Visual and Pupillary Pathway

LGN location

dorsolateral (up and out) aspect of the thalamus on the left and right side of the thalamus

main purpose of LGN

processing visual info from the retina and filtering the most relevant info to V1

LGN location

dorsolateral (up and out) aspect of the thalamus on the left and right side of the thalamus

main purpose of LGN

processing visual info from the retina and filtering the most relevant info to V1

what terminates in the LGN

RGC axons

what are the axons that leave the LGN called

optic radiations

what helps filter LGN output

input from the superior colliculus and feedback from the visual cortex regarding visual signal

what are the 6 layers of the LGN for

bottom up:

layers 1&2: magnocellular

layers 3-6: parvocellular

where are the koniocellular layers

in between the 6 layers of the LGN

what is retinotopic mapping

each layer of the LGN only gets input from one eye

type of input depends on where the object is in the VF

fibers from each eye that carry info from the same part of the VF lie next to each other in the LGN

an object located in the right hemifield of each eye will project to the layers of the LGN in the (right/left) side

left

what layers do crossed and uncrossed fibers go to

uncrossed: 2, 3, 5

crossed: 1, 4, 6

ex: if something is located in the right visual field, it will project to the left LGN; contralateral nasal retinal fibers (temporal field of right eye) will go to layers 1, 4, and 6, while ipsilateral temporal retinal fibers (nasal field of left eye) will go to layers 2, 3, and 5

if something moves from the superior peripheral to inferior peripheral visual field, where does it travel in the LGN

medial to lateral

where do macular fibers project in the LGN

large central wedge

where do optic radiations leave the LGN

posteriorly

BV processing (does/does not) occur at the LGN

does not

receptive fields of magno and parvo cells

center surround

are parvo or magno cells most sensitive to red-green

parvo

parvo cells are sensitive to (high/low) SF and (high/low) temporal frequency

high SF (fine details)

low TF (slow movements)

magno cells are sensitive to (high/low) SF and (high/low) temporal frequency

low SF (large details)

high TF (fast movements)

what cells have a higher speed of visual signal transmission and why

magno

have larger axons

what cells are monochromatic

magno cells

konio cells respond to:

blue yellow contrast

3 other names for the visual cortex

striate cortex

brodmann area 17

V1

borders/location of the visual cortex

outer surface of occipital lobe anteriorly towards the medial occipital lobe

ends anteriorly at the parieto-occipital sulcus

how is the visual cortex structured

6 layers

each layer has 2 maps (1 for each eye) of the opposite visual hemifield

what input drives V1

input from the LGN via optic radiations

V1 is the 1st location in the visual pathway to do what 2 things

• binocular processing

• evaluates visual input based on size, orientation, direction, shape, and texture

what layer of V1 receives primary visual input

layer 4

how are V1 cells organized

into ocular dominance columns that respond to visual input from only 1 eye

how are ocular dominance columns organized

hypercolumns that combine ocular dominance column with orientation column

4 types of cells in layer 4 of V1

non-oriented, simple, complex, end-stopped

non-oriented cells

cells with center-surround receptive fields that get input from the LGN

do not respond to stimulus orientation

simple cells

cells with elongated center-surround receptive fields that respond to stimulus orientation

stimulus has to be correct width, orientation, and position within the receptive field

also respond to edges, color, and depth

receptive fields likely product of multiple center surround LGN receptive fields

what type of cells are considered simple cells

P-cells

respond to color and edges

how are p-cells organized within V1

organized into blobs

blobs vs. interblobs

blobs: respond to color

interblobs: resppond to size and orientation

complex cells

respond to objects moving in a certain direction within a certain orientation

object needs to be located within the complex cell receptive field to get response, do not respond to object position in space

receptive fields do not have center-surround orientation, combined input from many simple cortical cells

what type of cells are complex cells

M-cells

respond to movement

end-stopped cells

respond to lines with a specific length and orientation

process combined input from multiple complex cells

role of V1 layers 2&3

processing layers that send axons to other layers

role of V1 layers 5&6

send axons to subcortical areas (superior colliculus, thalamus, midbrain, pons)

what layer provides feedback to the LGN and what is the purpose of that

layer 6

allows V1 to regulate its own input

extrastriate cortex

V2-V5

responsible for complex processing of visual info

2 main locations within extrastriate cortex

inferotemporal cortex: what

middle temporal cortex: where

what is the inferotemporal cortex responsible for

ventral pathway (what)

identification, object recognition, object constancy

what is the middle temporal cortex responsible for

dorsal pathway (where)

spatial relationship of object to surroundings, direction, velocity, motion

where does the superior colliculus get info from

V1

posterior optic tract fibers before they reach LGN

what does the superior colliculus control

saccades, visual orientation, foveation

SC does not analyze visual input for perception

where do frontal eye fields get info from

V1

2 main functions of frontal eye fields

pupil response to near objects

initiation of voluntary and reflex eye movement

what area of brain initiates voluntary saccades

superior colliculus and frontal eye fields

what is cortical magnification of the fovea

foveal visual input makes up large percentage of visual cortex

allows us to identify central fine details more easily

what does EOG stand for and what does it measure

electrooculogram

measures the difference in electrical charge between the front and back of the eye to assess RPE health

how is EOG performed

electrodes attached to inner and outer canthus of eye

patient is told to make a series of left and right eye movements under light and dark adapted conditions

