Visual System Flashcards
1/2 of Brain Mass Devoted to Visual Processing
- vast amount of usable information
- Perception: occipital cortex
- Visual memory: parietal & temporal lobes
- Brain stem/spinal cord: visual reflexes
- Circadian rhythm, general metabolic rate, hormonal function, mood- pineal gland & diencephalon
Visual Testing
- easily administered
- locates the lesion
- cognitive status: visual memory
- motor reflexes: postural reflex
- autonomic function: pupil dilation
- inner ear problem: eye movement
Incoming Light from Object of interest?
- focused on fovea
- refracted by cornea
- inverted through pupillary opening
- variably refracted by the lens (under control of suspensory ligaments/ciliary muscles)
- Projected on the fovea (pit) in center of the macula
Sclera
protection
Choroid
vascular layer, high blood flow
Fovea
devoid of blood vessels
Extraocular Muscles
-maintain visual axis on fovea
Retina
- external view of blood vessels & neural tissues
- more cell types than most organs
- retinal pigmented epithelial cells (pigment cells)
- provide barrier to retina from the choroid
- photoreceptors (cones & rods) come in contact with the RPE (cell bodies located in outer nuclear layer with projections lying in outer plexiform layer
- photoreceptor signal through the outer plexiform layer to the bipolar cells, whose cell bodies are in the inner nuclear layer, final layer of neurons are retinal ganglion cells
Regional Differences in the Retina
- photoreceptors line outermost surface
- pigmented epithelium support photoreceptors
- retinal pathway: photoreceptors to bipolars to ganglion cells
- Interneurons: horizontal cells (outer plexiform) amacrines (inner plexiform)
- ganglion cell axons coalesce to form optic nerve head; blind spot
- Fovea: all cellular elements except outer segments are displaced radially
Retinal Pigmented Epithelium
- layer that separates the choroid (vascular) from retina (neural)
- contains black pigment-melanin
- diseases of retina often affect tight junctions b/w the RPE and the retina-allows substances to leak in & out
- phagocytosis of outer rod segments, retinal nutrition, & protection of photoreceptors from light damage
Drusen
- autoflurescence from the dec. in effectiveness of RPE to eat rod outer segments every 10 days (more proteins left in RPE)
- key factor in dry macular degeneration
Rods
- named for shape of outer segment
- process Black & White (scotopic) info
- light is detected & transduced in outer segment
- synaptic expansion called the spherule
- rod outer segments undergo phagocytosis-with a new outer segment being formed approximately every 10 days
Cones
-named for shape of outer segment
-process color (photopic) info
-3 types of cones:
L-cones-long wavelengths (red)
M-cones-medium wavelengths (green)
S-cones-short wavelengths (blue)
-each of these responds to different color of light
-every color is represented by a unique combination of L,M, & S cones
-if one type of cone is absent b/c of genetic defects - person will be missing the corresponding opsin = color blind
-M & L
Function of Photoreceptors
- purpose is to absorb quanta of light & convert to an electrical signal
- both cones & rods undergo hyperpolarization in response to light
- only sensory system in which hyperpolariation is the response to stimulus
Visual Steps of Rods
- light in & converst 11-cis-retinal to all-trans retinal which activates the rod opsin (rhodopsin)
- active rhodopsin can activate GTP (activates cGMP phosphodiesterase)
- Active PDE lowers cGMP levels to hyperpolarize the membrane & close sodium & calcium channels (visual response)
- Na & Ca stuck in membrane, Ca begins to be pumped out through the Na/Ca exchanger, as Ca dec. cGMP levels rise & re-polarize the membrane to pre-stumulus levels (channel re-opens)
- SLOWLY: rhodopsin is dephosphorlated and all-trans-retinal is converted back to 11-cis-retinal
