Senses: Vision

What operates together to hold images STABLE on the retina?

* The vestibular and optokinetic systems operate together to hold images stable on the retina*

Contralateral superior quadrantanopia

*"Pie in the sky"* -Lesion of the temporal lobe (letters E and J)

Contralateral inferior quadrantanopia

*"Pie on the floor"* = Lesion of the parietal lobe (letters F and I) --- If have lesion on the right by superior MCA >Contralateral LEFT-LEFT hemi-quadrantanopia (Pie on the floor)

Scotoma

*A circumscribed region of pathological visual loss= BLIND* -Small deficit in the visual field resulting from pathological changes in some component of the primary visual pathway. -The location, size and shape of a monocular scotoma results from the location and extent of the retinal lesion. -Lesions of the retina can be due to retinal infarcts, hemorrhage, retinal degeneration, or infection ONE AREA affected

Attention Process

"Winner take all": Attention focused on LIMITED area combining ALL Local feature maps -When a subject attends visually to an object, neurons in the *posterior parietal cortex* responding to the object begin to discharge powerfully. -Closer attention recruits selective enhancement of cell activity in several regions of the cortex responding to the object of interest. -Synchrony of firing in similarly stimulated cells: mechanism of binding

Accommodation and lens

*Accommodation effectively INCREASES the refractive power of the lens* -The *power of accommodation* = The DIFFERENCE in refracting power between the resting and maximally accommodated eye. -Accommodation effectively SHORTENS focal length of lens. >Needed for NEAR vision >Light rays from an object >20 feet away that strike a lens are considered parallel >Light rays from an object CLOSER than 20 feet are DIVERGING and are brought to a focus farther back.

Major optical defects

*Ametropia*: Discrepancies of the various physical components of the eye cause a majority of the human population to have some form of refractive error -Emmetropia: Normal vision -Myopia: Nearsighted -Hyperopia: Farsighted

Optokinetic System

*CN II*: Used during sustained or slow head rotation (voluntary) -ACTIVATION of the optokinetic reflex requires a moving stimulus (moving pattern) that fills the field of vision. >*Optokinetic (railroad) nystagmus (OKN)* is composed of a pursuit eye movement to track the moving environment (utility poles, stripes on a drum etc.) and is then RESET with a FAST saccade. >PTO helps with tracking -Once put into action the optokinetic system maintains its effect until the field of vision STOPS moving. >Even AFTER stimulation stops it *remains in effect for some time* (sec) and helps to nullify post-rotatory eye movements. -Optokinetic system acts as a *BACK UP to the vestibular-ocular reflex*. >VOR by itself can only hold the image on the fovea steady during the first 30 sec of turning. >As the vestibulo-ocular compensation DECLINES, visual images of the seen world traverse the retina. >This stimulates the optokinetic system to *stabilize the retinal image*

Focusing on far objects occurs when...

*Ciliary nerve STOPS firing and the ciliary muscle RELAXES* 1.) Tension on the zonule fibers attached to the lens capsule is restored. 2.) The elastic lens flattens in shape (becomes LESS CONVEX). 3.) Effectively REDUCES the refractive power of the lens. 4.) Far point is the distance at or beyond which an object is in focus without accommodation (6 m (20 ft) for emmetropic eye). 5.) The parasympathetic nervous system STOPS firing-> PNS release of ACh on muscarinic ACh receptor in *ciliary muscle DECREASES* >Same effect with *atropine* which blocks mACh receptors so ciliary muscle *cannot contract* and the lens cannot accommodate-> NO FOCUS on near objects.

Commonly prescribed lenses used to refract light to focus image on the retina

*Convex* spherical lens: CONVERGES parallel light rays. -After passing through a convex lens, light rays that are PARALLEL to the axis of the lens CONVERGE to meet at a point called the *focal point (F)*. -*Focal length (f)*: The distance from the lens to the focal point. -Positive value ---- *Concave spherical lens*: DIVERGES parallel light rays. -No real image is formed by a concave lens -NO FOCAL POINT -Negative value

Astigmatism

*Corneal surface is NOT perfectly spherical* -Light rays do NOT form a point on the retina. -Corrected with lens that has DIFFERENT curvatures to compensate for the anomalies in the cornea.

Refracting power of a substance is measured in...

*Diopters (D)* -The refractive power of a lens equals the RECIPROCAL of the focal length of the lens in meters. Example: A lens with a focal length of 20 cm has a refractive power of +5D. D= 1/focal length (m) 1/0.2m= +5 m -A lens with a negative refractive power is a diverging lens.

Hyperopia

*Farsightedness* *Light rays are FOCUSED BEHIND the retina* -The eye is TOO short for its refractive power OR the refracting system is TOO weak. -Distant objects can be seen ONLY if the person *accommodates.* -Hyperope is continually *accommodating*. -Hyperope doesn't have a far point -The NEAR point is FARTHER than normal. -*Convex lens* is prescribed (positive D) to correct the problem. >Correct positive lens will cause *sufficient convergence* of the light rays to FOCUS images on the retina.

Argyll Robertson Pupil

*Sensory Defect-> CN2* -Constrict for Light (CN2)<<<<Constrict for near dissociation (CN III) -Near response intact-> Occipital lobe responsible -The pupils CONSTRICT much less in response to light than accommodation. -Neurosyphilis and diabetic lesions

Major differences between rods and cones (Table):

*Specialized neurons* RODS -HIGHLY sensitive to light -Low threshold -Best at dim light -Scotopic vision -Does have more photopigment and amount of light captured than cones -Saturated (bleached) by daylight -Low temporal resolution: Count spokes -Low flicker fusion rate: Cannot count spokes anymore -SLOW response/ longer to integrate -Sensitive to scattered light -Can tell there is something there but cannot see in great acuity ---- CONES -LOW sensitivity -HIGH threshold (Need a lot of light to reach) -Best at daylight -Saturated by intense light -HIGH flicker fusion rate -High temporal response -Fast response/integrates faster -Sensitive to DIRECT axial light rays -Too much light= SATURATE!= CANT SEE!

LGN Layers

6 Layers Each layer receives input from Only one eye -Ipsilateral eye in *layers 2, 3, and 5* -Contralateral eye in *layers 1, 4, and 6* -Large retinal ganglion cells called *Magnocellular cells* from the retina terminate in layers 1 and 2, where as small ganglion cells called *Parvocellular cells* terminate in layer 3, 4, 5, and 6.

Pretectum

A group of nuclei located at the junction of the thalamus and the midbrain (located in the midbrain) -These nuclei are important in the pupillary light reflex, relaying information from the retina to the Edinger-Westphal nucleus. -Extra-geniculate pathway (NOT LGN)

Parvocellular System (Inter-Blob System) Lesions

A lesion in the inferior temporal lobe results in *object agnosia* (defect in recognition of objects). -The patient is *unable to recognize faces*= *prosopagnosia*

Magnocellular System (Lesion)

A lesion in the system results in a DEFECT in perceiving *object motion* and FAILURE to produce eye movements to *track a target* -Results in movement *agnosia*= LOSS of sensory ability to recognize something familiar (DONT recognize the movement) >Loss of movement perception in a patient results in the inability to distinguish between moving and stationary objects. >Problems crossing street, not see lips moving, not see liquid pouring, etc

A lesion of the optic radiation fibers that curve downward..

A lesion of the optic radiation fibers that curve downward into the temporal lobe (*Meyer's Loop*) and terminate in the inferior bank of the *calcarine fissure*, causes a loss of vision in the UPPER quadrant of the contralateral half of the visual field of both eyes. *Contralateral superior quadrantanopia*

A lesion of the optic radiation fibers that curve upward..

