visual neuro final cards !! Flashcards
diabetes
haemorrhage
ischemia -> leaky vessels
basement membrane thickness increase
loss of pericytes -> increased vascular perm.
microaneurisms
stroke
blood vessel diameter can be a predictor
parkinsons
OPL thickening -> a-syn deposits
RNFL thinning and decreased macular thickness
alzheimers
b amyloid plaques can be seen using hyperspectral imaging
rnfl thinning bc decreased GCs
MS
loss of GCs
hypertension
ratio between art : vein thickness alters
art narrowing = increased pressure = squishes veins
blood retinal barrier breakdown
pupillary light reflex pathways - dilation
absence of light
sympathetic NS
sphincter muscles relax
dilate for emotion too
pupillary light reflex pathways - constriction
presence of light
parasympathetic NS
activate sphincter muscles
constrict for near vision
pupillary light reflex pathways - 3 neuron model
- hypothalamus -> thoracic s.c.
- thoracic sympathetic trunk -> long ciliary
- dilator muscle (release NA to a1 rec)
horner’s syndrome
pupillary light reflex pathways 3 neuron pathway disrupted
can’t dilate eye
lid droops
no sweating
blood vessel dilation in this area
accessory optic system
birds & fish -> main visual area
mammals -> large field motion
optokinesis & vestibular connections
nystagmus = involuntary eye movements
accessory optic system - inputs
MT/MST and V1
super colliculus
directing eye based on attention (and maintaining gaze on something)
humans -> in cortex
birds -> ventral and dorsal streams
bimodal and tri modal neurons
suprachiasmatic nucleus
input from: intrinsically photosensitive GCs
circadian rhythm
pulvinar nucleus of the thalamus - input and output
input -> both layers of SC
output -> wide to cortical visual areas & parietal cortex
pulvinar role
lesion =?
combine different pieces of information
lesion = facial rec. issues
activation for angry (closed mouth) and surprised facial expressions
simple vs complex cells (huber and wiesel)
simple -> small r.f., separate on and off, L4 and 6
complex -> large r.f., overlapping on and off, outside L4
issues with hubel and wiesel
- remove inhibition to striate cell = no orientation sel
- complex often respond to stimuli simple cells don’t -> so how can complex get input from simple?
- both complex and hypercomplex can be monosynaptically excited from LGN
- simple and complex distinction doesn’t apply at low contrast or after adaptation
saccades: FEF, PPC, DLPFC
fef: voluntary
ppc: reflex
dlpfc: inhib reflex
latency: vor vs okn
okn - 80ms
vor - 7ms
endogenous attention can be split into two types - what are they
spatial (attend to road while driving)
feature based (alll red cars in car park)
____ rf along ventral steam
increased
v1 v4 teo te
when do critical periods end?
- axonal growth stops = can’t change arbor length
- synaptic transmission fully matures
- neuromodulator activity decrease
why critical periods?
adapt developing ns to enviro, fine tune and calibrate cells
strabismic amblyopia
eye misalignment
double image
image doesn’t fall on fovea
anisometropic amblyopia
different glasses prescription between the two eyes -> dissimilar for the brain to connect
stimulus deprivation amblyopia
occluded optical axis
something blocking light from getting to retina
refractive error amblyopia
can be fixed w glasses
neural basis for amblyopia
brain prefers one eye, this can lead to cortical changes -> loss of OD columns for that eye
levi and hess drama !!!
hess -> neural dissarray (wrong info given to next step)
levi -> undersampling to incorrect sampling (rf size increase -> start acting like peripheral cells)
then daminin came in and said its the same thing
then levi revised saying neural noise impacts effectiveness of sampling
blindsight
MT (and pulvinar) bypasses V1 so even if someone has a full V1 lesion and cant see they can still go through a maze
