15-20 minutes then is fixed

Retinal detachment- unilateral flashing lights and floaters followed by peripheral to central curtain of darkness with pupillary defect. Does not improve spontaneously and requires prompt surgery

13
Q

What are the similarities and differences between central retinal artery occlusion [CRAO] and central retinal vein occlusion [CRVO] ?

A

Similarities:

  1. sudden, painless vision loss
  2. both present with afferent pupil defect

Differences

  1. CRAO - white,opaque retina with thin cherry red fovea; attenuated arterioles
  2. CRVO - retinal hemorrhages, venous engorgement, cotton-wool spots [white patches of retina that are microinfarcts]
  3. CRVO seen in hypertension, atherosclerotic vascular disease
14
Q

Why is CRAO a true ophthalmic emergency?

What is treatment?

A

It is a true emergency because permanent retinal damage can occur in 2hrs.

Treatment:
1. lowering intraocular pressure
2. attempting to induce arterial dilation to move the clot downstream
[treatment is of questionable efficacy]

15
Q

A 50 year old patient experiences painless transient vision loss in one eye. He says he has “attacks” where it looks as if a curtain were coming down over his vision. He said they develop in 30 seconds and usually last about 10minutes.

What is the Dx?
What is the pathological cause?
What is further treatment/assessment for the patient?
What is a person with this Dx at increased risk for?

A

Amaurosis fugax

It is caused by embolization from atherosclerotic plaques in the ipsilateral carotid [Hollenhorst plaque] or calcified heart valves

On fundic exam you may or may not see plaques lodged at the bifurcation of retinal arteries.

Requires complete neurological and medical assessment to determine the source of the embolus because these patients are at 4% increased risk of stroke w/in 5 years

16
Q

A 25 year old presents with sudden vision loss that is unilateral and painful on eye movement. She says it got progressively worse over about a week, but now it has stabilized.
Upon examination, you note an afferent pupillary defect. The optic disk shows swelling.

What is the most likely Dx?
What is the usual pathologic cause?
When should the patients vision improve?
What are possible lingering effects?
What are next steps for assessment/treatment?
A

Optic neuritis

  • usually caused by MS causing inflammation of the optic nerve due to demyelination
  • vision typically improves in 6-8 weeks
  • some lingering effects will be color vision and contrast sensitivity changes
  • MRI to look for evidence of MS, IV steroids/IFNb1a to delay onset of other symptoms of MS
17
Q

If a person is suspected of having optic neuritis, but does not show optic disk swelling, what is the likely location of the lesion?

A

Retrobulbar optic neuritis- lesion is further posterior to the nerve head

18
Q

What is the typical appearance of the optic disk with optic neuritis?

A
  1. blurred disk margins
  2. venous overfill
  3. hyperemia of the disk
19
Q

What is ischemic optic neuropathy?

How do you distinguish non-arteritic from arteritic?

A

Ischemic optic neuropathy is damage to the optic nerve head [disk] due to microvascular occlusion of the posterior ciliary arteries.

Non-arteritic:

  • 50 to 70
  • sudden loss in 1 eye that can be mild [20/30] to severe [counting fingers]
  • rarely progresses past day 3, but no recovery in affected eye
  • optic disc is pale/swollen for 4 to 8 weeks–> atrophy
  • risks: HTN, diabetes, cholesterol, smoking,CV disease

Arteritic:

  • 70-90 y
  • severe vision loss with no sensitivity to light
  • fever, weight loss, malaise, myalgia, temporal headache, jaw claudication, tenderness over temporal artery
  • ESR is over 60 [most over 90]
  • high risk of vision loss in other eye [treat with steroids to lower this risk]
20
Q

An 85 year old man presents with sudden severe vision loss in one eye. He has an APD. He has a fever and has been experiencing weight loss, malaise, myalgia, tenderness over temporal artery, and jaw claudication.

What test is a mandatory stat test for a presentation like this?

A

ESR to rule out arteritic ischemic optic neuropathy vs. non-arteritic

21
Q

What 4 things are on the DDx for papilledema?

A
  1. malignant HTN
  2. intracranial HTN from tumor or inflammation
  3. hydrocephalus
  4. idiopathic intracranial HTN [psedotumor cerebri
22
Q

How is papilledema differentiated from other causes of optic disk edema?