A lesion of the optic radiation fibers that curve upward into the *parietal lobe* and terminate in the upper bank of the calcarine fissure (cuneate) causes a loss of vision in the *LOWER quadrant of the contralateral half of the visual field of both eyes*

Lesions of the optic radiations of the internal capsule

A lesion of the optic radiation fibers that curve... -Downward to temporal lobe (Meyer's Loop) -Upward to parietal lobe

Aniscoria

SENSORY DEFECT *Unequal Pupils* -Normally in 10% of population -Hippus (spasing)-normalcontinual, symetric small CONTRACTIONS of pupil.

Saccadic System

Saccades, pursuit, and vergence eye movements, working together, acquire and HOLD images of objects of interest on the retina. -The *fastest of the eye movements* >Large saccades of 80 degrees have a peak velocity of 700°/sec) -They are ballistic (once started can't change): Can NOT change course of eye movement in response to subsequent changes in the target during the DELAY period. -Allow us to rapidly REDIRECT our line of sight (RESET) -Used in: reading , voluntary and involuntary changes in fixation, quick fast phase of vestibular and optokinetic nystagmus, and the Rapid Eye Movements in REM sleep. >Vestibular-> endolymph moving (transduce acceleration) -Tiny, *micro-saccades* (over a fraction of a degree of visual arc) PREVENT the visual image from disappearing due to retinal adaptation. >Ion channels could close but adapt in light receptors by opening the channels in the light --- YOU CHOOSE to do this Vergence eye movements: Occipital to midbrain (CN III-> EW nucleus-> ACh to ciliary muscle to relax)

Saccadic vs. smooth pursuit movements

Saccadic Speed: FAST Visual acuity during movement: Poor Target required: NO Maximum velocity: FASTEST Velocity under voluntary control: NO Stimulus to elicit a movement: Target displacement Latency: 200 msec (start to initial movements-> more synapses to occur) ----- Smooth pursuit movement Speed: SLOWER Visual acuity during movement: *Excellent* Target required: YES Maximum velocity: Slower Velocity under voluntary control: NO-> function of target velocity Stimulus to elicit a movement: Target velocity Latency: 130 seconds (VOR shorter with 2-3 synapses)

Refractive Index of glass

Speed in air/speed in glass 300,000 km/sec /200,000 km/sec = 1.5 Refractive Index (glass)

The Smooth Pursuit System

TRACKING This system generates *smooth following movements* of the eyes that closely match the pace of the target. -Once captured on the fovea by a saccadic eye movement an image of a moving target would soon slide off the fovea in the short interval between saccades. -*Smooth pursuit* eye movements KEEP targets on the fovea. -By using SLOW drifts, which move the fovea over the target and quick flicks, which are small saccades that return the fovea to the target, smooth pursuit eye movements MAINTAIN eye position with the target of interest.

Far Points

The CLOSEST distance an object can be placed and still be seen clearly WITHOUT accommodation -20 feet [6 m]= eye chart

Presbyopia

The ability of the lens to change shape decreases with age (*presbyopia*) -Associated with a *LOSS of elasticity* in the lens substance. >FAR point doesn't change with age. >NEAR point gets larger with age.

Refraction of light depends on...

The angle at which the beam of light strikes the interface between the two media. -Light rays will NOT be bent if they hit *perpendicular* to the surface. -The greater the CURVATURE of the surface the MORE the light will be bent (*refracted*).

Saccade and brain

The brain *suppresses the visual image* during the saccade so that the image is NOT blurred and we are *unconscious* of the eye movement.

Parvocellular System (Blob System)

This system processes COLOR -Color perception is a very sophisticated abstracting process. This pathway: -Starts from the small P (Pα) ganglion cells in the retina. -Synapses in the parvocellular subdivision of the LGN (some cells from the interlaminar layer also included) -Passes through V2 and V4, to the *inferior temporal cortex* -The neurons in this system respond SLOWLY and are capable of *HIGH resolution* >These cells are *color responsive*

Saccades (general)

To bring images of objects of interest onto the fovea

Nystagmus Quick Phase

To direct fovea toward the oncoming visual scene during SELF-rotation -To RESET the eye during prolonged rotation NOT have if unconscious

Smooth Pursuit (general)

To hold image of a moving target on the FOVEA -Count, watch, etc CONSCIOUS

Vergence

To move the eyes in opposite directions so that images of a single object are placed on BOTH fovea

Blind spot (Diagram)

Top eyes: ONLY right eye affected so lesion is in FRONT of the chiasm (lesion of retina, etc) -Only top right eye affected -Look with ophthalmoscope INFERIORLY as lesion is opposite of what the vision impairment is >Inferior ophthalmic artery could have ruptured to inferior retina >Can last for 10 minutes-> TIA (blocks and goes away) --- Lower eyes -Right: Blind eye -Left: Heminopsia -Originally: on optic chiasm -Now: Complete compression of nasal fibers

Visual Image

A visual image complete with movement, location, form, and color is accomplished by cellular processing of retinal information along 3 or more separate, parallel pathways in the cortex. -Visual perception is a creative, continuous transformational process --- Picture: Vase or two faces? -Retinal makes circular receptive fields in the contrasted areas -Cortex has visual input-> "connect the dots" where the contrast ("circles") are -Connect areas of contrast-> Fills it in

Smooth Pursuit positions (Graph)

A.) Smooth pursuit by a normal subject. -Top trace shows horizontal eye position -Bottom trace shows movement of the target (a small laser spot). -The eye movements consist mainly of *smooth tracking movements* with *occasional small saccades* -Overall: Follows the target perfectly B.) *Attempted smooth pursuit *in a patient with *Cerebellar disease* -Although the patient can generate some smooth following movements, their velocity (like the slope) is much LESS than that of the target. -Consequently, the patient has to make *"catch-up" saccades* to place the image of the target on the fovea. -JERKY movements due to*ATAXIC eye movements*= Cerebellar disease causing no smooth eye movements

increase in intracranial pressure

Any INCREASE in intracranial pressure is transmitted to the subarachnoid space surrounding the optic nerve and can be seen as a swelling of the optic disc= *papilledema*

Light passing to lens (Picture)

As incident ray goes into denser medium: Refracted CLOSER >Bent AWAY -- Cornea bends light (FIXED) -Light bends as goes to lens -LENS IS NOT FIXED in bending power-> Can change -Ach released from ciliary ganglion to ciliary muscle (muscarinic receptor) >This circular muscle will move FORWARD/bulges as contraction occurs >Suspensory ligaments DECREASE tension as CN III fires >Bulge forward-> lax of ligaments and lens will ROUND up (diopter strength increases: 20D- 34D (Relax ligaments)-> can do as NOT FIXED!!!!

Light entering eye is...

BENT= Refraction

Primary gaze positon

BOTH eyes straight ahead: all 12-extraocular muscles firing and balanced. Z) *Medial and lateral recti* contract reciprocally, moves the eye left or right. Y) *Superior and inferior recti* contract reciprocally, moves the eye up or down. X) *Superior and inferior obliques* rotate the eye to keep the visual field upright.