- now rhodopsin kinase comes back to re-phosphorylate rhodopsin which is bound by arrestin to render it inactive REPEAT
Phototransduction in cones
-simular to rods except there are 3 opsins with each corresponding to retinal in a specific manner
Bipolar Cells
- High deg. of convergence - 100 million receptor cells synapsing onto 1 million ganglion cells
- at the bipolar-ganglion cell synapse, amacrine cell synapse, amacrine cells detect major changes in activity levels
- cones & rods have their own bipolar cells with cone bipolar cells in the central retina & rod in the periphery
Ganglion Cells
- alpha: predominate in peripheral retina (most input from rods)
- extensive dendritic trees
- large axons
- participate little in color perception
- project to Magnocellular layer of lateral geniculate nucleus (location of object in space) - beta: primarily in central retina
- small receptive fields
- small dendritic arbors
- responsive to color stimuli
- project to parvocellular region in lateral geniculate nucleus - define color & texture of object
Fovea
- 1 photoreceptor/1 ganglion cell
- allows for crisp image representation
Central Visual Pathways
- visual image is reversed & inverted due to pinhole effect of pupil
- 180deg. visual field viewed by both eyes except 45deg. peripherally due to nose
- ganglion cell axons in optic nerve partially decussate in optic chiasm (only nasal fibers cross)
- optic tract projects to lateral geniculate
- optic radiations carry geniculate fibers to primary visual cortex in occipital lobe (all fibers are retinotopically organized)
- Left visual field is processed by right visual cortex
Visual Cortex Information
- cells that respond perferentially to input from one eye(ocular dominant) are segregated into layers in the lateral geniculate & the visual cortex
- the M pathway originates from magnocellular ganglion cells, projects to lateral geniculate layers 1 and 2, to layer 4C-alpha in cortex (space info)
- the P pathway originates from parvocellular ganglion cells, projects to lateral geniculate layers 3-6, to layer 4C-beta in cortex (form info)
Vision Related Diseases
- age related macular degeneration
- inherited retinal degeneration
- glaucoma
- retinal detachment
- diabetic retinopathy
- vascular insults
- multiple sclerosis
- pituitary tumor
- cortical infarctions/tumor
- visual migraines
What causes DR?
- Changes in vasculature
- angiogenic growth factors
- loss of angiostatic growth factors - Changes in neurons
- loss of photoreceptors
- loss of ganglion cell
Don’t Know!
Macular Degeneration VS Diabetic Retinopathy
AMD: DR:
Choroid NV retina NV
age induced no age effect
some genetic some genetic
lose central vision lose all vision
Dry AMD VS wet AMD
Dry AMD: Wet AMD:
Drusen Sometimes drusen
little vision loss vision loss
often in 1 eye progresses to both eyes
can progress to wet
Causes of AMD?
Treatments?
age
smoking
genetics
changes in angiogenic & angiostatic factors
Treatments:
laser coagulation
anti-angiogenic therapies: Avastin & Macugen
Scotomas
-blind spot that moves exactly as the eye moves
Floaters
-float around eye even when eye movement stops
Amblyopia
-“lazy eye”
Causes of Vision Loss
- Refractive Error
- Vitreous
- Cornea/Tear Film Anterior Chamber
- Optic Nerve or Optic Tract or Macula Chiasm
- Optic Radiations
- Occipital Cortex
“amaurosis fugax”
fleeting loss of vision
- transient ischemic attacks affecting vision in one eye for 5-10 min.
- result of platelet thrombin emboli from atheromatous plaques in the carotid artery on the same side
Loss of vision in both eyes simultaneously
-basilar artery insufficiency
Ocular History of Visual Loss
- loss in 1 or 2 eyes
- loss at distance and near
- gradual or sudden
- previous problem “lazy eye” trauma
- loss transient, recurrent, or constant
- pain?
- when was last eye exam?
Gradual, Progressive loss of vision?
-brain tumor
Sudden loss of vision in 1 eye?
- Older adults: vascular
- Younger: optic neuritis
Most common Causes of blurred vision?
