Eye Flashcards
Volitional saccades
conscious/free will
can be a screen for higher cortical function
Anti-saccade
consciously looking away from a stimulus
Memory saccade
remember spot, put gaze to where object was
Reflexitve saccades
looking at object of interest reflexively
coordinated through midbrain
Reflexive saccade pathway (object in the left)
Left visual field –> Right LGN of thalamus –> Right primary visual cortex, visual association cortex, frontal eye fields etc
–> R superior colliculus –> PPRF –> gaze to the left
Superior colliculus saccade
Retina –> visual layer of colliculus –> motor layer of colliculus –> gaze centres
Motor layer of colliculus receives extrapyramidal input
Pursuit movement components
cortical information from primary visual cortex/frontal eye fields
Cerebellar information for proprioception to stabilize information
Vestibular information to orient
CN III innervations
pupil
levator muscle
IO, SR, MR, IR
NOTE: nerve palsy –> unilateral ptosis, mydriasis is never nuclear
inferior rectus nucleus
dorsal - ipsilateral
Inferior oblique nucleus
intermediate - ipsilateral
medial rectus nucleus
ventral - ipsilateral
CN III location
intramedullarily related to: red nucleus (cerebellar connections) and cerebral peduncle (pyramidal tract)
tentorium and MCA/PCom jxn
cavernous sinus and pituitary
Superior orbital fissure and orbit
CN IV location
long course from dorsum of brainstem
through cavernous sinus and adjacent to pituitary gland
CN VI location
over petrous ridge
through cavernous sinus and adjacent to pituitary gland
Sup Rectus function
elevation and intorsion abduction
intorsion increase with adduction
Inf rectus function
depression and extorsion abduction
extorsion increases with adduction
Inferior oblique function
elevation and extorsion adduction
extorsion increases with abduction
Superior oblique function
depression and intorsion adduction
intorsion increases with abduction
Fixation system
Maintain fixation on a stationary target
Micromoevments to moev objects of regard on fovea
Necessary for vision
poorly localized in cortex
Fixation system dysfunction
global confusional states and dementia
anxiety
sedative/tranquilizers
Saccadic system
movement between targets on command
voluntary and fast eye movements
contralateral frontal cortex - projects via internal capsule to brainstem gaze centre
Saccade dysfunction
unilateral: horizontal gaze palsy
Bilateral: vertical gaze palsy
Disorders commonly seen (e.g. MCA infarct)
Pursuit system
tracking a slowly moving target
slow, involuntary eye movements
Occipital-parietal cortex
projects via internal capsule to brainstem
Pursuit dysfunction
cogwheel pursuit
Vergence system
occipital-parietal to midbrain pre-tectum
slow disconjugate eye movements
Non-optic reflex system
Oculocephalic reflex
caloric responses
Slow eye movements
Brainstem vestibular system
Frontal gaze palsy
horizontal gaze palsy (uses frontal eye field)
pursuit is ok (doesn’t use frontal eye field)
nuclei/downstream are okay
Dolls eyes movements
CT scan lesion
Look toward their lesion
Conjugate eye movements - no diplopia
Progressive supranuclear palsy (PSP)
gradual impairment of supranuclear gaze Vertical > horizontal Voluntary > pursuit > reflex relatively preserved vertical movements in non-optic reflexes axial dystonia dementia no convergence
Perinaud’s syndrome
vertical gaze palsy - can’t look up
lid retraction/ptosis
convergence-retraction nystagmus (all eye movements fire at the same time)
convergence poor, light reflex poor
lesion in pineal region compressing dorsal midbrain
Intranuclear ophthalmoplegia
Ipsilateral adduction weakness (MR)
MLF lesion - demyelination of heavily myelinated tract
could cause bilateral MLF lesions (MS hallmark)
Contralateral abducting nystagmus - vergence system attempt to compensate
Complete CN III palsy SSx
paralysis of all extraocular muscles except LR and SO
some abduction/depression/intorsion remain
–> down and out position at rest
pupil dilated and unresponsive to light –> involvement of parasympathetic fibers
CN III palsy cause
internal carotid artery aneurysm a common cause
CN VI palsy
horizontal diplopia
some patinets may tend to turn head toward affected eye to compensate
Choroid
vascular dark brown membrane (with melanin)
reduces light scatter within the eye
Ciliary body
ring of SM control eye movement via suspensory ligament
focusing vision
Outer pigmented layer (RPE) of the retina
absorbs light and prevents light scatter
role in photoreceptor regeneration
Inner neural layer of the retina
contains photoreceptors and neurons
Uveitis
more serious
often associated with systemic disease (autoimmune, infections, etc)
can be segmental
Blood supply to the eye
from internal carotid
ophthalmic artery arises at carotid siphon in cavernous sinus
2 end branches:
- posterior ciliary arteries (choroid, outer retina, optic disc)
- central retinal artery (inner retina)
Anterior ischemic optic neuropathy
due to ischemia in posterior ciliary arteries
see swollen infarcted optic disc, greyish
Central retinal artery occlusion
pale retina with a cherry red spot at fovea from shine-through of choroid
little inner retina at fovea
Rods
provide scotopic vision (dim light) - high sensitivity in the dark
Low spatial resolution - summation to one bipolar cell
Rhodopsin pigment
Cones
provide photopic vision (bright light)
colour vision - reflects type of opsin; R, G, B
X-chromosome
High resolution central vision
Photopigment
opsin + retinal
Phototransduction cascade