Eye pathway (Image)

Binocular vision (visual fields put together) via visual fields-> goes to fovea -VOR helps keep image to fovea

PNS Stimulation and no stimulation (Diagram)

CLOSE vision-> PNS stimulation-> Ciliary Muscle contracts >Suspensory ligaments RELAX >Lens CURVED (Becomes +34D) FAR vision-> No PNS stimulated-> Ciliary muscle relaxed -Suspensory ligament becomes TAUT (pulls back) -> Tension-> FLATTENS (Back to +20D) -Relaxed vision-> muscle not firing-> ligaments tighten-> flattens the lens to have distant vision

Binocular Movements

CONJUGATE GAZE MOVEMENTS = eyes moving in same direction -Six CARDINAL DIRECTIONS OF GAZE: Used *clinically* to isolate extraocular muscle dysfunction. >This DOES NOT represent actions of an individual extraocular muscle near its primary gaze position, but instead at its maximal functional use position. -*Yoked pairs* of extraocular muscles are used to move both eyes to the six cardinal positions of gaze.

Optokinetic

CONSCIOUS-> choose if want keep eye on something To hold image of the seen world STEADY on the retina during sustained head rotation or moving environment CN 2

Hyperpolarization of membrane potential

Causes a DECREASE in transmitter (Glu) release which changes the coding of APs.

Dark vs light effects on outer membrane (Picture)

Closed: Light sensitive Outer segment Open: Dark current depolarizing the cell -Ionotropic ligand is inside-> Ligand is inside-> *cGMP*!!

Retinotopic Map

Complete *retinotopic map* in the primary visual cortex = Striate cortex (Striped in the cortex) = *Brodmann's area 17= Visual area 1 (V1)*, is the FIRST level in CONSCIOUS visual processing -There are at least 10-20 other complete and partial retinotopic maps identified in the extrastriate cortex. -Like the somatic sensory system, the distinct receptive map obtained from the retina becomes the substrate for PARALLEL processing. -There are three major pathways that project from V1 striate cortex to various extrastriate cortical areas and process DISTINCT types of visual information.

Visual Circuits

Cortex interprets visual info -V1 to occipital lobe (contrasted visual info) ">CONNECTS the dots" >Circles from retina > Ventral Pathway: V1->V2->V4-> TEMPORAL Lobe Dorsal Pathway: V1-> V2-> MT-> PARIETAL Lobe

Dark vs light effect on photoreceptors

DARK -High [cGMP]= Channels OPEN -Dark= DEPOLARIZE >More conductance-> Sodium then calcium come into cell >Glutamate release to bipolar cell (#2) INCREASES LIGHT -Low [cGMP]= Channels CLOSE -Hyperpolarize-> no sodium or calcium into the cell >Transduction of light decreases sodium conductance in the outer segment of photoreceptors #1 (photoreceptor)-> #2 (Bipolar cell)-> #3 (ganglion cell) -Ganglion cell is only one with Na+/Ca++ channels capable of encoding and allowing APs to occur. -#1/#2: Membrane potentials

Physiological optics

DETECTION of electromagnetic waves Visible light: 400 nm- 750 nm wavelength 1.) *Intensity* of light is interpreted as BRIGHTNESS. 2.) *Wavelength* of light is interpreted as COLOR >High energy/low wavelength: Short wavelengths (blue 400nm) >Low energy/high wavelength: Long wavelengths (red 700nm)

Object <20 feet away

DIVERGING -Resting: viewing a DISTANT object (60D) >NO CN III firing (40 + 20-> 60= MINIMUM needed) - Young person resting: Viewing a near object and no accommodation (60D) -Older person actively trying to focus on a near object (best 61D). >40D + 21D-> 61D so cannot accommodate as well to NEAR objects even with best strength >NOT pathological but relates to aging where lens becomes STIFF -Young person ACTIVELY viewing a NEAR object with *max accommodation* (74D).

Secondary Gaze Positons

Direction from primary gaze: Look right (Cardinal gaze position) >Right eye: Lateral Rectus >Left eye: Medial Rectus Look left >Right eye: Medial Rectus >Left eye: Lateral Rectus

Tertiary Gaze positions

Direction from primary gaze: Look right and up >Right eye: Superior Rectus >Left eye: inferior Oblique Look Left and up >Right eye: Inferior Oblique >Left eye: Superior Rectus Look right and down: >Right eye: Inferior rectus >Left eye: Superior oblique Look left and down: >Right eye: Superior oblique >Left eye: Inferior Rectus

Eye position, target position, and eye velocity (Graph)

Eye does not immediately follow target-> need Saccadic eye movement to follow -There is a delay from target position moving from left to right and eyes moving the same way >saccadic eye movements have 200msec delay= LATENCY (from stimulus to onset of motor movements)

Frontal Eye Fields

FEF A region of the frontal lobe that lies in a rostral portion of the premotor cortex and that contains cells that *respond to visual and motor stimuli* (conscious)

Visual Attention

FOCUSES perception by facilitating coordination between the separate pathways -Distinct features cell: impossible concept as there cannot be a neuron for 1 thing each and only in the universe! -The Binding Problem >COMPLEX visual images are built at successively *higher processing centers* using inputs from the parallel pathways for movement, form, and color. -To express a specific COMBINATION of properties in the visual field at any given moment independent groups of cells each with a distinctive property MUST be brought TOGETHER in *temporary association* -Brain associates independent processing carried out in different cortical regions. -REQUIRES ATTENTION: Pre-attention and attention processes >"Circuit" that determines where to put the attention

Intorsion vs extorsion

Intorsion: UPPER POLE of eye moves INWARD-> Superior Oblique Extorsion: UPPER POLE of eye moves OUTWARD-> Inferior Oblique

Lesion of the PPRF or abducens nucleus will cause...

Ipsilateral horizontal gaze palsy. -Problem with moving BOTH eyes in directed gaze. Ex.) "Look to the right." Both eyes should move to the right

Parvocellular System (Inter-Blob System)

This neuronal pathway processes: -Detection of FORM -Stereopsis: Depth -Color information but NOT major pathway for it This system works at seeing *WHAT* rather than WHERE -Allows the subject to see stationary objects in *great detail* -Starts from the small *Parvocellular ganglion* cells in the retina. -Synapses in the *parvocellular layers of the LGN*. -Passes through V2 and V4 to the *inferior temporal cortex*. -The neurons in this system respond SLOWLY and are capable of *high resolution* >The analysis of color and form needs *high-resolution vision* >The neurons are sensitive to orientation of EDGES

Object >20 feet away

PARALLEL

Change from Dark-Light-Dark in mV (Graph)

Playing with an electrode to voltmeter 0 mV at beginning -Dark: -30mV as DEPOLARIZE (cGMP high and opens sodium channels) -Light: -60mV as HYPERPOLARIZE (sodium channels close/cGMP drops) -RECEPTOR POTENTIAL!

Phototransduction

Process where light is converted into *electrical signals* in the retina Photons become receptor potentials Attache to RPE --- Neurons: Rods and cones (20:1) -Do have transmitters at synaptic terminal (GLUTAMATE) Rods -Catch light in outer segment on Rodopsin-> constantly made and sloughed off -More rods than cones -Metabotropic receptors-> Rodopsins Cones -Intense light

Accommodation

adjustment of lens refractive power (can INCREASE 14 D). -Focusing on NEAR objects causes the ciliary nerve (*parasympathetic nervous system*) to DISCHARGE and the *ciliary muscle to contract* -Upon release of tension the elastic lens bulges into a more spherical shape and becomes more CONVEX (mostly at the anterior surface). -Accommodation is a SLOW process, with the lens requiring 0.5 sec to change its shape as the eye shifts from FAR to NEAR focusing.