-due to ocular problems
need glasses, cataract, macular degeneration, amblyopia, trauma
Visual Acuity
-Ability to Read standard size letters/symbols at specified distance
-Snellen chart (20 feet)
-VA Designated as Fraction (20/20 - normal)
numerator = testing distance
denominator = letter/symbol size
-patient wears glasses, read smallest line they can
-if unable to read largest letter, move patient closer
-this number becomes the numerator of the visual acuity fraction & the size of largest letter is bottom
( fingers, hand motion, light perception, no light)
Pupil Examination
- size in mm (each eye, symmetry)
- shape (round & regular)
- evaluate direct light reflex
- evaluate consensual light reflex
- check for afferent pupillary defect
- evaluate near reflex
Relative Afferent Pupillary Defect
- Extremely Important Pupil Sign
- If no retinal lesion seen, indicates an optic nerve conduction defect
- may be + (abnormal) even with normal disc and good VA
- if abnormal, additional study required
Test for RAPD
-normal is each pupil constricts as you move the light on them
Visual Field Examination
- confrontation - comparing patients VF to examiner
- Helpful at bedside, ER, office
- Methods: Finger Counting or Wiggling
-do not expect to find subtle VF defects by confrontation testing
Visual Field Defects
-Retinal or Optic Nerve lesion produces scotoma in 1 eye
-chiasmal compression produces bitemporal hemianopsia
-lesions behind chiasm produce homonymous hemianopsia (HH)
congruous HH - Occipital Cortex
Incongruous HH - More anterior
Optic Neuritis
- usually occurs in young, middle aged adults
- sudden loss of vision in one eye
- may have pain on motion of eye
- afferent pupillary defect present
- central visual field defect
- color desaturation in affected eye (RED)
- disc normal or swollen
Optic Neuritis: Signs & Treatment
- Retrobulbar ON - Optic Disc normal
- Papillitis - Optic Disc Swollen
- Vision loss progress over 10-14 days
- improves over 3 or more weeks
- prognosis for vision return good > 90%
- Treatment: +/- IV Corticosteroids
Importance of Optic Neuritis
- frequently seen in Multiple Sclerosis
- Patients presenting with optic neuritis may develop MS later
Evaluation: Neurological Examination
MRI
CSF Analysis
Lesion of Chiasm
- reduced VA 1 or 2 eyes
- bitemporal hemianopsia - asymmetric
- may develop optic atrophy - asymmetric
- most common cause - pituitary adenoma
- other causes - Meningioma, Craniopharyngioma, Aneurysm
Post Chiasmal Lesions
- produces Homonymous Hemianopsia
- Central Visual Acuity Good Unless Optic Tract Involved
- No Afferent Pupillary Defect Unless Optic Tract Involved
- No Optic atrophy unless optic tract involved
- may or may not have papilledema
- look for other neurological signs
Examination of Ocular Fundus
- margins of disc sharp?
- disc flat or elevated?
- disk color pink?
- disc pallor or hyperemia?
- spontaneous venous pulsations?
- optic cups normal size?
Optic Disc
- color
- contour
- circumference (margins)
- cup size
- spontaneous venous pulsations
- retina/vessels
Papilledema
- bilateral swelling of the optic discs secondary to increased intracranial pressure (ICP)
- indicates serious neurological problem
- evaluate patient immediately
- must exclude brain tumor & pseudotumor cerebri
- visual acuity normal
- visual field full with enlarged blind spot
- no pain on eye movement
- no afferent pupillary defect
- headaches, nausea, & vomiting: common due to the inc. ICP
- +/- 6th cranial nerve palsy
Signs of Papilledema
- both discs elevated & hyperemic
- disc margins blurred, indistinct
- small vessels at margin obscured
- retinal vessels tortuous, dilated
- hemorrhages & exudates
- spon. venous pulsations ABSENT
Ischemic Optic Neuropathy
- acute loss of vision in older patient
- usually only one eye
- afferent pupil defect present
- disc is swollen and PALE
- ischemia of disc (small vessel occlusion)
- altitudinal hemianopsia common
- must R/O Temporal Arteritis
Optic Atrophy
- suggested by pale color of disc
- usually poor vision & visual field defect
- may be caused by lesion in retina, optic nerve, chiasm, or optic tract
