Glaucoma and Visually Evoked Potentials (M2) Flashcards
What is glutamate excitotoxicity thought to be responsible for?
- acute ischemic pathologies such as stroke in the CNS
2. some chronic neurodegenerative disorders
What are thought to be the first cells affected by glaucoma? 1. So which pathway did functional tests target? 2
- parasol RGCs (larger RGCs)
2. magno pathway
What is the RGC death theory that suggests RGC axons pinched at the lamina cribosa, disrupting axoplasmic flow?
neurotrophin deprival hypothesis
What does ischemic anterior optic neuropathy result in?
optic nerve pallor but NOT optic nerve cupping
If a disease primarily affects the magno pathway, what does the patient have a decreased sensitivity to?
- low spatial frequencies
2. high temporal frequencies
What are FDT perimetry testing capable of catching?
some early damage to moderate glaucoma
What happens to the lamina cribosa during POAG?
- thinner laminar beams
2. bigger pored superiorly and inferiorly
What is the most important risk factor for primary open-angle glaucoma?
IOP
What can VEP be used for?
- measure of VA and contrast sensitivity in patients with communication difficulties
- helpful in cases of malingering
About what percentage of RGCs had to die in order for visual field defects to be detectable?
50%
Where is the initial damage to RGC axons during POAG?
lamina cribosa
What are the retinal neurons that are affected in glaucoma?
retinal ganglion cells (RGCs) only
What is most of the electrical activity detected using VEPs due to?
the fovea
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
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
- secondary degeneration
- continued progression of RGC death once IOP has been lowered
- neuroprotection