Pupillary Control (Picture)

subject on their back -Pretectum: Crosses ipsi and contra to release glutamate to EWN

Dark adaption

*Going from light environment to dark environment* Requires 30 min or longer for "scotopic" vision to become optimal. -Two thresholds: 1st is cone with high threshold, 2nd is rods low threshold. -Enormous rise in responsiveness to DIM light (*rods*). -Insufficient light to stimulate cones -Rods need to dark adapt from bright light to dark ---- GRAPH: Showing that cone adaption occurs as was in light going in dark; then rod adaption occurs -Cone adaption -Rod adaption: About 30 minutes needed for full adaption

Pons and eye movement

*Horizontal eye movement control center* -*Abducens nucleus* is a HORIZONTAL gaze center as it controls ipsilateral *lateral rectus and contralateral medial rectus*. -The *medial longitudinal fasciculus (MLF)* provides the interconnection between the occulomotor, trochlear, abducens, and vestibular nuclei. -*Paramedian pontine reticular formation (PPRF)* near the abducens nuclei provides output to the abducens from HIGHER cortical eye movement control centers. >PPRF= unconcious >Frontal eyes fields from cortex talks to CONTRALATERAL PPRF

Oculomotor Lesion (Pupil)

*IMPAIRED pupillary constriction* 1.) Results in a UNILATERAL *dilated pupil "blown pupil"* 2.) DECREASED or absent DIRECT response when light is shone in the affected eye as well as a decreased or absent consensual response when light is shone in the opposite eye UNCUS can also push on CN III and lead to damage DILATED and FIXED

Image and object (Picture)

*Image will be INVERTED (top-> bottom) and REVERSED on the retina (Right-> left) Flip object upside down and invert! -Refractive index in eye is about 1.33 -2 solutions: Aqueous and vitreous humor before getting to retina

LGN and vision

*Lateral geniculate nucleus (LGN)* of the thalamus in the diencephalon -MAIN input to the visual cerebral cortex (relay station) -WITHOUT this pathway visual perception is LOST= BLIND -Ninety percent of the retinal axons terminate in the lateral geniculate nucleus. -The *fovea* has a relatively larger representation than does the periphery of the retina. >Half of the neural mass in the LGN and visual cortex represents the FOVEA and the area just around it -Left half of the visual field is projected on the *right hemiretina* of each eye (lens) and sent (optic nerve & optic tract) to the right lateral geniculate nucleus.

Optical Properties of the eye

*Major refracting surface of the eye is the anterior surface of the cornea* -Anterior cornea SEPARATES two media (air and cornea) with very DIFFERENT refractive indices. > Cornea has a FIXED refractive power of 40 diopters. -The POSTERIOR surface of the cornea, the anterior and posterior surfaces of the lens are the other three refractive interfaces that light must pass through to reach the photoreceptors in the retina. >Together the cornea (40 D: fixed) and lens (20 D: NOT fixed) serve as a compound lens with a refractive power of *60 diopters* (1 / 0.017 m) and a refractive index of *1.33* >Lens can change power -> Can add 14 (20 +14= 34)-> 40+34= 74D (elevates!) -In the normal (emmetropic) eye the focal length is 17 mm.

Myopia

*Nearsightedness* Light rays are FOCUSED in front of the retina -The subject is UNABLE to bring DISTANT objects into clear focus. >The myopic person has NO mechanism to focus distant objects sharply on the retina. -The eye is TOO long for its refractive power OR cornea is too CURVED causing the refractive system to be TOO STRONG -Both the far and near point are closer than normal. -*Concave lens* are prescribed (negative D) to correct the problem -Correct negative lens will cause sufficient *divergence* of the light rays to bring DISTANT objects to FOCUS on the retina.

Types of eyeball movements

*Ocular Motor System*: One of the best understood examples of the integration of sensory and motor systems *Saccades, pursuit, and vergence eye movements*: working together, acquire and hold images of objects of interest on the retina.

On and Off Center Ganglion cells: Pathways

*On and off center ganglion cells are EQUALLY represented and provide 2 parallel pathways for processing information* -*M ganglion cells* have LARGE receptive fields and show a transient response to sustained illumination. >Concerned with detection of MOTION and gross features. >1/2 on and off center -*P ganglion cells* have SMALL cell bodies and receptive fields. >Concerned with detection of *fine detail and color* >1/2 on and off center

The optokinetic reflex

*Optokinetic (railroad) nystagmus (OKN)* A human's horizontal eye position as he sits still inside a vertically striped drum rotating slowly to his right. -Eye position is plotted against time. -Note that during the *slow phase* the eyes move in the same direction as the striped drum to keep the drum's stripes still or steady on the retina. -- Slow phase= Compensatory Fast phase= Saccades (The beats)

Retinal ganglion cell output determined by...

*Photoreceptors and interneurons*

Retinal Ganglion Cell Axon Projections

*Retinal ganglion cells* from both eyes send UNmyelinated axons from the retina to the optic disc where they become *myelinated* and form the bilateral optic NERVES (CN II). -The optic nerve travels DIRECTLY to the optic chiasm near the base of the *diencephalon* >ONLY axon fibers from the *nasal half* of each retina need to cross over at the optic chiasm to the *contralateral side*. -This partial crossing of retinal fibers at the optic chiasm allows corresponding points on the two retinas to be processed side by side in the same cerebral hemisphere. -The two left hemi-retinas project to the left visual cortex and the two right hemi-retinas project to the right visual cortex. -This separation of the right half of the visual field in the left optic TRACT and the left half of the visual field in the right optic TRACT is maintained in all the projections to the *subcortical nuclei* *The cross of the NASAL retinal fibers allows the entire hemifield of vision to be projected on the CONTRALATERAL visual cortex.* --- Lesions-> BLIND -Do left as left, right as right (Behind them) -Left 1/2 of visual fields processed in contra area-> Right V1 Cortex -When VF goes to lens-> gets inverted and flipped-> Retina will be split >Left visual field of left eye goes to *nasal hemi-retina* >Left visual field of right eyes goes to *temporal hemi-retina* -Cross at OPTIC CHIASM!!!! >Left half visual fields will joint at the optic chasm-> Drop glutamate at LGN -> Nasal fibers cross at optic chiasm

Photoreceptors

-Generate HYPERpolarization with light. -Have WEAK interactions with NEAR-by photoreceptors. -Receptive field defined by diameter of cell. -Do NOT fire APs

Retinal Ganglion Cells

*Spiking Cells* that can fire APs -Reflect the COMBINED signals from several photoreceptors and their interneurons. -Photoreceptors and interneurons display graded changes in membrane potential only >*Amacrine interneurons* may fire an occasional AP to boost electrotonic conduction of signal ->Know general idea -Retinal ganglion cells are never silent and are always *TONICALLY firing* >Light modulates the firing FREQUENCY of the ganglion cells. -Each retinal ganglion cell responds to and monitors light in a SPECIFIC area of the retina only. > Receptive fields of retinal ganglion cells are CIRCULAR

Eye movement control centers

*Supranuclear regulation* of eye movements found in brainstem, cerebellum, and forebrain including the basal ganglia -Brainstem Centers Controlling the eye movements: Pons and Midbrain

Near Point

*The CLOSEST point at which an object is CLEARLY seen* -The STRONGEST contraction of the ciliary muscle will FAIL to bring an object into focus if it is closer than the near point. -*Near point* is about 10 cm for normal humans under 30 years of age. -The NEAR point begins to recede in childhood and changes most noticeably in the mid-forties. ---- Both eyes turn (medial recti)-> closest object seen when close-> MAXIMAL contraction of ciliary muscle (lens still doesn't increase in power)