1) a photon converts 11-cis-retinal –> all-trans-retinal
2) activation of hundreds of G-protein transducin
3) transducin activates cGMP phosphodiesterase
4) each breaks down thousands of cGMP
5) decrease in [cGMP] closes Na channel –> hyperpolarization
Photoreceptor distribution
Fovea: no rods, just cones
Rods highest density at 20 degrees eccentricity
Rods/cones decline in density with increasing eccentricity
Physiologic blind spot
at the optic disc
Retinal ganglion cells gather to form optic nerve
no photoreceptors
Cone dystrophy/macular degeneration
central scotoma with poor central daytime vision
Retinitis pigmentosa
disease of rods
causes ring scotomata and nyctalopia (night blindness)
Bipolar cell - relay
from photoreceptors to retinal ganglion cells
Glutamate stimulation from photoreceptors
different bipolar cells for rods/cones
OFF/ON cells
Graded EPSP, not actional potential
OFF bipolar cells
active without light, excited by glutamate
ON bipolar cells
active with light, inhibited by glutamate (light reduces glutamate release)
Modulation of bipolar cells
by horizontal cells (at photoreceptor/bipolar cell synapse)
+ amacrine cells (at bipolar cell/retinal ganglion cell synapse)
Lateral inhibition by light in neighbouring regions –> centre-surround receptive organization
Parvocellular retinal ganglion cells
small cell bodies short dendrites small receptive fields sustained response to onset of light --> high spatial resolution, low temporal resolution
colour opponency
Magnocellular retinal ganglion cells
large cell bodies
long dendrites
large receptive fields
respond transiently to onset/offset of light
–> low spatial resolution, high temporal resolution
Papillomacular bundle
large bundle of RGC axons from fovea and macula
Temporal raphe
divides RGC fibers from upper and lower temporal retina (nasal visual field)
because they must curve around the large papillomacular bundle that is in the way
RGC fibers from nasal retina
temporal visual field
head straight to the optic disc
Central scotoma
optic neuritis
info from fovea –> disc all gone
Ceco-central scotoma
lesion closer to blind spot
hole contains lesion + blind spot
Nasal arcuate defect
inferior/superior reversed
lesion in arching fibers
e.g. glaucoma
Temporal wedge defect
on the other side of the blind spot
rare
Optic nerve
component of CNS
myelin provided by oligodendrocytes
each optic nerve ~106 axons
pass into cranium through optic canal, converge above pituitary at optic chiasm
Optic tract
continuation from optic chiasm
contains information from the contralateral hemifield of each eye
terminates in LGN
Pretectal nuclei
midbrain
pupil light reflex
Superior colliculus (vision)
rapid eye/head orientation
reflexive eye movements
Nucleus of optic tract/accessory optic system
supplement vestibular information in keeping gaze stable
Suprachiastmatic nuclei
hypothalamus
diurnal regulation of homeostasis
Lesions of optic chiasm
Bitemporal hemianopia
almost always due to mass effect, often a pituitary tumour
loss of nasal retinal fibers from both eyes
Lesions of optic tract
homonymous hemianopia
affect nasal fibers from the contralateral eye, temporal fibers from the ipsilateral eye.
Contralateral visual filed information lost
Usually partial and usually incongruous
Lesion to the Meyer loop
Contralateral superior quadrantanopia
fibers from upper portion of the contralateral visual field from both eyes
Lesion to the optic radiations
Contralateral inferior quadrantanopia
Lesion to the primary visual cortex
Contralateral homonymous hemianopia
loss of visual info from contralateral visual field
LGN layers
6:
- 2 where magnocellular RGC axons terminate (large cells) –> one for each eye
- 4 where parvocellular RGC axons terminate (smaller cells) –> two for each eye, in alteration
Receives some modulation from cortical regions
Retinotopic arrangement in LGN
Fovea - superior LVN
Peripheral field - inferior
Upper field - lateral
Lower - medial
Striate cortex
= primary visual cortex/V1, calcarine cortex
Initial stage of cortical processing
Info highly retinotopic (specific for location on retina)
information represented as linear segments/boundaries - cells organized in regular array of orientation columns
Cortical magnification of central vision>peripheral
Striate lesions
Highly congruous homonymous defects in contralateral hemifield
Occipital pole lesion
hemi-central scotoma
None-occipital pole lesion consequence
Macula-sparing hemianopia
Superior bank lesion
inferior quadrantanopia
Inferior bank lesion
superior quadrantanopia
Extra-striate cortex
visual information fans into parallel distributed hierarchy of specialized modules beyond V1
less concerned with retinotopic location; more concerned with specific stimuli
2 streams
Dorsal (occipital-parietal) stream
"where" stream motion processing (v5) stereopsis saccadic targeting manual reaching depth perception eye and hand movements
Ventral (occipito-temporal) stream
"what" stream colour processing (V4) object recognition (words, faces)
Lesions to components in dorsal stream
Akkinetopsia - rare
Hemineglect
Astereopsis (no depth perception)
Balint’s syndrome
Balint’s syndrome
triad of:
ocular motor apraxia –> poor targeting of eye movements to targets
optic ataxia –> misreaching for visual object
Simultanagnosia –> inability to attend to >1 object at a time
Lesions of components in ventral stream
Achromatopsia (cerebral loss of colour vision)
General visual object agnosia
Prosopagnosia: impaired recognition of faces
Alexia