A

Papilledema :
bilateral and usually asymmetric
-normal visual acuity
- normal pupillary light response

Other optic disc swelling is:

  • unilateral
  • decreased visual acuity
  • APD
23
Q

What should papilledema be considered until proven otherwise?
What are the steps to determine the cause of the papilledema?

A

intracranial mass until proven otherwise!!

  1. MRI/CT if negative–>
  2. Lumbar puncture with measurement of opening pressure to rule out psuedotumor cerebri, CSF infection, inflammation, neoplasm
24
Q

How does the VF exam change if papilledema remains?

A

Initially the VF reveals a large blind spot. If the nerves remain swollen, axons will die and there will be nerve fiber layer VF defects –> blindness

25
Q

What will be the associated VF defect for a lesion at the optic nerve?
What are the 3 problems with optic nerve damage?
What will the optic disk look like?

A

VF= monocular loss of vision in the ipsilateral eye

  1. monocular central visual acuity loss
  2. color vision defect
  3. APD [Marcus Gunn]

Optic disk may be swollen, pale or normal

26
Q

What will be the associated field defect for a lesion at the optic nerve merging with the chiasm?

A

Monocular vision loss ipsilateral

Temporal field defect of contralateral eye

27
Q

What will be the associated field defect for a lesion of the optic chiasm?

A

bitemporal hemianopia [cannot see in either peripheral/temporal visual field]

  • may or may not be associated with loss of visual acuity
28
Q

What will be the associated field defect for a lesion in the left optic tract?

A

Homonymous hemianopia [you lose the right visual field in both eyes]

29
Q

What is the associated field defect for a lesion in the left geniculate body?

A

Same as for the optic tract -hononymous hemianopsia of the right side

30
Q

What is the associated field defect for a lesion in the left temporal lobe [left inferior optic radiation, Meyer’s loop]?

A

right upper quadrant defect [superior quadrantanopia]

31
Q

What is the associated defect for a lesion of the parietal lobe [left superior optic radiation]?

A

right lower quadrant defect

32
Q

What is the associated visual defect for a lesion of the occipital lobe ?

A

homonymous hemianopsia of the opposite side with macular sparing

33
Q

What is the effect of a retrochiasmal lesion on visual acuity?

A

Retrochiasmal defects do NOT cause central acuity loss [you can have 20/20 with one half a macula] unless other structures are affected or the lesion is bilateral

34
Q

The more _________ the lesion occurs in the post-chiasmal pathway, the more likely the defects will be congruous.

A

Posterior -
Fibers serving corresponding parts of the two retinas lie increasingly closer together as the fibers travel back into the occipital cortex

35
Q

What are chiasmal syndromes almost always caused by?

A

compression of the chiasm by a tumor, aneurysm or other mass lesion

  • one or both optic nerves/tracts are often involved
  • slow progressive visual loss [any age]
  • bitemporal VF loss, respecting the vertical meridian
36
Q

If there is compression of the chiasm, there should be bitemporal hemianopsia that respects the vertical meridian. If you do a vision map and notice spillover, what does this tell you about the defect?

A

Spillover represents the compression of a portion of the ipsilateral optic nerve superimposed on the chiasm compression

37
Q

With retrochiasmal lesions, where are incongruous VF defects most likely to occur?
Congruous?

A
Incongruous = optic tract, temporal, parietal lobes
Congruous = occipital cortex
38
Q

What are possible causes of retrochiasmal lesions?

What is necessary for localization?

A
  1. stroke
  2. mass
  3. aneurysm
  4. AV malformation

Localization depends on VF defect AND other neurological deficits like hemiparesis and aphasia.
Occipital lobe defects = pure VF defect

39
Q

What is the effect of homonymous hemianopia on visual acuity and pupillary response?

A
  1. no reduced acuity unless bilateral

2. no APD unless concurrent disease of optic nerve

40
Q

What is functional vision loss?

What will exams show?

A

Vision loss without organic basis [hysterical or malingering]

Exams will show results incompatible with organic blindness
ex. claimed complete blindness in one eye, but they have normal stereopsis and no APD