Visual Processing Pathways

*The pathways are interconnected and parallel* -Receptive fields become complex -Retinal disassembles image to contrast-> Lateral geniculate nucleus in Thalamus only relays the info-> Brodman's Area 17 (V1) processes info in Primary visual cortex (Puts the image back together)-> Sends to magnocellular or parvocellular pathway -1/2 on center 1/2 off center *Magnocellular System*: The WHERE MOTION -Parietal Lobe -Tracking where the motion is going-> Following it *Parvocellular System*: The WHAT motion -INFERIOR Temporal Lobe -Processes color: Interblob and blob system -Color and form-> High acuity ganglion (discrimination) --- Moving V2->V3->V4 etc becomes more complex for neuron to become fire= putting picture back together in cortex as retina disassembles the picture originally

Retinal image

*The retinal image (RI) is an inversion and reversal of the visual field (VF)* -Must distinguish between retinal image and visual field. -*Retinal image*: *Inverted and reversed* image of the visual field on the retina. >Retina divided into temporal hemi-retina (lateral to the fovea) and nasal hemi-retina (nasal to the fovea). -*Visual field*: View of the world by two eyes WITHOUT head movement. >Foveas of both eyes fixed on a single point in space allows the visual field to be divided into right and left halves. -Binocular zone -Mononclear zone

Accommodation (Near) Reflex

*To bring near objects in focus on the retina, a three part reflex is invoked using CN III* 1.) Lens refractive power INCREASES: accommodation-> PNS 2.) Pupil CONSTRICTS: INCREASES depth of field and SUPPRESSES optical aberrations-> PNS >DEPTH of focus: RANGE of distance from the eye in which an object appears CLEAR WITHOUT change in accommodation. >Depth of focus is INVERSELY proportional to pupil size. 3.) Eyes CONVERGE: Dysconjugate eye movement >Simultaneous CONTRACTION of medial recti muscles

The vestibular System

*Used during BRIEF or RAPID head rotation* This system generates the VOR (vestibular-ocular reflex) active all the time. -The VOR promptly compensates for natural head movements which are usually *rapid and transient* by generating an eye movement which is *equal and opposite* of the head movement in space. -This is ineffective with steady continuous rotations as the compensatory eye movements cease after 30 secONDS >ROTATORY nystagmus

Visual Cortex

*V1= Brodmann's area 17= striate cortex* -Occipital cortex is 2 mm THICK and has 6 layers of cells and lies on the banks of the *calcarine fissure* in the occipital lobe. -Retinotopic Map: The left visual hemifields of the left and right eyes are mapped to the primary visual cortex of the right (contralateral) cerebral hemisphere. -The fovea is mapped to the *occipital pole* -The axons from the *lateral geniculate neurons* terminate in *layer 4* of the visual cortex on pyramidal cells. 1.) The cortical pyramidal cells are projection neurons and they project to other brain regions as well as to interconnecting neurons in local areas

Midbrain and eye movements

*Vertical and vergence eye movement control centers= VV movements* VERTICAL: Vertical eye movements are initiated by a supranuclear center in the *rostral midbrain reticular formation and pretectal area* -This area controls the superior and inferior rectus muscles and the inferior and superior oblique muscles. -Dorsal region controls upward gaze >*Pineal tumor* or lesion of dorsal region causes impaired upward gaze -Ventral region controls downward gaze >Lesion of ventral region causes impaired downward gaze VERGENCE: Vergence eye movements are initiated in the *midbrain reticular formation* -This area controls the convergence (medial recti muscles) and divergence (lateral rectus muscles) of the eyeballs. -Descending control from *occipital and parietal cortex* control eye movements for near and far vision. >Parietal

Magnocellular System

*WHERE-> Parietal Lobe* Processes: -Motion and spatial relationships -Stereopsis ( 3-D vison)= DEPTH perception -This system works at seeing WHERE rather than WHAT (Tell coming toward you) Pathway: -Starts from the large *Magnocellular ganglion* cells in the retina. -Synapses in the magnocellular layers of the LGN. -Passes through *V2, V3, V4, V5* (middle temporal area - MT) to other cortical areas. -The neurons in this system are INSENSITIVE to color and color contrasts. >The neurons in this system respond RAPIDLY but transiently. -The analysis of depth, brightness, and texture is done rapidly but at LOW resolution.

opsin undergoes conformational change to...

*metarhodopsin II* -Active form of rhodopsin STIMULATES a G protein: *TRANSDUCIN* -Active form of rhodopsin QUICKLY breaks up into *opsin and all-trans retinal.* -All-trans retinal transported to the *retinal pigmented epithelium (RPE)* layer for isomerization back to *11-cis retinal* -The GTP bound, α subunit of transducin activates a phosphodiesterase (PDE) which hydrolyzes cGMP to GMP. -The photoreceptor response to light is to DECREASE THE CONCENTRATION OF THE SECOND MESSENGER and decrease cGMP. -Biochemical cascade is used to amplify this response. -Light ON: Activates Rodopsin-> Activates FIVE HUNDRED TRANSDUCIN molecules (AMPLIFICATION)-> 500 active transducin molecules-> Activate 500 PDE molecules -> Hydrolyzes 500,000 molecules of cGMP -The DECREASE in [cGMP] causes sodium channels to CLOSE, DECREASING the sodium current in the outer segment of the photoreceptor. -HYPERPOLARIZE

Retinal Layers (Picture)

-#1 cell= Rod or cone (Photoreceptors) >Light will cause HYPERPOLARIZATION-> becomes more negative (<-60mV) >Light becomes a receptor potential! -#2 cell= Bipolar Cell >2 processes -#3 cell- Ganglion cells >TRAVELS >In the inner layer >NOT myelinated so light can get thru axons >Axons release glutamate traveling to optic disc (To CN II) to THALAMUS (LGN) >Myelinated AFTER going down OPTIC DISC ->Oligodendrocytes -Optic disc (Diencephalon) >Blind spot: NO PHOTORECEPTORS >Dilate pupils give Atropine (block muscarinic cholinergic receptor) -Will see Dura mater, Arachnoid mater, subarachnoid space (CSF), and Pia Mater >Dura mater outer surface of optic disc (HARD) >After pia mater-> SEE AXONS -Aqueous humor: Clear watery liquid that supplies nutrients -Vitreous Humor: Thick, gelatinous substance-> maintains shape of eye and phagocytic cells that remove blood and other debris -Light will hit INNER layer-> go thru the layers-> Absorbed in the pigments (*Retinal Pigment Epithelium= RPE*) >Needed to see crisp images-> RPE absorbs light >Black absorbs light -Light goes to photoreceptors THEN will move up the layers to get to optic disc REMEMBER: Light goes from vitreous humor to RPE

CN VI lesion and MLF lesion

-A lesion of the abducens nerve will cause diplopia (CN VI palsy ipsilateral). -A lesion of the abducens nucleus will cause ipsilateral, lateral gaze palsy. >Will never be able to took laterally with the ipsilateral eye/Both eyes cannot look to the lesioned side -A lesion of the abducens nucleus AND ipsilateral MLF will cause ipsilateral, lateral gaze palsy AND an internuclear ophthalmoplegia (INO). >"one and a half syndrome." -A lesion of the cerebral hemisphere FEF (frontal eye field) will cause gaze to the side of the lesion ---- Supranuclear: Abducens nucleus, PPRF, FEF Infranuclear: Nerve or axon

Pupillary Abnormalities

-Aniscoria -Argyll Robertson Pupil -CN 3 Lesion -Horner's Syndrome

Retrochiasmal Lesions

-Areas of lesion include the optic tract, LGN, optic radiations, or visual cortex. -ALL lesions generally cause homonymous (the same region of the visual field for both eyes is involved) visual field deficits. -Lesions of the optic tract (relatively uncommon), entire optic radiations, or entire primary visual cortex on one side of the brain cause a *contralateral homonymous hemianopia* (D, G or H below).