- multiple causes
- atrophy with large optic cups (usually open-angle glaucoma)
Chronic Open Angle Glaucoma
- ocular disease usually associated with inc. IOP
- optic nerve is damaged
- characterized by enlargement of optic cup & eventual pallor (atrophy)
- early visual field loss (asymptomatic)
- loss of central vision - LATE
Strabismus: Paralytic
non-comitant
- adult
- angle of deviation varies in different fields of gaze
- diplopia
- no amblyopia
- muscle weakness identified
Strabismus: Non-paralytic
comitant
- early childhood
- angle of deviation remains constant in different fields of gaze
- no diplopia
- amblyopia
- no muscle weakness identified
Tropia
- visible deviation always
- ESOtropia - inward “crossed eyes”
- EXOtropia - outward “wall eyes”
- HYPERtropia - upward
- HYPOtropia - downward
Phoria
-aligned unless fusion
Tests to verify Ocular Alignment
- Alternate Cover Test: cover 1 eye, then the other, look for motion of the eye that has just been uncovered
- Light Reflex Test: observe symmetry of corneal light reflexes
Duction
- movement of one eye
- Adduction: move in toward nose
- Abduction: move out toward ear
- Supraduction (elevation) move up
- Infraduction (depression) move down
Version
- movement of both eyes in same direction
- Dextroversion: right gaze
- Levoversion: left gaze
- Supraversion: up gaze
- Infraversion: down gaze
Evaluation of Eye Movements
- Versions or Ductions
- have patients keep head still
- have patient follow a light or your finger into the 6 cardinal positions
- move slowly
Vergence
-movement of both eyes in opposite directions
-Convergence: movement of both eyes toward nose (IN)
near reflex - convergence, accommodation, Miosis
-Divergence: movement of both eyes away from the nose (out)
divergence poorly developed in humans except to return from converged position
Intorsion
- rotation of the 12 o’clock position of the cornea toward the nose
- superior rectus & superior oblique muscles are intorters
Extorsion
- rotation of the 12 o’clock position of the cornea away from the nose
- inferior rectus & inferior oblique muscles are extorters
Vertical Alignment of Eyes
- Anatomy of Muscle Origins & Insertions is the Key to Understanding this concept
- The Primary, Secondary, & Tertiary Actions of the Vertical Recti & Obliques, Depend on Whether the Eye is Abducted or Adducted
Nystagmus
-to & fro, oscillations of eyes (horizontal, vertical, rotary)
Jerk Nystagmus
-slow then fast recovery (neurologic)
Pendular Nystagmus
-equal amplitude to & fro (poor vision)
Diplopia
- double vision
- sees 2 images with both eyes open
- differentiate from monocular diplopia (ocular causes)
- indicates acquired weakness from EOM
- Commonly III, IV, or VI Nerve Palsy
- Deviation varies with Gaze Direction
- deviation greatest in direction of action of weak muscle
- look for maximal under action of EOM in one field of gaze
Horizontal Diplopia
-weak LR or MR
Vertical Diplopia
-Weak SO, IO, SR, IR
Cranial Nerve III Palsy
(oculomotor)
- weakness or MR, SR, IR, IO
- Ptosis (weakness of Levator)
- Non-reactive pupil (Sphincter)
- Eye is down & out
- may be partial or total
- Serious Clinical Sign
Posterior Communicating Artery Aneurysm
- important cause of III nerve palsy with pupil involved
- III nerve palsy + headache is aneurysm until proven otherwise - image immediately
Microvascular III Nerve Palsy
- III Nerve Palsy with Normal Pupil
- Usually Middle-aged or Elderly Patient
- Diabetes or HTN Common
- May have Mild Pain at Onset
- Recovery WIthin 3 to 4 months
Cranial Nerve VI Palsy
(abducens)
-weakness of LR with ESOtropia
-ESOtropia and Diplopia Inc. on gaze to the side of the lesion
-non-localizing neurologic sign
Causes: inc. ICP, Tumor, Trauma, Stroke, Microvascular
Cranial Nerve IV Palsy
(trochlear)
-paresis or superior oblique muscle
-produces vertical or oblique diplopia
-spontaneous head tilt to opposite side
Causes: head trauma, microvascular, congenital
-hypertropia on side of weak SO
-Diplopia & deviation inc. on gaze to side opposite weak SO
-diplopia & deviation inc. on forced head tilt to same side as weak SO