electrical potential is recorded over 30 minute period

when is electrical potential the lowest during EOG and what is this called

8 minutes of dark adaptation

dark trough

when is electrical potential the highest during EOG and what is this called

10 minutes of light adaptation

light rise

what is the arden ratio

light rise/dark trough

indicates health of RPE

what are arden ratio norms

greater than 1.8: normal

less than 1.65: very abnormal

1.65-1.8: subnormal

what can the EOG be clinically used for

diagnoses of diseases that impact RPE: Best’s, Stargardt’s, advanced drusen, RPE anomalies

not useful for disease differentiation, useful for confirmation

what does ERG stand for and what does it measure

electroretinogram

records retinal graded potentials in response to light to measure outer retinal activity

what layer of the retina is the ERG not assessing and why

ganglion cell layer

ERG assesses graded potential and GCL uses action potential

process of performing ERG

• patient is maximally dilated and dark adapted for 45 minutes

• retina is flooded with various light stimuli

• patient is tested under dark and light adapted conditions to isolate rod and cone function

how is rod function isolated in ERG

using blue flash with slow flicker in dim background

how is cone function isolated in ERG

using red flash with fast flicker in bright background

what are the 3 waves of the ERG response

A wave: negative wave

B wave: positive wave

C wave: positive wave

what does each ERG wave represent

A wave: negative wave represents photoreceptor activity

B wave: positive wave represents bipolar and muller cells

C wave: positive wave represents RPE cells

which wave is rarely used clinically and why

C wave: tests for RPE cell function but if RPE function needs to be tested EOG is test of choice

how is an electronegative ERG classified

loss of B-wave

what is contribution of rods vs. cones to b-wave under dark adapted conditions

rods:cones ratio in retina: 13:1

rods contribute 75% and cones contribute 25% to dark-adapted b-wave amplitude

what are pattern ERGs used for

target RGCs by using a complex stimulus

what are multifocal ERGs used for

record responses of multiple retinal locations allowing for retinal disease to be localized

what are serial ERGs used for

track foreign bodies in the retina

what clinical signs classify retinitis pigmentosa

bone-spicule pigmentation, vessel attenuation, waxy optic disc pallor

what does an ERG look like in early vs. late RP cases

early: scotopic (rod) ERG response is abnormal

late: ERG is completely extinguished due to poor function of rods and cones

what does VEP stand for and what does it measure

visually evoked potential

electrical response of brain activity to visual stimulus

how is VEP performed

• wires placed on scalp overlying V1 in back of head

• patient looks at alternating checkerboard display

how long does response in visual cortex to visual stimuli take

100 milliseconds

normal vs. abnormal VEP

normal: large positive wave that peaks at 90-110 msec after stimulus presented

abnormal: waves that peak after 110 msecs

limitations of VEP

VEP tells you that there is something wrong between the fovea and V1, but it cannot tell you where

what diseases can be diagnosed with VEP

ON tumors, optic neuritis, retinal disorders, demyelinating disease

path of afferent pupillary fibers in light response

travel with RGC fibers to posterior 1/3 of optic tract, where they exit and synapse in the pretectal nucleus of the midbrain

fibers project from the pretectal nucleus contra and ipsilateral and go to the EW nucleus (tectotegmental tract)

what does damage to the tectotegmental tract (path to EW nucleus from midbrain/pretectal nucleus) lead to

argyll-robertson pupil

what characterizes argyll-robertson pupil

light-near dissociation

since the issue is at the path from the pretectal nucleus to the EW nucleus (light response), the near response is unaffected (path from FEF to EW)

pupils will not constrict for light, but will constrict for near

ARP = Accommodative Response Present

what disease is argyll-robertson pupil associated with

tertiary syphillis

path of pre-ganglion PS fibers from EW nucleus

leave each EW nucleus and go to ciliary ganglion in the orbit

path of post-ganglionic PS fibers in light response

go from ciliary ganglion to iris sphincter and ciliary muscles

where do efferent PS fibers for miosis and accommodation begin

EW nucleus

anisocoria is always a response of:

efferent pathology

when does near reflex triad occur

fixation is shifted from far to near object

what mediates pupillary constriction in the near reflex triad

frontal eye field

how does the pupil response innervation change in near reflex triad vs regular pupillary constriction

since it is mediated by the FEFs instead of the pretectal nucleus, the FEF activates the EW nucleus instead

from there, the fibers do the same projection to the ciliary ganglion, and then the sphincter and CM

efferent pathway stays the same but afferent pathway changes

how does the sympathetic NS impact pupil size

controls supranuclear activity, causing decreased EW activity

EW activity is what prompts pupillary constriction, so sympathetic innervation causes an increase in pupil size

when uninhibited, how do EW neurons function

continuously fire action potentials to sphincter for miosis

what happens to pupil size during sleep or anesthesia, and why

supranuclear control is inhibited so the SNS cannot control the EW nucleus

increase in EW activity causes miotic pupils

prectectal nucleus is associated with ______ while FEF is associated with _______

light response

near response

what is the main disease tested for with EOG and ERG

EOG: Best’s

ERG: RP

what CN is the EW nucleus part of

CN III

disease that causes damage at the ciliary ganglion

adie’s tonic pupil

how will Adie’s tonic pupil present

ADie’s: Acute Dilated pupil

since the issue is at the ciliary ganglion, both light and near response will be affected

light response is worse: segmental constriction and wormlike movement of pupil

also blur at near due to loss of accommodation from ciliary ganglion

what systemic side effect is common in Adie’s

loss of deep tendon reflexes

how is Adie’s tonic pupil diagnosed and why

.125% of pilocarpine in the eye will constrict the pupil

sphincter muscle is not getting any innervation/acetylcholine (super-sensitized muscle) so any little amount of cholinergic innervation will make it constrict