Hypercolumn of the primary visual cortex

-Bring left and right eye together: Ocular dominant columns >L: Ipsi >R: Contra >L and R fuse vision of fields at V1 -Simple Cell for North and South in layer 5 -> gives ORIENTATION >Simple cells only fire in correct orientation >Cells in the V1 cortex detects edges based on convergence info from receptive fields -Blobs: Dispersed throughout >Fire within blob: See full of color >Fire outside of blob: NO color >First conscious recognition of color in the brain

Rhodopsin (Pathway)

-Cis fits -Trans does not fit -*Metarhodopsin II*: Activates G protein (Severeal minutes in living eye) -Doesn't last for too long -Trans must become 11-cis again (in 30 minutes) and combine with opsin to become rhodopsin ---- Chromophore is LIGHT LOVING-> 11-Cis -Source of vitamin A -Change in amino acid (help for seeing different wavelengths) can cause BLINDNESS

Near reflex triad

-Convergence of the eyes is one of three reflexes elicited by interest in a near object. -*Accommodation* of the lens: INCREASES lens STRENGTH to bring near objects into focus. (PNS). -CONSTRICTION of the pupil: sharpens the image on the retina and INCREASES the depth of field (PNS)

Off-center, on-surround ganglion cells

-Fire SLOWER/INHIBITED when light is directed to the center of the receptive field. -Fire faster when light directed to the surround of the center area. -Rapid INCREASE in firing rate indicates rapid DECREASE in light intensity. -Unresponsive to DIFFUSE light.

On-center, off-surround ganglion cells

-Fire faster when light directed to the CENTER of the receptive field. -Fire slower when light directed to the surround of the center area. -Rapid INCREASE in firing rate indicates RAPID increase in light intensity. -Unresponsive to DIFFUSE light. ---- Light on center= HIGH APs Light on surrounding: NO FIRING

Subcortical Nuclei

-Hypothalamus: Ganglion cell axons receiving information from photoreceptors containing *melanopsin* monitor NOT features but overall LIGHT levels. >The *suprachiasmatic nucleus* in the hypothalamus is the termination of the retinohypothalamic pathway. >Required for normal circadian rhythms. -*Pretectum in the diencephalon*: Controls pupillary light reflexes. >Also depends on photoreceptors containing melanopsin and monitors LIGHT levels. -*Superior colliculus*: Controls head and eye movements in response to visual and other sensory input. -*Lateral geniculate nucleus (LGN)* of the thalamus in the diencephalon: MAIN input to the visual cerebral cortex.

Vision

-Light waves must fall on sensory receptors: photoreceptors. -Photoreceptors must transduce light signal into electrochemical signal (Receptor Potential) RP. >With light hyper polarization (shine light = -90mV) -Nervous system must encode and analyze light signal. >CNII-> LGN (Thalamus) -> V1 (Occipital Lobe)

Horner's Syndrome (Pupil)

-Miosis caused by *loss of SNS innervation* of the *iris dilator muscle* -Impaired dilation of the pupil but still REACTIVE to light. -Massively LARGE pontine lesion (BILATERAL disruption of the descending sympathetic pathways) may result in *"pontine pupils"*= Both pinpoint pupils with REACTION to light

Interaction of photoreceptors, retinal interneurons, and ganglion cells.

-Photoreceptors synapse with bipolar cells. -Bipolar cells synapse with ganglion cells. -On-center bipolar cells synapse with on-center ganglion cells. -Off-center bipolar cells synapse with off-center ganglion cells. -*Ganglion cells spike or generate APs when THRESHOLD is reached*

Retinal pathway to primary visual cortex

-Primary visual cortex= Brodmann's area 17

Bipolar Cells

-Receptive fields similar to ganglion cells. -Concentric, mutually antagonistic -Do NOT fire APs

Horizontal Cells

-Respond to light with HYPERpolarization -Do not fire APs GEN

Retinotopic Map (Picture)

-Retinal receptive fields making circles on contrasted areas sending axons to LGN -LGN: "relay station" >Layers 2, 3, 5 ("2+3=5") >IPSI EYES -Converging on one cortical neuron from LGN-> cortical simple cell (Pyramidal Shape) >Go to layer IV of primary visual cortex -V1 cortex in LINGULA (Occipital Lobe) -Electrode of occipital lobe (North and South) >No APs East, west, Northeast, etc >Fires APs when put North and South

The right visual hemifield will project to the...

-Right eye: Nasal hemi-retina -Left eye: Temporal hemi-retina.

RAPD

-Sensory defects= CN2 -BEFORE the chiasm -*RAPD*: Relative afferent pupillary defect (Marcus Gunn Pupil)-> SWING flashlight -Lesion in the retina, eye, or optic nerve (BEFORE the optic chiasm) -Can be blind -DECREASED or absent light sensitivity in the AFFECTED eye with a failure of the two pupils to constrict

Near Points

-The closest distance an object can be placed and still be seen CLEARLY with accommodation -Age dependent

Ocular Motor System

-Two principle types of eyeball movements: >Eye movements that change the line of sight (CONSCIOUS) >Eye movements that keep the retinal image STEADY (UNCONSCIOUS) -ALL eye ball movements accomplished by the six muscles of each eye. >Muscular control of eye movements: In most eye movements, both eyes move together with three pairs of antagonistic muscles per eye >There is strong inhibitory interaction (reciprocal innervation) which is important in governing the motor nuclei for these muscles. >The movement of eye muscles is among the fastest in the body. T ->hey do not pull against gravity and always have the same mechanical load. -Binocular movements

The optical density of the two transparent media

-When light enters a medium of HIGHER optical density it is bent TOWARD a line *perpendicular* (normal) to the surface. -When light enters a medium of LOWER optical density it is bent AWAY from a line perpendicular (normal) to the surface.

Mechanics of saccadic eye movements

1.) There is a reaction DELAY of 200 msec between the appearance of the target of interest and the onset of eye movement. 2.) A typical saccadic eye movement *accelerates rapidly* reaching its peak velocity between one third and one half of the way through the movement. 3.) The eye gently *decelerates* but usually STOPS moving abruptly.

Relationship between the regions of the visual field and the retinal image

1.) upper half of visual field projects to the lower (inferior, ventral) half of the retina. 2.) Lower half of visual field projects to the upper (superior, dorsal) half of the retina. 3.) Right half of visual field projects to the left half of the retina. 4.) left half of visual field projects to the right half of the retina. Example: Damage to the INFERIOR half of the retina of one eye causes a monocular deficit in the UPPER half of the visual field of that eye.

