visual system

cornea

avascular, transparent, want it to be domed - if not causes astigmatism, can be transplanted

glaucoma

obstruction of reabsorption aqueous fluid leads to buildup of pressure, can compress retina and lead to blindness

aqueous humor

made by ciliary epithelium, absorbed at canal of schlemm
flows from posterior chamber to anterior chamber

vitreous humor

in posterior chamber

cataracts

clouding of lens

ciliary muscle

controlled by CN III, thickens lens for focus on near objects

zonule fibers

ciliary muscle contraction causes them to slacken leading to more curvature of lens

lens elasticity

after 40 begins to decrease leading to presbyopia (inability to focus on near objects)

fovea

center of vision where you can see detail, removes other layers and goes directly to photoreceptors
more info in visual cortex for processing of info from fovea

photoreceptor layer

outer layer where rods and cones are located, create AP, light info goes through multiple layers before being transduced

ganglion cell layer

origin of optic nerve fibers, not connected to photoreceptors, inner layer
multiple connections between ganglion and outer layer for processing before info sent to brain

retinal pigment epithelium

post to photoreceptor layer, provide nutrition and protection for rods and cones
retinal detachment usually between neural retina and RPE, if not reattached quickly death occurs

optic disk

no photoreceptors present, how optic nerve exits, blind spot

cones

high density in middle retina (fovea), color/precise vision
red, green, blue cones: lots of width to what they respond to, not precise to one color domain

rods

primarily in periphery, best at info in low light conditions

color blind

defect in at least one type of cone

phototransduction

level of glutamate constantly release, effect of light is to up or down regulate cyclic GMP
photon leads to hyperpolarization and decrease in glutamate (turning off rods/cones)
amount depends on how many structures affected by photon energy

action stream

dorsal, post parietal cortex, specifies how you move/visual guidance, motion analysis, “where”

perception stream

ventral, occipitotemporal region, visual identification of objects, “what”

subcortical projection pathways

sup colliculus for orientation and visually guiding eye/neck movement
pretectal area for pupillary responses

meyer’s loop

some fibers enter temporal lobe to get to VI, can be affected with lesion

geniculocalcarine fibers

lat geniculate to VI cortex, pass through post limb internal capsule

lesion to optic nerve

visual loss in one eye

lesion to optic chiasm

bilat loss of lateral visual fields

lesion to optic tract

loss of contra visual field

lesion to optic radiation

loss of part of contra visual field depending on extent of lesion

supranuclear control for horizontal gaze

coordination between CN VI and III via MLF
abducens nucleus drives oculomotor, paramedian pontine reticular formation (PPRF) helps coordinate

lesion of abducens nerve

CN VI palsy, ipsi side does not abduct, oculomotor still gets info, peripheral problem

lesion of abducens nucleus

ipsi lat rectus cannot fire, no info sent through MLF so contra med rectus does not fire either

internuclear ophthalmoplegia

lesion to MLF, abducens and oculomotor disconnected so lat rectus fires but contra med rectus cannot, nystagmus on side abducting due to diplopia

1 ½ syndrome

abducens nucleus and MLF lesion, no movement to side with nuclear damage and to contra side can abduct but opp eye does not adduct due to loss MLF - leads to nystagmus

supranuclear control for vertical gaze

oculomotor primarily controls movement
rostral midbrain reticular formation, pretectal area

superior colliculus

orchestrates visually guided movements, coordinates reflexive orientation movement of eyes and head via MLF and tectospinal tract
maps of visual, auditory, body converge in sup colliculus

frontal eye fields

control voluntary and memory guided eye movement, generate saccades in contra direction via connection to contra PPRF and sup colliculus

parieto-occipital-temporal cortex

smooth pursuit in ipsi direction
connects to vestibular nuclei, cerebellum, PPRF

right and wrong way eyes

right way eyes: cortical lesion, look toward intact side of body
wrong way eyes: look toward impaired side of body

saccades

rapid eye movements, shifts target into field of view, switch vision between objects
during saccades visual system suppresses input - not aware of movement
regulated by PPRF

smooth pursuit

foveal movements for stable viewing of moving objects, pursue with eyes and keep relatively stable
lateral parietal and mid temporal areas determine speed and direction of target, project to vestibulo-cerebellum/vestibular nuclei/CN III, IV, and VI

optokinetic reflex

following moving objects until outside field and then returning to new target in field
slow phase (smooth pursuit): lesions of vestibular nuclei or cerebellum disrupt
nystagmus (fast phase, similar to saccadic movement): regulated by frontal eye fields projecting to contra PPRF

consciousness for reflexes

needed for accommodation (specifically occipital lobe) but not pupillary or VOR

loss of vision

describe by referring to visual field deficit
blindness in one eye, bitemporal hemianopsia, homonymous hemianopsia, sup homonymous quadrantanopia

nearsighted

myopia

farsighted

presbyopia

cortical blindness

bilat loss of visual cortex causes loss of awareness of visual info
blind sight: may still be able to orient to objects and be aware of light/dark but lack conscious awareness, from direct connections to hypothalamus and midbrain

papilledema

swelling of optic disk indicative of increased ICP
increased ICP compresses optic nerve leading to axoplasmic stasis causing swelling

disorders of eye movement

damage to CN, MLF, vestibular system

damage to vestibulo-cerebellum

inability to smoothly pursue targets

pathological nystagmus

abnormal oscillations in eyes without external stimulation

damage to frontal eye field

temporary ipsi gaze deviation, look toward damaged side but this resolves due to bilat control

damage to parieto-occipital eye field

inadequate eye pursuit, compensatory saccades to catch up to object, don’t get info on entire arc of movement