Glaucoma and Visually Evoked Potentials (M2) Flashcards Preview

II. Neurophysiology and Perception > Glaucoma and Visually Evoked Potentials (M2) > Flashcards

Flashcards in Glaucoma and Visually Evoked Potentials (M2) Deck (26):
1

What is glutamate excitotoxicity thought to be responsible for?

1. acute ischemic pathologies such as stroke in the CNS
2. some chronic neurodegenerative disorders

2

What are thought to be the first cells affected by glaucoma? 1. So which pathway did functional tests target? 2

1. parasol RGCs (larger RGCs)
2. magno pathway

3

What is the RGC death theory that suggests RGC axons pinched at the lamina cribosa, disrupting axoplasmic flow?

neurotrophin deprival hypothesis

4

What does ischemic anterior optic neuropathy result in?

optic nerve pallor but NOT optic nerve cupping

5

If a disease primarily affects the magno pathway, what does the patient have a decreased sensitivity to?

1. low spatial frequencies
2. high temporal frequencies

6

What are FDT perimetry testing capable of catching?

some early damage to moderate glaucoma

7

What happens to the lamina cribosa during POAG?

1. thinner laminar beams
2. bigger pored superiorly and inferiorly

8

What is the most important risk factor for primary open-angle glaucoma?

IOP

9

What can VEP be used for?

1. measure of VA and contrast sensitivity in patients with communication difficulties
2. helpful in cases of malingering

10

About what percentage of RGCs had to die in order for visual field defects to be detectable?

50%

11

Where is the initial damage to RGC axons during POAG?

lamina cribosa

12

What are the retinal neurons that are affected in glaucoma?

retinal ganglion cells (RGCs) only

13

What is most of the electrical activity detected using VEPs due to?

the fovea

14

What is the idea that there should be tests that use specific stimuli that target distinct populations of RGCs (target magno vs. parvo vs. konio)?

multi-channel theory

15

What is the idea that as retinal ganglion cells die ,they are capable of releasing signals that can cause adjacent RGCs to die? 1. What does this hypothesis help to explain? 2. What are the therapeutic types that are designed to prevent this? 3

1. secondary degeneration
2. continued progression of RGC death once IOP has been lowered
3. neuroprotection

16

At what wavelength is there a greater sensitivity to color versus flicker?

less than 475nm

17

What can measure the small waves of activity generated in the occipital lobe when the eyes are stimulated with complex stimuli?

visually evoked potentials electrodes

18

What does neurotrophin deprivation in RGCs cause the cell to do?

program apoptosis

19

What is the idea that the decreasing blood supply to the optic nerve results in RGC death called?

vascular compromise

20

What is the most commonly attempted method to obtain neuroprotection? 1. Why? 2

1. blocking glutamate receptors
2. most common excitatory neuron in the retina and involved in the vertical pathway

21

What does the activation of glutamate receptors cause for cells? 1. When is this a problem? 2

1. calcium ions enter into neurons through channels
2. too much calcium triggers apoptosis

22

Why is SWAP successful at catching glaucoma earlier if it targets the konio pathway?

redundancy in the visual system when a pretty non-specific stimulus is used

23

What is the rank of glaucoma in terms of leading causes of blindness in the world? 1. America? 2

1. second (glaucoma #1)
2. second (ARMD #1)

24

What tests are decreased with open-angle glaucoma?

CFF's decreased

25

What is the test that has grating alternating at over 25 Hz which causes an illusion in which you see double the actual gratings? 1. What is varied in the test? 2

1. FDT perimetry (frequency doubling)
2. contrast varied and threshold of detection determined

26

At what wavelength is there a greater sensitivity to flicker versus color?

between 575 and 600nm