Target Movement vs. Eye movement

1st: Sacchadic movements 2nd: Smooth pursuit movements FEF starts it off with catch up saccade PTO does movement consciously (Smooth pursuit-> conscious decision)

Retinal Ganglion Cell (Picture)

2 types of bipolar cells: AMPA and mGlu (1/2 of each receptors-> different receptors on bipolar cells) -Glutamate release ionotropically (AMPA, Canine, and NMDA) -Inhibition of Glutamate release metabotropically (mGLUR)

Transduction of light signal in the retina

3 Steps 1.) Transduction of light signal into a change in membrane CONDUCTANCE 2.) Change in membrane conductance into a change in *membrane potential (mV)* 3.) Change in membrane potential into a change in CODING of APs

Forebrain and Eye movements

Forebrain centers controlling eye movements send information from cerebral cortex to the brainstem centers and the superior colliculi. 1.) *Frontal eye fields*: Stimulate the PPRF and generate conjugate eye movements (*saccades*) to the *contralateral side* >Lesion of the frontal eye field causes both eyes to *gaze toward the lesioned side* >Conscious 2.) Parieto-occipito-temporal cortex (PTO) stimulates smooth pursuit *eye movements in the ipsilateral direction*-> TRACKING >3,4, and 6 Both are conscious movements (voluntary)

Anatomy of the Eye

Fovea: Cones >Pupil lines perfectly with it -Optic disc: NO CONES= BLIND SPOT >See with ophthalmoscope

Master Map of image (Diagram)

Fused and found feature details-> temporary findings of features-> 1 stimuli -First imagine the "Canvas": Color, size, distance, etc -Then specific area-> "lips"-> BOUND to a specific area (temporary binding)

A decrease in outer segment membrane sodium conductance causes....

HYPERPOLARIZATION of the photoreceptor -In the light INTRAcellular [cGMP] is LOW which keeps the sodium channels SHUT and slows or stops the steady inward sodium current. -This causes the photoreceptor to HYPERpolarize and reach a resting membrane potential of -60 mV in the light. -By hyperpolarizing the photoreceptor LESS glutamate transmitter is released from the photoreceptors to the bipolar and horizontal cells during the light.

Optical Abnormalities (Diagram)

Hyperopia (Top) Myopia (Bottom)

Increase in sodium conductance (Dark)

In the DARK INTRAcellular [cGMP] is high keeping sodium channels OPEN and a steady inward sodium current (Dark Current). -The sodium channel is a transduction channel in the cell membrane which is similar to a DIRECT ligand-gated channel. -It INCREASES NON-selectively cation conductance into the cell when there is a RISE in cGMP levels on the cytoplasmic side. -This keeps the photoreceptor DEPOLARIZED at a dark resting membrane potential of - 30 mV. -The DEpolarization of the photoreceptor maintains a steady release of GLUTAMATE from the secretory terminals of the cells in the dark.

Recognition of Complex forms

Inferior Temporal Cortex (ITC): Necessary for normal visual learning and perception (See differences between animals, faces, etc) -ITC removal impairs visual recognition of *shapes and patterns* only. -Other basic visual perceptions are OK (acuity, motion, color, etc). -ITC cells are selective for specific COMPLEX patterns. -Face recognition, etc. -Have very LARGE receptive fields 25°X 25° -Some cells respond to the ENTIRE visual field ---- Diagram showing Time vs APs in ITC >Top ITC only fires adequate stimulus to certain image-> need specific stimulus to fire >Electrode tells you adequate stimulus is a full fledged face ->Mixed faces won't stimulate as high ->Hand have little stimulus >Bottom ITC fires best when monkey face is to the side Damage can't recognize facial profiles

Depth of focus of eye (Large versus small)

Large depth of focus: -Pupil is constricted and the depth of focus is VERY LARGE >Move closer or farther away-> Still be in focus on the retina Small depth of focus: Depth of focus is SMALL-> Out of focus image on the retina

The left visual hemifield will project to the...

Left eye: Nasal hemi-retina Right eye: Temporal hemi-retina

Lens (Diagram)

Lens reverse and invert the image! -Pic should be reverse and inverted! -Visual field to retina >Lens will take superior part-> INVERTS it (Top of the visual field projected to bottom or INFERIOR part of the retina) -TOP VF goes to bottom retina (vice versa) >Bottom fibers damaged of retina-> SKY can't see! >Cuneate and Lingula (separated by calcarine fissure) ->Cuneate sees bottom VF ->Lingula sees top VF (damaged these fibers= can't see sky!)

Parvocellular System (Blob System) Lesion

Lesion of the *V4 cortex* results in the total LOSS of color vision= *achromatopsia* -No recognition of color: Cones work fine but when get here then there is a problem -SHADES OF GRAY= Monochromatic world

Bitemoporal hemianopsia

Lesion of the CROSSING axons from the nasal hemiretinas that carry information about the TEMPORAL visual fields Lesions caused by MID-sagittal transection or pressure from pituitary tumor, hypothalamic tumor Nasal fibers are in trouble!

Prechiasmal

Lesions PRIOR to the *optic chiasm* -Lesion of the retina = *Monocular scotoma* -If SEVERE enough could cause lesion of the entire retina (monocular vision loss). -Lesion of the optic nerve = *Monocular vision loss* -Lesions include: Glaucoma, optic neuritis, ELEVATED intracranial pressure

Mononuclear Zone

Light from EXTREME TEMPORAL portions of the visual field projects ONLY to the one ipsilateral nasal hemi-retina.

Binocular Zone

Light from central region of the visual field enters BOTH eyes -A single point on the binocular portion of one visual hemifield projects onto different regions of the two retinas. Ex: A point of light in the binocular half of the left visual hemi-field falls upon the nasal hemiretina of the left eye and the temporal hemiretina of the right eye.

Refraction

Light rays passing from one medium to another will change their VELOCITY 1.) The *refractive index* is a measure of optical DENSITY. (Speed in air/speed in glass)

Vergence eye movements

MIDBRAIN Vergence eye movements align the fovea of each eye with targets located at different distances from the observer. -Only type of eye movement which causes the eyes to move in OPPOSITE directions >vergence eye movements are disjunctive (disconjugate) eye movements -Line of sight for each eye CONVERGES with NEAR object of interest and DIVERGES with FAR object of interest.

Demyelination of oligodendrocytes can lead to...

Multiple Sclerosis -Sensory problem= *Temporarily Blind* >Oligodendrocytes will try to re-myelinate Myelinated AFTER the optic disc

Far and Near points

Myopia: Can't see at distance because image FAILS in front of retina (Far point affected) Normal: Far and near points are fine Hyperopia: Close vision deficient (near point affected) -INCREASES lens strength further >Cannot see neared-> image now falls behind retina

Accommodation Response

NEAR vision or object moving from far to near -*Pupillary Constriction*: Activated by signals from the visual cortex to the *pretectal nuclei* and *Edinger-Westphal nuclei:* >*Supranuclear* control of pupils by *occipitomesencephalic pathways* -20 feet/ 6 meters

Lesions at the optic chiasm

NON-homonymous deficit in vision-> Two different parts of the visual field are DEFICIENT following ONE lesion -Bitemoporal hemianopsia -Binasal hemianopsia

Near point and far point (Diagram)

Near point: Can't see nearer-> image now FALLS behind the retina >Cannot focus and will be a BLURRY circle Far point: Don't need ACCOMMODATION and image falls on retina

Extraocular Eye Muscles

No UMNs for the CN III, IV, and VI CN III: Superior Rectus, Inferior Rectus, Medial Rectus, Inferior Oblique CN IV: Superior Oblique CN VI: Lateral Rectus

Subcortical Nuclei (Picture)

Occipital lobe includes: -Cuneate -Lingula -Nasal hemi-retina cross contralaterally at optic chasm-< will pass areas such as hypothalamus, pre-tectum, superior colliculus >90% of fibers go to LGN (Layers 2,3, and 5-> relay) >Out and around, posterior to V1 (OPTIC RADIATIONS to Lingula and cuneate) >Fibers that end up in Lingula= *Meyer's Loop* ->That part of the optic radiation that runs in the caudal portion of the temporal lobe.

On-center, off-surround ganglion cells VS. Off-center, on-surround ganglion cells

On Center Ganglion Cell: Neurons INCREASE firing when there is a spot of light in the CENTER of their receptive field and the rest of their receptive field is DARK. -Light: Causes EPSP to increase on bipolar cell as there is NO mGlu causing NO Hyperpolarization-> K+ stay inside the cell allowing for DEPOLARIZATION without elevated glutamate -Dark causes increase in glutamate BUT IPSPs form= mGlu receptor (causes hyper polarization-> K+ opens) Off Center Ganglion Cell: These neurons INCREASE their firing when there is a RISE of light on the periphery of their receptive field and the center of the field is DARK. -Light will cause IPSP to release-> ganglion cell is hyperpolarized -Dark will cause depolarization (glutamate release increases) >AMPA receptor present: Glutamate released in the dark-> EPSP!

Papilledema

Optic disc SWELLING that is caused by increased intracranial PRESSURE. -HIGH PRESSURE -Optic disc will move forward -Do not puncture because will cause LOW resistance!

Pupillary Control

Pupillary constriction with light-> Best seen in DARK conditions (extra-geniculate pathway) -Shine spot of light into right eye -Light activates retinal ganglion cells of the right retina and fibers (CN 2) project to both right and left (BILATERALLY) optic tracts (cross over at the optic chiasm). -Fibers in the *extrageniculate pathway* continue in the brachium of the superior colliculus (PAST the lateral geniculate nucleus) to synapse in the pretectal nuclei just rostral to the midbrain. -After synapsing in the pretectal area, the fibers continue BILATERALLY (in the posterior commissure) to the *Edinger-Westphal nucleus* -The postganglionic PNS innervation causes the pupillary *constrictor muscles* to contract and the pupils become smaller (*miosis*). -NOTE: the light shone in the right eye causes the DIRECT RESPONSE in the same eye and a *CONSENSUAL RESPONSE* in the left eye because information crosses bilaterally at MULTIPLE levels EXTRA-geniculate pathway involved NOT LGN!

Binasal hemianopsia

RARE 1.) Lesion of the NON-crossing axons from the temporal hemiretinas that carry INFO about the NASAL visual fields. 2.) Lesion caused by *calcified internal carotid arteries* (ONE carotid artery?).

Major differences between the photoreceptor neural system:

RODS -LOW acuity -High convergence -Achromatic -ONE photopigment-> *Rhodopsin* ---- CONES -HIGH acuity -LOW amount of convergence -Concentrated in FOVEA -Chromatic -3 photopigments-> 3 cone opsins (basis for color vision)

Pre-attention Process

Rapid SCAN will detect objects and basic elementary visual properties. -Color, orientation, size, and direction of movement -"Feature maps"

Receptive fields of retinal ganglion cells

Receptive fields of retinal ganglion cells are CIRCULAR -Smallest receptive fields are in the *fovea* 0.25 mm= 1o >Just cone->bipolar->ganglion (SMALL) -Largest receptive fields are in the periphery where activity is low 3 o to 5 o >RODS -Ganglion receptive fields are NOT homogeneous. -There is lateral INHIBITION to promote contrast within receptive fields. -Each receptive field has a circular center zone and an antagonistic surround zone.

Visual System

Reflects KEY characteristic of the visual system: The retinal cells signal CONTRAST rather than absolute intensity of light On-center, off-surround ganglion cells OR Off-center, on-surround ganglion cells -- Brain only attends contrasted areas

Retinal Detachment

Retina PEELS away from its underlying layer of support tissue -Initial detachment may be localized or broad, but without rapid treatment the entire retina may detach, leading to vision loss and *blindness* -Get patient so can get retinal layer back against RPE >Put heavy gas bubble to hold it and get it back-> REPAIR-> CAN SEE AGAIN!

Oculomotor system (Fovea and Retina)

The oculomotor system functions to keep the fovea in the retina directed and fixed on the subject of interest -The fovea is the region of the retina with the *greatest acuity* and the oculomotor system effectively keeps *images centered on this small region* (about 5 degrees), even though we have a LARGE visual field (about 200 degrees). -Images moving over the retina at velocities as LOW as a few degrees per second can degrade visual acuity. >Micro-eye movements keep the image steady on the retina. -Since our eyes (retinas) are fixed to our heads, unwanted, unexpected head movements are the disturbance that is most likely to affect our vision. >For best vision, even the tiny cardiac pulsations (VOR) transmitted to the head must be compensated for. -Class of eye movements: >Vestibular (VOR) >Optokinetic >Smooth pursuit >Nystagmus quick phages >Saccades >Vergence

Rhodopsin

The photopigment *rhodopsin* is an INDIRECT ligand-gated transmembrane receptor located on the INTRAcellular disk membranes of rods. -Composed of a protein: *opsin and a chromophore*: RETINAL= the ligand. -*Retinal* is the light absorbing, aldehyde form of *vitamin A (carrots)*. >Deficiency of vitamin A (retinol) leads to *night blindness*. -Prebound ligand (retinal) is INACTIVE and is waiting for a photon of light to isomerize and become active. -Retinal *nonactive form in the DARK*: 11-cis isomer of retinal. -*Retinal active form in the LIGHT*: ALL-trans isomer of retinal. -In active state retinal NO LONGER FITS into its binding site in opsin (photoisomerization).

Blind Spot

The region of visual space that falls on the optic disk -Due to the lack of photoreceptors in the optic disk, objects that lie completely within the blind spot are not perceived.

Vestibular Nystagmus

The trace shows eye position of a subject in a chair rotated (right) clockwise at a constant rate in the dark -At the beginning of the trace the eye moves SLOWLY at the same speed as the chair (slow phase) and occasionally make RAPID resetting movements (QUICK phase). -The speed of the slow phase GRADUALLY decreases until the eye NO LONGER moves regularly. --- Head moves right-> endolymph and eyes move to the left (eyes will RESET to the right-> rotatory nystagmus) ->Not occur if unconscious >Slow eye movements (compensatory-> will cause the eye movements to lag behind with endolymph) >The "reset" saccadic movements will be to the right

VOR

The vestibulo-ocular reflex -A human subject's *horizontal eye position* as he is rotated rightward in total darkness. -Horizontal position is plotted against time. -Eye position is always plotted as degrees of rotation. -The subject begins to rotate at 50 degrees per second and the eyes move LEFTWARD to hold the eyes still in space. -Note that the eyes move in the direction OPPOSITE to the head. -When the eyes become too eccentric they move BACK toward the center of the orbit with a quick phase movement. -The reflex gradually habituates and has DISAPPEARED by about 30 seconds. EYE space= EYE orbit + HEAD space -Image is steady on FOVEA

VOR (General)

UNCONSCIOUS (Very fast) Vestibulo-ocular reflex To hold images of the seen world STEADY on the retina during brief head movements CN 8 involved

Right eye position vs left eye position (mergence graph)

Vergence eye movements induced during binocular viewing conditions. -Eye movements were recorded by electro-oculography (EOG), -The time scale, at top, is in seconds. A.) The subject alternates fixation between a far (F) and a near (N) target located in the midsagittal plane. >They are combined with saccades to realign the visual axes. B.) The subject fixates the examiner's finger as it is slowly brought in along the midsagittal plane toward the subject's nose and then out again. >Small saccades are superimposed upon the vergence movement. --- MR-> Near LR-> Far B-> Blinking= may see artifacts

Luminance (Graph)

Wiede range of intensities -CONES >Help see good color vision and best acuity >*Scotopic vision range*: Vision of DIM light where only RODS function >Reach saturation= BLEACHED (white colored) -Mesopic: Vision in light levels at which RODS and CONES function -RODS >No color vision >POOR acuity >Photopic: High light levels only mediated by cone cells